Tokushima University / Educator and Researcher Directory --- Yamazaki, Naoshi

Personal Web Page

https://researchmap.jp/read0183917 (researchmap)

https://orcid.org/0000-0002-5950-134X (ORCID)

Field of Study

○	Molecular and Cellular Biology

Subject of Study

○	遺伝子発現調節，生体エネルギー産生機構 (gene expression, U1 snRNA, RNAスプライシング, brown adipose tissue, carnitine)

Book / Paper

Book:

1.	Yasuo Shinohara, Kazuaki Kajimoto, Naoshi Yamazaki and Hiroshi Terada : ミトコンドリア学(内海耕造・井上正康監修), KYORITSU SHUPPAN.CO.,LTD, Tokyo, Nov. 2001.
2.	Naoshi Yamazaki, Yasuo Shinohara and Hiroshi Terada : ミトコンドリア学(内海耕造・井上正康監修), KYORITSU SHUPPAN.CO.,LTD, Tokyo, Nov. 2001.
3.	Naoshi Yamazaki and Hiroshi Terada : タンパク質と核酸の分離精製(寺田弘編集), 株式会社廣川書店, Tokyo, Jun. 2001.

Academic Paper (Judged Full Paper):

1.	Tsutsumi Toshihiko, Taira Satoshi, Matsuda Risa, Kageyama Chieko, Wada Mamiko, Kitayama Tomoya, Morioka Norimitsu, Morita Katsuya, Tsuboi Kazuhito, Naoshi Yamazaki, Jun-ichi Kido, Toshihiko Nagata, Dohi Toshihiro and Akira Tokumura : Lysophospholipase D activity on oral mucosa cells in whole mixed human saliva involves in production of bioactive lysophosphatidic acid from lysophosphatidylcholine., Prostaglandins & Other Lipid Mediators, Vol.174, 106881, 2024.
2.	Naoshi Yamazaki, Chiho Ohtsuka and Kentaro Kogure : Weak electric current increases ceramide levels by inducing ceramide synthase expression, Journal of Asian Association of Schools of Pharmacy, Vol.13, 1-5, 2024. (Link to Publication Site) ● Publication site (DOI): 10.62100/jaasp.2024.13101 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.62100/jaasp.2024.13101 (DOI: 10.62100/jaasp.2024.13101)
3.	Kiri Akieda, Kazuto Takegawa, Takeshi Ito, Gaku Nagayama, Naoshi Yamazaki, Yuka Nagasaki, Kohei Nishino, Hidetaka Kosako and Yasuo Shinohara : Unique Behavior of Bacterially Expressed Rat Carnitine Palmitoyltransferase 2 and Its Catalytic Activity, Biological & Pharmaceutical Bulletin, Vol.47, No.1, 23-27, 2024. (Summary) Mammalian type 2 carnitine parmitoyltransferase (EC 2.3.1.21), abbreviated as CPT2, is an enzyme involved in the translocation of fatty acid into the mitochondrial matrix space, and catalyzes the reaction acylcarnitine + CoA = acyl-CoA + carnitine. When rat CPT2 was expressed in Escherichia coli, its behavior was dependent on the presence or absence of i) its mitochondrial localization sequence and ii) a short amino acid sequence thought to anchor it to the mitochondrial inner membrane: CPT2 containing both sequences behaved as a hydrophobic protein, while recombinant CPT2 lacking both regions behaved as a water soluble protein; if only one region was present, the resultant proteins were observed in both fractions. Because relatively few protein species could be obtained from bacterial lysates as insoluble pellets under the experimental conditions used, selective enrichment of recombinant CPT2 protein containing both hydrophobic sequences was easily achieved. Furthermore, when CPT2 enriched in insoluble fraction was resuspended in an appropriate medium, it showed catalytic activity typical of CPT2: it was completely suppressed by the CPT2 inhibitor, ST1326, but not by the CPT1 inhibitor, malonyl-CoA. Therefore, we conclude that the bacterial expression system is an effective tool for characterization studies of mammalian CPT2. (Keyword) Animals (Tokushima University Institutional Repository) ● Metadata: 115728 (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b23-00612 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38171776 ● Search Scopus @ Elsevier (PMID): 38171776 ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.b23-00612 (Tokushima University Institutional Repository: 115728, DOI: 10.1248/bpb.b23-00612, PubMed: 38171776)
4.	Toshihiko Tsutsumi, Kohei Kawabata, Naoshi Yamazaki, Kenji Tsukigawa, Hiroyuki Nishi and Akira Tokumura : Extracellular and intracellular productions of lysophosphatidic acids and cyclic phosphatidic acids by lysophospholipase D from exogenously added lysophosphatidylcholines to cultured NRK52E cells, Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, Vol.1868, No.9, 159349, 2023. (Summary) Lysophosphatidic acid (LPA) is a bioactive lysophospholipid that is a notable biomarker of kidney injury. However, it is not clear how LPA is produced in renal cells. In this study, we explored LPA generation and its enzymatic pathway in a rat kidney-derived cell, NRK52E cells. Culturing of NRK52E cells with acyl lysophosphatidylcholine (acyl LPC), or lyso-platelet activating factor (lysoPAF, alkyl LPC) was resulted in increased extracellular level of choline, co-product with LPA by lysophospholipase D (lysoPLD). Their activities were enhanced by addition of calcium ions to the cell culture medium, but failed to be inhibited by S32826, an autotaxin (ATX)-specific inhibitor. Liquid chromatography-tandem mass spectrometric analysis revealed the small, but significant extracellular production of acyl LPA/cyclic phosphatidic acid (cPA) and alkyl LPA/cPA. The mRNA expression of glycerophosphodiesterase (GDE) 7 with lysoPLD activity was elevated in confluent NRK52E cells cultured over 3 days. GDE7 plasmid-transfection of NRK52E cells augmented both extracellular and intracellular productions of LPAs (acyl and alkyl) as well as extracellular productions of cPAs (acyl and alkyl) from exogenous LPCs (acyl and alkyl). These results suggest that intact NRK52E cells are able to produce choline and LPA/cPA from exogenous LPCs through the enzymatic action of GDE7 that is located on the plasma membranes and intracellular membranes. (Keyword) Choline / Cyclic phosphatidic acid / Glycerophosphodiesterase 7 / lysophosphatidic acid / Lysophosphatidylcholine / NRK52E cells (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbalip.2023.159349 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37295607 ● Summary page in Scopus @ Elsevier: 2-s2.0-85161996639 (DOI: 10.1016/j.bbalip.2023.159349, PubMed: 37295607, Elsevier: Scopus)
5.	Kazuto Takegawa, Takeshi Ito, Atsushi Yamamoto, Naoshi Yamazaki, Mitsuru Shindo and Yasuo Shinohara : KH-17, a simplified derivative of bongkrekic acid, weakly inhibits the mitochondrial ADP/ATP carrier from both sides of the inner mitochondrial membrane, Chemical Biology & Drug Design, Vol.101, No.4, 865-872, 2023. (Summary) Two natural products, bongkrekic acid and carboxyatractyloside, are known to specifically inhibit the mitochondrial ADP/ATP carrier from its matrix side and cytosolic side, respectively, in concentration ranges of 10-6 M. In the present study, we investigated the manner of action of a synthetic bongkrekic acid derivative, KH-17, lacking three methyl groups, one methoxy group, and five internal double bonds, on the mitochondrial ADP/ATP carrier. At slightly acidic pH, KH-17 inhibited mitochondrial [3 H]ADP uptake, but its inhibitory action was about 10 times weaker than that of its parental compound, bongkrekic acid. The main site of action of KH-17 was confirmed as the matrix side of the ADP/ATP carrier by experiments using submitochondrial particles, which have an inside-out orientation of the inner mitochondrial membrane. However, when we added KH-17 to mitochondria at neutral pH, it had a weak inhibitory effect on [3 H]ADP uptake, and its inhibitory strength was similar to that of bongkrekic acid. These results indicated that KH-17 weakly inhibits the ADP/ATP carrier not only from the matrix side but also from the cytosolic side. To ascertain whether this interpretation was correct, we examined the effects of KH-17 and carboxyatractyloside on mitochondrial [3 H]ADP uptake at two [3 H]ADP concentrations. We found that both KH-17 and carboxyatractyloside showed a stronger inhibitory effect at the lower [3 H]ADP concentration. Therefore, we concluded that the bongkrekic acid derivative, KH-17, weakly inhibits the mitochondrial ADP/ATP carrier from both sides of the inner mitochondrial membrane. These results suggested that the elimination of three methyl groups, one methoxy group, and five internal double bonds present in bongkrekic acid altered its manner of action towards the mitochondrial ADP/ATP carrier. Our data will help to improve our understanding of the interaction between bongkrekic acid and the mitochondrial ADP/ATP carrier. (Link to Publication Site) ● Publication site (DOI): 10.1111/cbdd.14194 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36527173 ● Search Scopus @ Elsevier (PMID): 36527173 ● Search Scopus @ Elsevier (DOI): 10.1111/cbdd.14194 (DOI: 10.1111/cbdd.14194, PubMed: 36527173)
6.	Yuto Horii, Toshiki Iniwa, Masayoshi Onitsuka, Jun Tsukimoto, Yuki Tanaka, Hironobu Ike, Yuri Fukushi, Haruna Andoh, Yoshie Takeuchi, So-ichiro Nishioka, Daisuke Tsuji, Mariko Ikuo, Naoshi Yamazaki, Yoshiharu Takiguchi, Naozumi Ishimaru and Kouji Itou : Reversal of neuroinflammation in novel galactosialidosis model mice by single intracerebroventricular administration of CHO-derived human recombinant cathepsin A precursor protein., Molecular Therapy. Methods & Clinical Development, Vol.25, No.June, 297-310, 2022. (Tokushima University Institutional Repository) ● Metadata: 117739 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.omtm.2022.04.001 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.omtm.2022.04.001 (Tokushima University Institutional Repository: 117739, DOI: 10.1016/j.omtm.2022.04.001)
7.	Yoshinobu Fujiwara, Takeshi Ito, Atsumi Toiyama, Takenori Yamamoto, Naoshi Yamazaki, Mitsuru Shindo and Yasuo Shinohara : Suramin Inhibits Mitochondrial ADP/ATP Carrier, Not Only from the Cytosolic Side But Also from the Matrix Side, of the Mitochondrial Inner Membrane, BPB Reports, Vol.4, No.3, 92-97, 2021. (Summary) <p>Suramin was earlier reported to show inhibitory effects on the mitochondrial ADP/ATP carrier. However, two important questions, i) whether it shows a specific inhibition of the ADP/ATP carrier when applied to isolated mitochondria, and ii) whether it inhibits the mitochondrial ADP/ATP carrier only from the cytosolic side or from the matrix side, as has been observed with its canonical inhibitors of carboxyatractyloside or bongkrekic acid, remain to be answered. In the present study, we sought exact answers to these questions. As for the first question, suramin showed certain inhibitory effects on the mitochondrial respiratory chain; and at a concentration of 25 μM it showed strong inhibition of the mitochondrial ADP/ATP carrier. This property was due to its weaker inhibitory effects on the mitochondrial ADP/ATP carrier than those of carboxyatractyloside or bongkrekic acid. As for the second question, suramin inhibited the ADP/ATP carrier from both sides of the mitochondrial inner membrane. Thus, suramin was concluded to be utilizable as a new type of inhibitor for the ADP/ATP carrier; but we must pay attention to its side-effects, especially when it is applied to whole mitochondria.</p> (Link to Publication Site) ● Publication site (DOI): 10.1248/bpbreports.4.3_92 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390851398296418688 ● Search Scopus @ Elsevier (DOI): 10.1248/bpbreports.4.3_92 (DOI: 10.1248/bpbreports.4.3_92, CiNii: 1390851398296418688)
8.	Toshihiko Tsutsumi, Risa Matsuda, Katsuya Morito, Kohei Kawabata, Miho Yokota, Miki Nikawadori, Manami Inoue-Fujiwara, Satoshi Kawashima, Mayumi Hidaka, Takenori Yamamoto, Naoshi Yamazaki, Tamotsu Tanaka, Yasuo Shinohara, Hiroyuki Nishi and Akira Tokumura : Identification of human glycerophosphodiesterase 3 as an ectophospholipase C that converts the G protein-coupled receptor 55 agonist lysophosphatidylinositol to bioactive monoacylglycerols in cultured mammalian cells., Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, Vol.1865, No.9, 158761, 2020. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbalip.2020.158761 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbalip.2020.158761 (DOI: 10.1016/j.bbalip.2020.158761)
9.	Tasuku Torao, Miyuki Mimura, Yasufumi Ohshima, Kohki Fujikawa, Mahadi Hasan, Tatsuharu Shimokawa, Naoshi Yamazaki, Hidenori ANDO, Tatsuhiro Ishida, Tatsuya Fukuta, Tamotsu Tanaka and Kentaro Kogure : Characteristics of unique endocytosis induced by weak current for cytoplasmic drug delivery, International Journal of Pharmaceutics, Vol.576, 119010, 2020. (Tokushima University Institutional Repository) ● Metadata: 114728 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijpharm.2019.119010 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.ijpharm.2019.119010 (Tokushima University Institutional Repository: 114728, DOI: 10.1016/j.ijpharm.2019.119010)
10.	Naoshi Yamazaki, Keisuke Kanazawa, Maria Kimura, Hironobu Ike, Makiko Shinomiya, Shouko Tanaka, Yasuo Shinohara, Noriaki Minakawa, Kouji Itou and Yoshiharu Takiguchi : Use of modified U1 small nuclear RNA for rescue from exon 7 skipping caused by 5-splice site mutation of human cathepsin A gene, Gene, Vol.677, 41-48, 2018. (Summary) Cathepsin A (CTSA) is a multifunctional lysosomal enzyme, and its hereditary defect causes an autosomal recessive disorder called galactosialidosis. In a certain number of galactosialidosis patients, a base substitution from adenine to guanine is observed at the +3 position of the 7th intron (IVS7 +3a>g) of the CTSA gene. With this mutation, a splicing error occurs; and consequently mRNA lacking the 7th exon is produced. This skipping of exon 7 causes a frame shift of the transcripts, resulting in a non-functional CTSA protein and hence galactosialidosis. This mutation seems to make the interaction between the 5'-splice site of intron 7 of pre-mRNA and U1 small nuclear RNA (U1 snRNA) much weaker. In the present study, to produce properly spliced mRNA from the CTSA gene harboring this IVS7 +3a>g mutation, we examined the possible usefulness of modified U1 snRNA that could interact with the mutated 5'-splice site. Toward this goal, we first prepared a model system using a mutant CTSA mini gene plasmid for delivery into HeLa cells. Then, we examined the effectiveness of modified U1 snRNA on the formation of properly spliced mRNA from this mutant CTSA mini gene. As a result, we succeeded in obtaining improved formation of properly spliced CTSA mRNA. Our results suggest the usefulness of modified U1 snRNA for rescue from exon 7 skipping caused by the IVS7 +3a>g mutation of the CTSA gene. (Keyword) Cathepsin A / Cell Line, Tumor / Exons / HeLa Cells / Humans / Introns / Mutation / RNA Precursors / RNA Splice Sites / RNA Splicing / RNA, Messenger / RNA, Small Nuclear (Tokushima University Institutional Repository) ● Metadata: 111998 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.gene.2018.07.030 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30010039 ● Summary page in Scopus @ Elsevier: 2-s2.0-85050244217 (Tokushima University Institutional Repository: 111998, DOI: 10.1016/j.gene.2018.07.030, PubMed: 30010039, Elsevier: Scopus)
11.	Iffat Sonia Ara Rahman, Kazuhito Tsuboi, Zahir Hussain, Ryouhei Yamashita, Yoko Okamoto, Toru Uyama, Naoshi Yamazaki, Tamotsu Tanaka, Akira Tokumura and Natsuo Ueda : Calcium-dependent generation of N-acylethanolamines and lysophosphatidic acids by glycerophosphodiesterase GDE7., Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, Vol.1861, No.12 pt A, 1881-1892, 2016. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbalip.2016.09.008 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27637550 ● Summary page in Scopus @ Elsevier: 2-s2.0-84988489470 (DOI: 10.1016/j.bbalip.2016.09.008, PubMed: 27637550, Elsevier: Scopus)
12.	Noriko Saito-Tarashima, Hirotaka Kira, Tomoya Wada, Kazuya Miki, Shiho Ide, Naoshi Yamazaki, Akira Matsuda and Noriaki Minakawa : Groove modification of siRNA duplexes to elucidate siRNA-protein interactions using 7-bromo-7-deazaadenosine and 3-bromo-3-deazaadenosine as chemical probes, Organic & Biomolecular Chemistry, Vol.14, No.47, 11096-11105, 2016. (Summary) Elucidation of dynamic interactions between RNA and proteins is essential for understanding the biological processes regulated by RNA, such as RNA interference (RNAi). In this study, the logical chemical probes, comprising 7-bromo-7-deazaadenosine (Br(7)C(7)A) and 3-bromo-3-deazaadenosine (Br(3)C(3)A), to investigate small interfering RNA (siRNA)-RNAi related protein interactions, were developed. The bromo substituents of Br(7)C(7)A and Br(3)C(3)A are expected to be located in the major and the minor grooves, respectively, and to act as a steric hindrance in each groove when these chemical probes are incorporated into siRNAs. A comprehensive investigation using siRNAs containing these chemical probes revealed that (i) Br(3)C(3)A(s) at the 5'-end of the passenger strand enhanced their RNAi activity, and (ii) the direction of RISC assembly is determined by the interaction between Argonaute2, which is the main component of RISC, and siRNA in the minor groove near the 5'-end of the passenger strand. Utilization of these chemical probes enables the investigation of the dynamic interactions between RNA and proteins. (Link to Publication Site) ● Publication site (DOI): 10.1039/c6ob01866a (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27714245 ● Summary page in Scopus @ Elsevier: 2-s2.0-84999752038 (DOI: 10.1039/c6ob01866a, PubMed: 27714245, Elsevier: Scopus)
13.	Yota Saito, Yosuke Hashimoto, Mai Arai, Noriko Saito-Tarashima, Tadashi Miyazawa, Kazuya Miki, Mayumi Takahashi, Kazuhiro Furukawa, Naoshi Yamazaki, Akira Matsuda, Tatsuhiro Ishida and Noriaki Minakawa : Chemistry, properties, and in vitro and in vivo applications of 2'-O-methoxyethyl-4'-thioRNA, a novel hybrid type of chemically modified RNA., ChemBioChem, Vol.15, No.17, 2535-2540, 2014. (Summary) We report the synthesis, properties, and in vitro and in vivo applications of 2'-O-methoxyethyl-4'-thioRNA (MOE-SRNA), a novel type of hybrid chemically modified RNA. In its hybridization with complementary RNA, MOE-SRNA showed a moderate improvement of Tm value (+3.4 °C relative to an RNA:RNA duplex). However, the results of a comprehensive comparison of the nuclease stability of MOE-SRNA relative to 2'-O-methoxyethylRNA (MOERNA), 2'-O-methyl-4'-thioRNA (Me-SRNA), 2'-O-methylRNA (MeRNA), 4'-thioRNA (SRNA), and natural RNA revealed that MOE-SRNA had the highest stability (t1/2 >48 h in human plasma). Because of the favorable properties of MOE-SRNA, we evaluated its in vitro and in vivo potencies as an anti-microRNA oligonucleotide against miR-21. Although the in vitro potency of MOE-SRNA was moderate, its in vivo potency was significant for the suppression of tumor growth (similar to that of MOERNA). (Keyword) Animals / Cell Proliferation / HeLa Cells / Humans / Mice / Mice, Inbred BALB C / Mice, Nude / MicroRNAs / Neoplasms / Nucleic Acid Conformation / RNA / RNA Stability / Tumor Cells, Cultured (Link to Publication Site) ● Publication site (DOI): 10.1002/cbic.201402398 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25314258 ● Summary page in Scopus @ Elsevier: 2-s2.0-84915745333 (DOI: 10.1002/cbic.201402398, PubMed: 25314258, Elsevier: Scopus)
14.	Takuya Hada, Takenori Yamamoto, Atsushi Yamamoto, Kazuto Ohkura, Naoshi Yamazaki, Yoshiharu Takiguchi and Yasuo Shinohara : Comparison of the catalytic activities of three isozymes of carnitine palmitoyltransferase 1 expressed in COS7 cells, Applied Biochemistry and Biotechnology, Vol.172, No.3, 1486-1496, 2014. (Summary) The enzyme carnitine palmitoyltransferase 1 (CPT1) catalyzes the transfer of an acyl group from acyl-CoA to carnitine to form acylcarnitine, and three isozymes of it, 1a, 1b, and 1c, have been identified. Interestingly, the 1c isozyme was reported to show no enzymatic activity, but it was not clearly demonstrated whether this inactivity was due to its dysfunction or due to its poor expression. In the present study, we (a) expressed individual CPT1 isozymes in COS7 cells, (b) evaluated quantitatively their expression levels by Western blotting using the three bacterially expressed CPT1 isozymes as standards, and (c) evaluated their catalytic activities. With these experiments, we successfully demonstrated that the absence of the enzymatic activity of the 1c isozyme was due to its dysfunction. In addition, experiments on the preparation of standard CPT1 isozymes revealed that the 1c isozyme did not show the standard relationship between migration in an SDS-PAGE gel and molecular size. We further tried to determine why the 1c isozyme was inert by preparing chimeric CPT1 between 1a and 1c, but no clear conclusion could be drawn because one of the chimeric CPT1s was not sufficiently expressed. (Keyword) Acyl Coenzyme A / Animals / COS Cells / Carnitine O-Palmitoyltransferase / Cercopithecus aethiops / Electrophoresis, Polyacrylamide Gel / Gene Expression Regulation / Isoenzymes / Kinetics / Mitochondria, Liver (Link to Publication Site) ● Publication site (DOI): 10.1007/s12010-013-0619-y (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24222496 ● Summary page in Scopus @ Elsevier: 2-s2.0-84896316059 (DOI: 10.1007/s12010-013-0619-y, PubMed: 24222496, Elsevier: Scopus)
15.	Yusaku Kikuchi, Naoshi Yamazaki, Noriko Tarashima, Kazuhiro Furukawa, Yoshiharu Takiguchi, Kouji Itou and Noriaki Minakawa : Gene suppression via U1 small nuclear RNA interference (U1i) machinery using oligonucleotides containing 2'-modified-4'-thionucleosides, Bioorganic & Medicinal Chemistry, Vol.21, No.17, 5292-5296, 2013. (Summary) Gene suppression via U1 small nuclear RNA interference (U1i) is considered to be one of the most attractive approaches, and takes the place of general antisense, RNA interference (RNAi), and anti-micro RNA machineries. Since the U1i can be induced by short oligonucleotides (ONs), namely U1 adaptors consisting of a 'target domain' and a 'U1 domain', we prepared adaptor ONs using 2'-modified-4'-thionucleosides developed by our group, and evaluated their U1i activity. As a result, the desired gene suppression via U1i was observed in ONs prepared as a combination of 2'-fluoro-4'-thionucleoside and 2'-fluoronucleoside units as well as only 2'-fluoronucleoside units, while those prepared as combination of 2'-OMe nucleoside/2'-OMe-4'-thionucleoside and 2'-fluoronucleoside units did not show significant activity. Measurement of Tm values indicated that a higher hybridization ability of adaptor ONs with complementary RNA is one of the important factors to show potent U1i activity. (Tokushima University Institutional Repository) ● Metadata: 113344 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bmc.2013.06.023 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23871495 ● Search Scopus @ Elsevier (PMID): 23871495 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bmc.2013.06.023 (Tokushima University Institutional Repository: 113344, DOI: 10.1016/j.bmc.2013.06.023, PubMed: 23871495)
16.	Takuya Hada, Yumiko Kato, Eriko Obana, Atsushi Yamamoto, Naoshi Yamazaki, Mitsuru Hashimoto, Takenori Yamamoto and Yasuo Shinohara : Comparison of two expression systems using COS7 cells and yeast cells for expression of heart/muscle-type carnitine palmitoyltransferase 1, Protein Expression and Purification, Vol.82, No.1, 192-196, 2012. (Summary) Carnitine palmitoyltransferase 1 (CPT1), catalyzing the transfer of the acyl group from acyl-CoA to carnitine to form acylcarnitine, is located at the outer mitochondrial membrane. Because it is easily inactivated by solubilization, expression systems using living cells are essential for its functional characterization. COS7 cells or yeast cells are often utilized for this purpose; however, the advantages/disadvantages of the use of these cells or the question as to how the CPT1 enzyme expressed by these cells differs are still uncertain. In this study, we characterized the heart/muscle-type isozyme of rat CPT1 (CPT1b) expressed by these two cellular expression systems. The mitochondrial fraction prepared from yeast cells expressing CPT1b showed 25% higher CPT1 activity than that obtained from COS7 cells. However, the expression level of CPT1b in the former was 3.8 times lower than that in the latter; and thus, under the present experimental conditions, the specific activity of CPT1b expressed in yeast cells was estimated to be approximately five times higher than that expressed in COS7 cells. Possible reasons for this difference are discussed. (Tokushima University Institutional Repository) ● Metadata: 114016 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.pep.2012.01.006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22266133 ● Search Scopus @ Elsevier (PMID): 22266133 ● Search Scopus @ Elsevier (DOI): 10.1016/j.pep.2012.01.006 (Tokushima University Institutional Repository: 114016, DOI: 10.1016/j.pep.2012.01.006, PubMed: 22266133)
17.	Tomomi Ishido, Naoshi Yamazaki, Mitsuru Ishikawa and Ken Hirano : Characterization of DNA polymerase from Danio rerio by overexpression in E. coli using the in vivo/in vitro compatible pIVEX plasmid., Microbial Cell Factories, Vol.10, 84, 2011. (Summary) Eukaryotic DNA polymerase β (pol β), the polymerase thought to be responsible for DNA repair synthesis, has been extensively characterized in rats and humans. However, pol β has not been purified or enzymatically characterized from the model fish species Danio rerio (zebrafish). We used the in vitro/in vivo dual expression system plasmid, pIVEX, to express Danio rerio pol β (Danio pol β) for biochemical characterization. Danio pol β encoded by the in vitro/in vivo-compatible pIVEX plasmid was expressed in E. coli BL21(DE3), BL21(DE3)pLysS, and KRX, and in vitro as a C-terminal His-tagged protein. Danio pol β expressed in vitro was subject to proteolysis; therefore, bacterial overexpression was used to produce the protein for kinetic analyses. KRX cells were preferred because of their reduced propensity for leaky expression of pol β. The cDNA of Danio rerio pol β encodes a protein of 337 amino acids, which is 2-3 amino acids longer than other pol β proteins, and contains a P63D amino acid substitution, unlike mammalian pol βs. This substitution lies in a hairpin sequence within an 8-kDa domain, likely to be important in DNA binding. We performed extensive biochemical characterization of Danio pol β in comparison with rat pol β, which revealed its sensitivity to metal ion activators (Mn2+ and Mg2+), its optimum salt concentration (10 mM KCl and 50 mM NaCl), alkaline pH optimum (pH 9.0), and low temperature optimum (30°C). Substituting Mn2+ for Mg2+ resulted in 8.6-fold higher catalytic efficiency (kcat/Km). Our characterization of pol β from a model fish organism contributes to the study of the function and evolution of DNA polymerases, which are emerging as important cellular targets for chemical intervention in the development of anticancer agents. (Keyword) Amino Acid Sequence / Animals / DNA Polymerase beta / Enzyme Stability / Escherichia coli / Fish Proteins / Gene Expression / Kinetics / Molecular Sequence Data / Plasmids / Protein Structure, Tertiary / Rats / Recombinant Fusion Proteins / Sequence Homology, Amino Acid / Zebrafish (Link to Publication Site) ● Publication site (DOI): 10.1186/1475-2859-10-84 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22018137 ● Search Scopus @ Elsevier (PMID): 22018137 ● Search Scopus @ Elsevier (DOI): 10.1186/1475-2859-10-84 (DOI: 10.1186/1475-2859-10-84, PubMed: 22018137)
18.	Tatsuaki Tagami, Takuya Suzuki, Kiyomi Hirose, Jose Mario Barichello, Naoshi Yamazaki, Tomohiro Asai, Naoto Oku, Tatsuhiro Ishida and Hiroshi Kiwada : Argonaute2 is a potential target for siRNA-based cancer therapy for HT1080 human fibrosarcoma., Drug Delivery and Translational Research, Vol.1, No.4, 277-288, 2011. (Link to Publication Site) ● Publication site (DOI): 10.1007/s13346-011-0025-3 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1007/s13346-011-0025-3 (DOI: 10.1007/s13346-011-0025-3)
19.	Naoto Okada, Takenori Yamamoto, Masahiro Watanabe, Yuuya Yoshimura, Eriko Obana, Naoshi Yamazaki, Kazuyoshi Kawazoe, Yasuo Shinohara and Kazuo Minakuchi : Identification of TMEM45B as a protein clearly showing thermal aggregation in SDS-PAGE gels and dissection of its amino acid sequence responsible for this aggregation., Protein Expression and Purification, Vol.77, No.1, 118-123, 2011. (Summary) SDS-PAGE is one of the most powerful experimental techniques used for the separation of proteins, and most proteins are separated according to their molecular size by this technique. However, exceptional proteins showing abnormal behavior in SDS-PAGE gels are known to exist. Thermal aggregation, rarely observed with membrane proteins, is one of the exceptional behaviors of proteins during SDS-PAGE, but detailed characterization of this aggregation has not yet been achieved. In the present study, we found that a putative membrane protein, TMEM45B, very clearly showed properties of thermal aggregation when it was expressed in COS7 cells and subjected to SDS-PAGE. We dissected the region of TMEM45B responsible for this aggregation, and found that of the seven putative transmembrane domains, a region comprising the 4th to 7th ones was essential for the thermal aggregation properties. We also demonstrated that these transmembrane domains, 4th to 7th, of TMEM45B conferred thermal aggregation properties on other proteins, by fusing this amino acid sequence to target proteins. The molecular mechanism causing thermal aggregation by TMEM45B is still uncertain, but TMEM45B could be utilized as a nice model to show clear thermal aggregation in SDS-PAGE gels. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.pep.2011.01.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21277373 ● Search Scopus @ Elsevier (PMID): 21277373 ● Search Scopus @ Elsevier (DOI): 10.1016/j.pep.2011.01.011 (DOI: 10.1016/j.pep.2011.01.011, PubMed: 21277373)
20.	Ken Hirano, Yuichiro Yoshida, Tomomi Ishido, Yukihisa Wada, Naoji Moriya, Naoshi Yamazaki, Yoshiyuki Mizushina, Yoshinobu Baba and Mitsuru Ishikawa : Consecutive incorporation of fluorophore-labeled nucleotides by mammalian DNA polymerase beta, Analytical Biochemistry: Methods in the Biological Sciences, Vol.405, No.2, 160-167, 2010. (Summary) In the present study, we investigated mammalian polymerases that consecutively incorporate various fluorophore-labeled nucleotides. We found that rat DNA polymerase beta (pol beta) consecutively incorporated fluorophore-labeled nucleotides to a greater extent than four bacterial polymerases, Sequenase Version 2.0, Vent(R) (exo-), DNA polymerase IIIalpha and the Klenow fragment, and the mammalian polymerases DNA polymerase alpha and human DNA polymerase delta, under mesophilic conditions. Furthermore, we investigated the kinetics of correct or mismatched incorporation with labeled nucleotides during synthesis by rat pol beta. The kinetic parameters K(m) and k(cat) were measured and used for evaluating: (i) the discrimination against correct pair incorporation of labeled nucleotides relative to unlabeled nucleotides; and (ii) the fidelity for all nucleotide combinations of mismatched pairs in the presence of labeled or unlabeled nucleotides. We also investigated the effect of fluorophore-labeled nucleotides on terminal deoxynucleotidyl transferase activity of rat pol beta. We have demonstrated for the first time that mammalian pol beta can consecutively incorporate various fluorophore-labeled dNTPs. These findings suggest that pol beta is useful for high-density labeling of DNA probes and single-molecule sequencing for high-speed genome analysis. (Keyword) Animals / DNA Nucleotidylexotransferase / DNA Polymerase III / DNA Polymerase beta / DNA Probes / Fluorescein / Fluorescent Dyes / Humans / Nucleotides / Rats (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ab.2010.06.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20570644 ● Search Scopus @ Elsevier (PMID): 20570644 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ab.2010.06.005 (DOI: 10.1016/j.ab.2010.06.005, PubMed: 20570644)
21.	Taisuke Matsuo, Atsushi Yamamoto, Takenori Yamamoto, Kaoru Otsuki, Naoshi Yamazaki, Masatoshi Kataoka, Hiroshi Terada and Yasuo Shinohara : Replacement of C305 in heart/muscle-type isozyme of human carnitine palmitoyltransferase I with aspartic acid and other amino acids., Biochemical Genetics, Vol.48, No.3-4, 193-201, 2010. (Summary) Liver- and heart/muscle-type isozymes of human carnitine palmitoyltransferase I (L- and M-CPTI, respectively) show a certain similarity in their amino acid sequences, and mutation studies on the conserved amino acids between these two isozymes often show essentially the same effects on their enzymatic properties. Earlier mutation studies on C305 in human M-CPTI and its counterpart residue, C304, in human L-CPTI showed distinct effects of the mutations, especially in the aspect of enzyme stability; however, simple comparison of these effects on the conserved Cys residue between L- and M-CPTI was difficult, because these studies were carried out using different expression systems and distinct amino acids as replacements. In the present study, we carried out mutation studies on the C305 in human M-CPTI using COS cells for the expression system. Our results showed that C305 was replaceable with aspartic acid but that substitution with other amino acids caused both loss of function and reduced expression. (Keyword) Amino Acid Sequence / Amino Acid Substitution / Amino Acids / Animals / Aspartic Acid / COS Cells / Carnitine O-Palmitoyltransferase / Cercopithecus aethiops / Cysteine / Gene Expression Regulation, Enzymologic / Humans / Isoenzymes / Muscle, Skeletal / Mutagenesis, Site-Directed / Myocardium / Organ Specificity (Link to Publication Site) ● Publication site (DOI): 10.1007/s10528-009-9301-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19937377 ● Summary page in Scopus @ Elsevier: 2-s2.0-77950859558 (DOI: 10.1007/s10528-009-9301-z, PubMed: 19937377, Elsevier: Scopus)
22.	Tatsuaki Tagami, Kazuya Nakamura, Taro Shimizu, Naoshi Yamazaki, Tatsuhiro Ishida and Hiroshi Kiwada : CpG motifs in pDNA-sequences increase anti-PEG IgM production induced by PEG-coated pDNA-lipoplexes., Journal of Controlled Release, Vol.142, No.2, 160-166, 2010. (Summary) Gene therapy is largely dependent on the development of efficient delivery vehicles. To prolong their circulating time, PEGylation of the surface of a delivery vehicle is frequently applied. However, we have reported previously that anti-PEG IgM produced by intravenous injection of PEG-coated liposome is responsible for enhanced clearance of second dose PEG-coated liposomes, which is known as the "accelerated blood clearance (ABC) phenomenon." A similar phenomenon has been observed with PEG-coated pDNA-lipoplexes (PDCLs) upon their repeated injection. But the effect of the sequence of pDNA in PDCLs on inducing the ABC phenomenon has not been thoroughly investigated. Here, we focus on CpG motifs in pDNA, which are known to have a potent immune-stimulatory activity. PDCLs with non-CpG pDNA (PNDCL) diminished the anti-PEG IgM response, resulting in significant accumulation of a second dose in tumor tissue, comparable to that of a single injection, but not in enhanced accumulation in liver. In addition, PDCL induced proliferation of IgM(+) splenic cells including B cells. These results suggest that the CpG motif is a major cause of the induction of the ABC phenomenon when PDCLs are repeatedly injected. Immunogenicity is a relevant point of concern for non-viral delivery systems. Our results indicate that the use of non-CpG pDNA may allow meaningful repeated dosing of pDNA formulations without the induction of a strong immune reaction and thus may have important implications for therapeutic use of liposomal formulations of nucleic acids. (Keyword) Animals / B-Lymphocytes / Cell Proliferation / CpG Islands / DNA / Immunoglobulin M / Liposomes / Male / Mice / Mice, Inbred BALB C / Mice, Nude / Polyethylene Glycols (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jconrel.2009.10.017 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19850094 ● Search Scopus @ Elsevier (PMID): 19850094 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jconrel.2009.10.017 (DOI: 10.1016/j.jconrel.2009.10.017, PubMed: 19850094)
23.	Akiko Yamada, Takenori Yamamoto, Yuya Yoshimura, Shunichi Gouda, Satoshi Kawashima, Naoshi Yamazaki, Kikuji Yamashita, Masatoshi Kataoka, Toshihiko Nagata, Hiroshi Terada and Yasuo Shinohara : Ca2+-induced permeability transition can be observed even in yeast mitochondria under optimized experimental conditions., Biochimica et Biophysica Acta (BBA) - Bioenergetics, Vol.1787, No.12, 1486-1491, 2009. (Summary) Yeast mitochondria have generally been believed not to undergo the permeability transition (PT) by the accumulation of Ca(2+) within the mitochondrial matrix, unlike mammalian mitochondria. However, the reason why the yeast PT is not induced by Ca(2+) has remained obscure. In this study, we examined in detail the effects of Ca(2+) on yeast mitochondria under various conditions. As a result, we discovered that the PT could be induced even in yeast mitochondria by externally added Ca(2+) under optimized experimental conditions. The 2 essential parameters for proper observation of the PT-inducing effects of Ca(2+) were the concentrations of the respiratory substrate and that of inorganic phosphate (Pi) in the incubation medium. The yeast mitochondrial PT induced by Ca(2+) was found to be insensitive to cyclosporin A and suppressed in the presence of a high concentration of Pi. Furthermore, when the PT was induced in yeast mitochondria by Ca(2+), the release of cytochrome c from mitochondria was also observed. (Keyword) calcium / Cytochromes c / Mitochondrial Membrane Transport Proteins / Yeasts (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbabio.2009.07.001 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19616504 ● Search Scopus @ Elsevier (PMID): 19616504 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbabio.2009.07.001 (DOI: 10.1016/j.bbabio.2009.07.001, PubMed: 19616504)
24.	Takenori Yamamoto, Atsushi Yamamoto, Masahiro Watanabe, Taisuke Matsuo, Naoshi Yamazaki, Masatoshi Kataoka, Hiroshi Terada and Yasuo Shinohara : Classification of FABP isoforms and tissues based on quantitative evaluation of transcript levels of these isoforms in various rat tissues., Biotechnology Letters, Vol.31, No.11, 1695-1701, 2009. (Summary) In mammals, 10 isoforms of fatty acid-binding protein (FABP) are expressed in various tissues. To understand the role of multiple FABP isoforms, we have quantitatively examined the transcript levels of individual FABP isoforms in each of various tissues by Northern blotting using synthesized RNAs corresponding to the mRNA of each isoform as external standards. As a result, absolute transcript levels of individual FABP isoforms expressed in each tissue were successfully determined. The 10 FABP isoforms were classified into three categories: (1) isoforms FABP7 and 12 were not markedly expressed in any tissue examined; (2) isoforms showing certain transcript levels in multiple tissues; and (3) isoforms FABP6, 8, and 9, expressed at certain levels in one particular tissue. Based on the expression profiles of the isoforms, individual tissues were also classified into three groups: (1) tissues in which high-level expression of FABP isoforms was not observed, (2) tissues in which multiple FABP isoforms were expressed at certain levels, and (3) tissues in which a single FABP isoform was dominantly expressed at a certain level. These results give a better understanding of the meaning of the presence of multiple FABP isoforms in mammals. (Keyword) Animals / DNA Probes / DNA, Complementary / Fatty Acid-Binding Proteins / Gene Expression Profiling / Gene Expression Regulation / Organ Specificity / Protein Isoforms / RNA, Messenger / Rats (Link to Publication Site) ● Publication site (DOI): 10.1007/s10529-009-0065-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19565192 ● Search Scopus @ Elsevier (PMID): 19565192 ● Search Scopus @ Elsevier (DOI): 10.1007/s10529-009-0065-7 (DOI: 10.1007/s10529-009-0065-7, PubMed: 19565192)
25.	Akiko Yamada, Takenori Yamamoto, Naoshi Yamazaki, Kikuji Yamashita, Masatoshi Kataoka, Toshihiko Nagata, Hiroshi Terada and Yasuo Shinohara : Differential permeabilization effects of Ca2+ and valinomycin on the inner and outer mitochondrial membranes as revealed by proteomics analysis of proteins released from mitochondria., Molecular & Cellular Proteomics, Vol.8, No.6, 1265-1277, 2009. (Summary) It is well established that cytochrome c is released from mitochondria when the permeability transition (PT) of this organelle is induced by Ca2+. Our previous study showed that valinomycin also caused the release of cytochrome c from mitochondria but without inducing this PT (Shinohara, Y., Almofti, M. R., Yamamoto, T., Ishida, T., Kita, F., Kanzaki, H., Ohnishi, M., Yamashita, K., Shimizu, S., and Terada, H. (2002) Permeability transition-independent release of mitochondrial cytochrome c induced by valinomycin. Eur. J. Biochem. 269, 5224-5230). These results indicate that cytochrome c may be released from mitochondria with or without the induction of PT. In the present study, we examined the protein species released from valinomycin- and Ca2+-treated mitochondria by LC-MS/MS analysis. As a result, the proteins located in the intermembrane space were found to be specifically released from valinomycin-treated mitochondria, whereas those in the intermembrane space and in the matrix were released from Ca2+-treated mitochondria. These results were confirmed by Western analysis. Furthermore to examine how the protein release occurred, we examined the correlation between the species of released proteins and those of the abundant proteins in mitochondria. Consequently most of the proteins released from mitochondria treated with either agent were highly expressed proteins in mitochondria, indicating that the release occurred not selectively but in a manner dependent on the concentration of the proteins. Based on these results, the permeabilization effects of Ca2+ and valinomycin on the inner and outer mitochondrial membranes are discussed. (Keyword) Amino Acid Sequence / Animals / Blotting, Western / Calcium / Cell Membrane Permeability / Electrophoresis, Polyacrylamide Gel / Intracellular Membranes / Microscopy, Electron, Transmission / Mitochondria, Liver / Molecular Sequence Data / Proteins / Proteomics / Rats / Valinomycin (Link to Publication Site) ● Publication site (DOI): 10.1074/mcp.M800377-MCP200 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19218587 ● Search Scopus @ Elsevier (PMID): 19218587 ● Search Scopus @ Elsevier (DOI): 10.1074/mcp.M800377-MCP200 (DOI: 10.1074/mcp.M800377-MCP200, PubMed: 19218587)
26.	Taisuke Matsuo, Eriko Obana, Takenori Yamamoto, Rei Kakuhata, Naoshi Yamazaki, Masatoshi Kataoka, Yoshinobu Baba, Tomoshige Hori and Yasuo Shinohara : Construction of plasmids suitable for in vitro synthesis of full-length mRNAs having a 3'-poly(A)+tail., Biotechnology Letters, Vol.31, No.2, 203-207, 2009. (Summary) In vitro synthesized mRNAs are often used as calibrants in gene expression analysis. In the case of an analytical procedure for gene expression containing a process of reverse transcription such as microarray analysis, full-length mRNAs having a 3'-poly(A)+tail are required as calibrants. However, the preparation of full-length mRNAs having a 3'-poly(A)+tail by using ordinary plasmid vectors is difficult. In this study, we established two plasmid vectors in which the nucleotide sequence corresponding to the 3'-poly(A)+tail were included. By simply inserting full-length cDNAs lacking their 3'-poly(A)+tail into established plasmid vectors, full-length mRNAs having a 3'-poly(A)+tail were successfully prepared. (Keyword) Base Sequence / Gene Expression Profiling / Genetic Vectors / Japan / Molecular Sequence Data / Oligonucleotide Array Sequence Analysis / Plasmids / RNA Probes / RNA, Messenger / Reference Standards (Link to Publication Site) ● Publication site (DOI): 10.1007/s10529-008-9847-6 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18810330 ● Summary page in Scopus @ Elsevier: 2-s2.0-58149196389 (DOI: 10.1007/s10529-008-9847-6, PubMed: 18810330, Elsevier: Scopus)
27.	Taisuke Matsuo, Takenori Yamamoto, Chie Katsuda, Kanami Niiyama, Atsushi Yamamoto, Naoshi Yamazaki, Kazuto Ohkura, Masatoshi Kataoka and Yasuo Shinohara : Substitution of certain amino acids in a short peptide causes a significant difference in their immunoreactivities with antibodies against different epitopes: evidence for possible folding of the peptide on a nitrocellulose or PVDF membrane., Biologicals, Vol.37, No.1, 44-47, 2009. (Summary) Substitution of amino acids in a peptide caused remarkable differences in its immunoreactivities with antibodies against 3 epitopes in the immobilized peptide. The observed differences in immunoreactivities among the peptides were not due to the differences in efficiencies of their transfer onto nitrocellulose or PVDF membranes. Rather, possible folding of the peptide on the membrane was considered to be the reason for their distinct immunoreactivities with the antibodies. (Keyword) Amino Acid Sequence / Amino Acid Substitution / Antibodies / Antigen-Antibody Reactions / Collodion / Epitopes / Membranes, Artificial / Molecular Sequence Data / Peptide Fragments / Polyvinyls / Protein Folding (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biologicals.2008.10.001 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19022683 ● Search Scopus @ Elsevier (PMID): 19022683 ● Search Scopus @ Elsevier (DOI): 10.1016/j.biologicals.2008.10.001 (DOI: 10.1016/j.biologicals.2008.10.001, PubMed: 19022683)
28.	Akihiro Iwahashi, Aoi Ishii, Naoshi Yamazaki, Mutsuru Hashimoto, Kazuto Okura, Masatoshi Kataoka, Eiji Majima, Hiroshi Terada and Yasuo Shinohara : Functionally important conserved length of C-terminal regions of yeast and bovine ADP/ATP carriers, identified by deletion mutants studies, and water accessibility of the amino acids at the C-terminal region of the yeast carrier., Mitochondrion, Vol.8, No.2, 196-204, 2008. (Summary) Comparison of the amino acid sequence of yeast type 2 ADP/ATP carrier (yAAC2) with that of bovine type 1 AAC (bAAC1) revealed that the N- and C-terminus of yAAC2 are 15- and 6-amino acids longer, respectively, than those of bAAC1. In the present study, we focused on the difference in the C-terminal region between yAAC2 and bAAC1. Deletion of first six residues of C-terminus of yAAC did not markedly affect the function of yAAC2; however, further deletion of 1 amino acid (7th amino acid from the C-terminus) destroyed its function. On the contrary, deletion of the first amino acid residue of the C-terminus of bAAC1 caused failure of its functional expression in yeast mitochondria. Based on these results, we concluded that the 6-amino acid residue extension of the C-terminus of yAAC2 was not necessary for the function of this carrier and that the remainder of the C-terminal region of yAAC2, having a length conserved with that of bAAC1, is important for the transport function of AACs. We next prepared various single-Cys mutants in which each of 32 residues in the C-terminus of yAAC2 was replaced by a Cys residue. Since all mutants were successfully expressed in yeast mitochondria, we examined the reactivity of these cysteine residues with the membrane-impermeable sulfhydryl reagent eosin 5-maleimide (EMA). As a result, all cysteine residues that replaced the 9 continuous amino acids in Met310-Lys318 showed high reactivity with EMA regardless of the presence of carboxyatractyloside or bongkrekic acid; and so this region was concluded to be exposed to the water-accessible environment. Furthermore, based on the reactivities of cysteine residues that replaced amino acids in the sixth transmembrane segment, the probable structural features of the C-terminal region of this carrier in the presence of bongkrekic acid were discussed. (Keyword) Amino Acid Sequence / Animals / Bongkrekic Acid / Cattle / Eosine Yellowish-(YS) / Gene Deletion / Mitochondrial ADP, ATP Translocases / Molecular Sequence Data / Protein Conformation / Saccharomyces cerevisiae Proteins / Sequence Alignment / Transformation, Genetic (Link to Publication Site) ● Publication site (DOI): 10.1016/j.mito.2008.01.004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18313366 ● Search Scopus @ Elsevier (PMID): 18313366 ● Search Scopus @ Elsevier (DOI): 10.1016/j.mito.2008.01.004 (DOI: 10.1016/j.mito.2008.01.004, PubMed: 18313366)
29.	Naoshi Yamazaki, Taisuke Matsuo, Miho Kurata, Makiko Suzuki, Takehisa Fujiwaki, Seiji Yamaguchi, Hiroshi Terada and Yasuo Shinohara : Substitutions of Three Amino Acids in Human Heart/Muscle Type Carnitine Palmitoyltransferase I Caused by Single Nucleotide Polymorphisms, Biochemical Genetics, Vol.46, No.1-2, 54-63, 2008. (Summary) Heart/muscle type carnitine palmitoyltransferase I (M-CPTI) catalyzes the rate-limiting step of mitochondrial long-chain fatty acid (LCFA) oxidation in muscle and adipose tissue. Three replacements of nucleotides resulting in missense mutations of I66V, S427C, and E531K were observed in the M-CPTI gene of patients showing abnormal fatty acid metabolism. These nucleotide replacements were found to be common single nucleotide polymorphisms (SNPs) of this gene and not specific to patients. The question of whether these missense mutations caused by SNPs alter the functional properties of M-CPTI remains unanswered. Thus, we examined whether these missense mutations are associated with any changes in the enzymatic properties of M-CPTI. None of these mutations was found to cause remarkable alteration of its enzymatic properties. Based on the comparison of amino acid sequences of M-CPTI among different animal species, the roles of these amino acids in the enzyme are discussed. (Keyword) Amino Acid Substitution / Animals / COS Cells / Carnitine O-Palmitoyltransferase / Cercopithecus aethiops / Fatty Acids / Humans / Lipid Metabolism / Lipid Metabolism, Inborn Errors / Mitochondria, Heart / Mutation, Missense / Myocardium / Oxidation-Reduction / Polymorphism, Single Nucleotide (Link to Publication Site) ● Publication site (DOI): 10.1007/s10528-007-9129-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17987377 ● Search Scopus @ Elsevier (PMID): 17987377 ● Search Scopus @ Elsevier (DOI): 10.1007/s10528-007-9129-3 (DOI: 10.1007/s10528-007-9129-3, PubMed: 17987377)
30.	Rei Kakuhata, Masahiro Watanabe, Takenori Yamamoto, Eriko Obana, Naoshi Yamazaki, Masatoshi Kataoka, Toshihiko Ooie, Yoshinobu Baba, Tomoshige Hori and Yasuo Shinohara : Importance of probe location for quantitative comparison of signal intensities among genes in microarray analysis., Journal of Biochemical and Biophysical Methods, Vol.70, No.6, 926-931, 2008. (Summary) In our previous studies, we demonstrated that expression levels of genes determined by Agilent oligoarray system, code G4130A, could be quantitatively evaluated by spike-in of synthetic full-length mRNAs as standards [Kakuhata R, Watanabe M, Yamamoto T, Akamine R, Yamazaki N, Kataoka M, et al. Possible utilization of in vitro synthesized mRNAs specifically expressed in certain tissues as standards for quantitative evaluation of the results of microarray analysis, J Biochem Biophys Methods 2007;70:755-60]. However, in its successor version (Agilent oligo array system, code G4131F), which was established to enable gene expression analysis over a much wider dynamic range, multiple probes are often utilized for evaluation of expression levels of individual genes; and they showed markedly distinct signal intensities. This result indicates that the observed signal intensities in this new version seemed not to simply reflect the transcript levels of individual genes. To understand the factors influencing the signal intensities of probes, we characterized the properties of the probes used in this new array system and the cRNAs formed during the labeling process. Analysis of cRNAs in the reaction mixture, which were hybridized with the arrays, revealed that the cRNAs were not fully transcribed under the conditions used. For this reason, probes located at the 5' side of the message were found to give lower signals than those at the 3' end; and the observed signal intensities were dependent upon the location of probes in the mRNA. Analysis of the correlation between signal intensities and locations on mRNAs for larger numbers of probes also supported the idea that probe location is one of the major determinants of signal intensities of probes in microarray analysis. (Keyword) Animals / DNA Probes / DNA-Directed RNA Polymerases / Male / Microarray Analysis / RNA / Rats / Rats, Wistar / Transcription, Genetic / Viral Proteins (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jprot.2007.12.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18241926 ● Search Scopus @ Elsevier (PMID): 18241926 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jprot.2007.12.005 (DOI: 10.1016/j.jprot.2007.12.005, PubMed: 18241926)
31.	Masahiro Watanabe, Takenori Yamamoto, Rei Kakuhata, Naoto Okada, Kazuaki Kajimoto, Naoshi Yamazaki, Masatoshi Kataoka, Yoshinobu Baba, Toshiaki Tamaki and Yasuo Shinohara : Synchronized changes in transcript levels of genes activating cold exposure-induced thermogenesis in brown adipose tissue of experimental animals., Biochimica et Biophysica Acta (BBA) - Bioenergetics, Vol.1777, No.1, 104-112, 2008. (Summary) To identify genes whose expression in brown adipose tissue (BAT) is up- or down-regulated in cold-exposed rats, we performed microarray analysis of RNA samples prepared from the BAT of cold-exposed rats and of rats kept at room temperature. Previously reported elevations of transcript levels of uncoupling protein (UCP1), type II iodothyronine deiodinase (DIO2), and type III adenylate cyclase (AC3) in the BAT of cold-exposed rats over those in that of rats maintained at room temperature were confirmed. In addition to these changes, remarkable elevations of the transcript levels of several genes that seemed to be associated with the processes of cell-cycle regulation and DNA replication were detected in the BAT of cold-exposed rats, possibly reflecting the significant proliferation of brown adipocytes in response to cold exposure. Up-regulation of the gene encoding sarcomeric mitochondrial type creatine kinase in the BAT of cold-exposed rats was also detected by microarray analysis, but subsequent Northern analysis revealed that the expression of not only the sarcomeric mitochondrial type enzyme, but also that of 2 other subtypes, i.e., cytoplasmic brain type and cytoplasmic muscle type, was elevated in the BAT of cold-exposed rats. Microarray analysis also revealed a significant expression of myoglobin in BAT and its elevation in the BAT of cold-exposed rats, and this result was supported by calibrated Northern analysis. On the contrary, several genes such as regulator of G-protein signaling 2 and IMP dehydrogenase 1 were down-regulated in the BAT of cold-exposed rats. The physiological meaning of these changes accompanying cold exposure was discussed. (Keyword) Adenylate Cyclase / Adipose Tissue, Brown / Amino Acid Sequence / Animals / Cold Temperature / Creatine Kinase / Gene Expression Regulation / Iodide Peroxidase / Ion Channels / Male / Mitochondrial Proteins / Molecular Sequence Data / Oligonucleotide Array Sequence Analysis / RNA, Messenger / Rats / Rats, Wistar / Thermogenesis / Voltage-Dependent Anion Channel 1 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbabio.2007.10.014 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18036333 ● Search Scopus @ Elsevier (PMID): 18036333 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbabio.2007.10.014 (DOI: 10.1016/j.bbabio.2007.10.014, PubMed: 18036333)
32.	Rei Kakuhata, Masahiro Watanabe, Takenori Yamamoto, Rie Akamine, Naoshi Yamazaki, Masatoshi Kataoka, Satoshi Fukuoka, Mitsuru Ishikawa, Toshihiko Ooie, Yoshinobu Baba, Tomoshige Hori and Yasuo Shinohara : Possible utilization of in vitro synthesized mRNAs specifically expressed in certain tissues as standards for quantitative evaluation of the results of microarray analysis., Journal of Biochemical and Biophysical Methods, Vol.70, No.5, 755-760, 2007. (Summary) To examine the possible usefulness of in vitro synthesized RNA as standards in microarray analysis, we prepared full-length mRNAs encoded by 3 rat metabolic genes for heart/muscle type carnitine palmitoyltransferase I (M-CPTI), uncoupling protein (UCP1), and heart/muscle type fatty acid-binding protein (H-FABP). Artificial RNA samples were prepared by adding known amounts of these synthetic mRNAs to total RNA from rat liver, and transcript levels of various genes were compared between the prepared artificial RNA samples and total RNA samples of rat liver by using an Agilent oligo microarray system. Upon the addition of these synthetic RNAs, signals from the DNA spots corresponding to these 3 genes were elevated, but those from the DNA spots representing other genes were not markedly influenced. Using the ratio of the increase in signal intensity of DNA spot to the amount of added RNA, we estimated the expression levels of several genes and compared them with the absolute expression levels determined by calibrated Northern analysis. As a result, the absolute transcript levels of 3 genes encoding acidic ribosomal phosphoprotein P0, type-1 voltage-dependent anion channel (VDAC1), and type-2 glucose transporter (GLUT2) were successfully estimated by this procedure. Furthermore, genes specifically expressed in certain tissues such as UCP1 were concluded to be good candidates as standards for use in microarray analysis. (Keyword) Animals / Base Sequence / Carnitine O-Palmitoyltransferase / DNA Primers / DNA, Complementary / Fatty Acid-Binding Proteins / Gene Expression / Ion Channels / Mitochondrial Proteins / Oligonucleotide Array Sequence Analysis / RNA, Messenger / Rats / Tissue Distribution / Transcription, Genetic (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jbbm.2007.04.004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17512601 ● Search Scopus @ Elsevier (PMID): 17512601 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jbbm.2007.04.004 (DOI: 10.1016/j.jbbm.2007.04.004, PubMed: 17512601)
33.	Rie Akamine, Takenori Yamamoto, Masahiro Watanabe, Naoshi Yamazaki, Masatoshi Kataoka, Mitsuru Ishikawa, Toshihiko Ooie, Yoshinobu Baba and Yasuo Shinohara : Usefulness of the 5' region of the cDNA encoding acidic ribosomal phosphoprotein P0 conserved among rats, mice, and humans as a standard probe for gene expression analysis in different tissues and animal species., Journal of Biochemical and Biophysical Methods, Vol.70, No.3, 481-486, 2007. (Summary) Housekeeping genes are often used as internal standards for gene expression analysis. When steady-state transcript levels of 4 typically used housekeeping genes, i.e., beta-actin, glyceraldehyde 3-phosphate dehydrogenase, cyclophilin, and acidic ribosomal phosphoprotein P0 (36B4), were evaluated in various rat tissues, the 36B4 gene seemed to be the most suitable as a standard to compare the expression levels of genes among different tissues. Next, for possible quantitative comparison of the expression level of this gene among different animal species, we compared the nucleotide sequence of the cDNA of 36B4 among rats, mice, and humans. As a result, highly conserved regions showing more than 97.5% identities were observed in the 5' portion of its open reading frame. When samples of synthesized mRNA encoding rat, mouse, and human 36B4 were hybridized with the entire cDNA encoding rat 36B4 as a probe, hybridization signals of mRNAs of mouse and human 36B4 were much weaker than those of mRNA encoding rat 36B4. However, when they were hybridized with an oligonucleotide probe corresponding to the highly conserved regions, they showed similar signal intensities. Thus, these highly conserved regions of the cDNA encoding 36B4 were concluded to be an effective standard for use in gene expression analysis. (Keyword) Animals / Base Sequence / Conserved Sequence / DNA, Complementary / Gene Expression Profiling / Humans / Mice / Molecular Sequence Data / Phosphoproteins / RNA, Messenger / Rats / Ribosomal Proteins / Sequence Homology, Nucleic Acid / Species Specificity / Tissue Distribution / Transcription, Genetic (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jbbm.2006.11.008 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17196660 ● Search Scopus @ Elsevier (PMID): 17196660 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jbbm.2006.11.008 (DOI: 10.1016/j.jbbm.2006.11.008, PubMed: 17196660)
34.	Takenori Yamamoto, Akiko Yamada, Masahiro Watanabe, Yuya Yoshimura, Naoshi Yamazaki, Yoshiyuki Yoshimura, Takashi Yamauchi, Masatoshi Kataoka, Toshihiko Nagata, Hiroshi Terada and Yasuo Shinohara : VDAC1, having a shorter N-terminus than VDAC2 but showing the same migration in an SDS-polyacrylamide gel, is the predominant form expressed in mitochondria of various tissues., Journal of Proteome Research, Vol.5, No.12, 3336-3344, 2006. (Summary) The voltage-dependent anion channel (VDAC) is a pore-forming protein expressed in the outer membrane of eukaryotic mitochondria. Three isoforms of it, i.e., VDAC1, VDAC2, and VDAC3, are known to be expressed in mammals; however, the question as to which is the main isoform in mitochondria is still unanswered. To address this question, we first prepared standard VDACs by using a bacterial expression system and raised various antibodies against them by using synthetic peptides as immunogens. Of the three bacterially expressed VDAC isoforms, VDAC3 showed faster migration in SDS-polyacrylamide gels than VDAC1 and VDAC2, although VDAC2 is longer than VDAC1 and VDAC3, due to a 12-amino acid extension of its N-terminal region. Even with careful structural characterization of the expressed VDACs by LC-MS/MS analysis, serious structural modifications of VDACs causing changes in their migration in SDS-polyacrylamide gels were not detected. Next, immunoreactivities of the raised antibodies toward these bacterially expressed VDAC isoforms were evaluated. Trials to prepare specific antibodies against the three individual VDAC isoforms were not successful except in the case of VDAC1. However, using a synthetic peptide corresponding to the highly conserved region among the three VDACs, we were successful in preparing an antibody showing essentially equal immunoreactivities toward all three VDACs. When mitochondrial outer membrane proteins of various rat tissues were subjected to 2-dimensional electrophoresis followed by immunoblotting with this antibody, six immunoreactive protein spots were detected. These spots were characterized by LC-MS/MS analysis, and the signal intensities among the spots were compared. As a result, the signal intensity of the spot representing VDAC1 was the highest, and thus, VDAC1 was concluded to be the most abundantly expressed of the three VDAC isoforms in mammalian mitochondria. (Keyword) Amino Acid Sequence / Animals / Base Sequence / Chromatography, Liquid / DNA Primers / Electrophoresis, Gel, Two-Dimensional / Electrophoresis, Polyacrylamide Gel / Immunoblotting / Mass Spectrometry / Mitochondrial Proteins / Molecular Sequence Data / Protein Isoforms / Rats / Sequence Analysis, DNA / Voltage-Dependent Anion Channel 1 (Link to Publication Site) ● Publication site (DOI): 10.1021/pr060291w (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17137335 ● Search Scopus @ Elsevier (PMID): 17137335 ● Search Scopus @ Elsevier (DOI): 10.1021/pr060291w (DOI: 10.1021/pr060291w, PubMed: 17137335)
35.	Akihiro Iwahashi, Yoshitaka Kihira, Eiji Majima, Hiroshi Terada, Naoshi Yamazaki, Masatoshi Kataoka and Yasuo Shinohara : The structure of the second cytosolic loop of the yeast mitochondrial ADP/ATP carrier AAC2 is dependent on the conformational state, Mitochondrion, Vol.6, No.5, 245-251, 2006. (Summary) To detect structural changes in the second cytosolic loop of the mitochondrial ADP/ATP carrier of Saccharomyces cerevisiae AAC2, we prepared 20 single cysteine mutants by replacing each amino acid in the S213 to L232 region. All single cysteine mutants were fully functional, because they could restore growth on glycerol of a yeast strain lacking functional ADP/ATP carriers. First, these single-Cys mutants were treated with carboxyatractyloside to lock the carrier in the cytosolic state or with bongkrekic acid to generate the matrix state, and then with the membrane-impermeable SH reagent eosin-5-maleimide (EMA) to probe accessibility. The amino acid residues S213C, L214C, F231C and L232C were not labeled, indicating that these 4 residues must have been buried in the membrane, whereas the region between residues K215 and S230 is accessible to labeling and must, therefore, have protruded into the aqueous phase. Residue L218C showed strong resistance against EMA labeling regardless of the state of the carrier, but the reason for such behavior is unclear. On the contrary, the labeling of the residues between F227C and S230C was strongly dependent on the state of the carrier. Thus, the C-terminal region of the second cytosolic loop in AAC2 changes its environment when the carrier cycles between the matrix and cytosolic state. (Keyword) Amino Acid Substitution / Cysteine / Cytosol / Eosine Yellowish-(YS) / Mitochondria / Mitochondrial ADP, ATP Translocases / Molecular Sequence Data / Mutation / Protein Conformation / Saccharomyces cerevisiae / Saccharomyces cerevisiae Proteins (Link to Publication Site) ● Publication site (DOI): 10.1016/j.mito.2006.07.007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16962388 ● Search Scopus @ Elsevier (PMID): 16962388 ● Search Scopus @ Elsevier (DOI): 10.1016/j.mito.2006.07.007 (DOI: 10.1016/j.mito.2006.07.007, PubMed: 16962388)
36.	Mari Ogino, Jun-ichi Kido, Mika Bando, Noriko Hayashi, Chie Wada -Mihara, Toshihiko Nagata, Fusanori Nishimura, Y. Soga, Shogo Takashiba, T. Kubota, M. Itagaki, Yasuko Shimada, H. Tai, Hiromasa Yoshie, Naoshi Yamazaki, Yasuo Shinohara and Masatoshi Kataoka : Alpha 2 integrin +807 polymorphism in drug-induced gingival overgrowth, Journal of Dental Research, Vol.84, No.12, 1183-1186, 2005. (Summary) Alpha2 integrin on fibroblasts is reported to play an important role in the induction of drug-induced gingival overgrowth, which is characterized by excessive accumulation of type I collagen in gingival connective tissue. Silent polymorphism 807 T/C within the alpha2 integrin gene is associated with high/low alpha2 integrin expression. The aim of this study was to test the hypothesis that expression of alpha2 integrin 807 T/C polymorphism correlates with drug-induced gingival overgrowth. A case-control study comparing 136 subjects taking calcium channel blockers (72 with vs. 64 without drug-induced gingival overgrowth) demonstrated that the frequency of the +807 C allele was significantly higher in the case group than in the controls (odds ratio, 3.61; 95% confidence interval, 2.14 - 6.10; P < 0.05). The present findings suggest that the alpha2 +807 C allele is one of the genetic risk factors for drug-induced gingival overgrowth. (Keyword) drug-induced gingival overgrowth / Alpha 2 integrin / SNP / collagen phagocytosis (Link to Publication Site) ● Publication site (DOI): 10.1177/154405910508401217 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16304451 ● Search Scopus @ Elsevier (PMID): 16304451 ● Search Scopus @ Elsevier (DOI): 10.1177/154405910508401217 (DOI: 10.1177/154405910508401217, PubMed: 16304451)
37.	Kazuaki Kajimoto, Takiko Daikoku, Fumiyo Kita, Naoshi Yamazaki, Masatoshi Kataoka, Yoshinobu Baba, Hiroshi Terada and Yasuo Shinohara : PCR-select subtraction for characterization of messages differentially expressed in brown compared with white adipose tissue., Molecular Genetics and Metabolism, Vol.80, No.1-2, 255-261, 2003. (Summary) To understand the energy metabolism occurring in brown adipose tissue (BAT), we subtracted the messages expressed in white adipose tissue (WAT) from those in BAT. Thereby we succeeded in identifying 37 cDNA clones as being significantly expressed in BAT but not in WAT. Of these, 24 clones were found to code for mitochondrial proteins. Since BAT is well known to have a higher mitochondrial content than WAT, these results would seem to reflect simply the differences in mitochondrial content between BAT and WAT. To examine this possibility, we next measured the amount of mitochondrial DNA (mtDNA) in various rat tissues. As a result, the mtDNA copy number per cell was found to be markedly different among the tissues analyzed, and the highest value of about 5.3x10(4) copies per cell was observed with the rat brain. BAT showed a value similar to that of brain, but this value was only about 3.5-fold higher than that for WAT. Since observed differences in mitochondrial content between BAT and WAT was smaller than those observed with transcript levels of proteins, we conclude that the observed differences in the transcript levels of certain proteins between BAT and WAT reflect the functional differences between BAT and WAT, and do not reflect the differences in mitochondrial content between BAT and WAT. (Keyword) Adipose Tissue / Adipose Tissue, Brown / Animals / Blotting, Northern / Brain / Cloning, Molecular / DNA, Complementary / DNA, Mitochondrial / Gene Expression Profiling / Mitochondria / Mitochondrial Proteins / Polymerase Chain Reaction / RNA, Messenger / Rats / Rats, Wistar (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ymgme.2003.08.006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14567975 ● Search Scopus @ Elsevier (PMID): 14567975 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ymgme.2003.08.006 (DOI: 10.1016/j.ymgme.2003.08.006, PubMed: 14567975)
38.	Naoshi Yamazaki, Yasuhisa Yamanaka, Yoshiko Hashimoto, Takayuki Hiramatsu, Yasuo Shinohara and Hiroshi Terada : The gene encoding muscle-type carnitine palmitoyltransferase I: comparison of the 5'-upstream region of human and rodent genes, The Journal of Biochemistry, Vol.133, No.4, 523-532, 2003. (Summary) Muscle-type carnitine palmitoyltransferase I (M-CPTI) is the key enzyme for fatty acid beta-oxidation in heart and skeletal muscles and in adipose tissue. So far, M-CPTI mRNA has been detected in white adipocytes from epididymal fat pads of rats and humans, but not in mouse adipocytes. To characterize the gene expression of M-CPTI in mice, we isolated the genomic DNA encoding mouse M-CPTI and determined its transcription initiation site. As a result, the mouse M-CPTI gene seemed to have multiple initiation sites, as in the case of the rat and human genes. Furthermore, the conserved nucleotide sequence of the response element for peroxisome proliferators was shown to exist in the upstream of the mouse gene as in that of the rat and human genes. From these observations, we suggest that the anomalous expression of M-CPTI in mouse adipocytes reported previously may be regulated by factors other than peroxisome proliferators. Previously, we reported that there were transcripts containing regions of both CK/EK-beta and M-CPTI genes in humans. In this study, we found that such transcripts also exist in rodents and that the amounts of the transcripts containing regions of both of these genes did not depend on the expression level of CK/EK-beta. (Keyword) Actins / Adipocytes / Adipose Tissue, Brown / Amino Acid Sequence / Animals / Base Sequence / Carnitine O-Palmitoyltransferase / Choline Kinase / DNA, Complementary / Genes / Humans / Mice / Molecular Sequence Data / Muscles / Phosphotransferases (Alcohol Group Acceptor) / Rats / Response Elements / Reverse Transcriptase Polymerase Chain Reaction / Transcription, Genetic (Link to Publication Site) ● Publication site (DOI): 10.1093/jb/mvg069 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12761301 ● Search Scopus @ Elsevier (PMID): 12761301 ● Search Scopus @ Elsevier (DOI): 10.1093/jb/mvg069 (DOI: 10.1093/jb/mvg069, PubMed: 12761301)
39.	Kazuaki Kajimoto, Takiko Daikoku, Naoshi Yamazaki, Hiroshi Terada and Yasuo Shinohara : Expression profiles of three isoforms of inositol 1,4,5-trisphosphate receptor in brown adipose tissue of the rat., Biochemical Pharmacology, Vol.65, No.6, 995-998, 2003. (Summary) The thermogenic function of brown adipose tissue (BAT) is known to be mainly regulated by a signal transduction cascade via beta-adrenoceptor. However, recent studies indicated that the alpha-adrenoceptor and its downstream signal transduction cascade, causing elevation of the cellular Ca(2+) level, are also important for the regulation of this function of BAT. In the present study, expression profiles of 3 isoforms of the inositol 1,4,5-trisphosphate (IP(3)) receptor, known as one of the major components of the machinery regulating the intracellular Ca(2+) concentration in the BAT of rats, were investigated by Northern analysis. Of these three IP(3) receptor isoforms, the type 2 one was found to be the most abundant of the three in BAT. Furthermore, when rats were exposed to the cold, under which condition the thermogenic function of BAT is known to be stimulated, the expression levels of types 1 and 2 isoforms of IP(3) receptor were remarkably elevated. The results of Western analysis supported the predominant expression of the type 2 isoform in BAT. However, different from the results of Northern analysis, the expression levels of types 1 and 2 isoforms of IP(3) receptor protein in BAT were not influenced by exposure of the animals to the cold. (Keyword) Adipose Tissue, Brown / Animals / Blotting, Northern / Calcium Channels / Energy Metabolism / Gene Expression Profiling / Inositol 1,4,5-Trisphosphate Receptors / Male / Protein Isoforms / Rats / Rats, Wistar / Receptors, Cytoplasmic and Nuclear (Link to Publication Site) ● Publication site (DOI): 10.1016/S0006-2952(02)01664-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12623131 ● Search Scopus @ Elsevier (PMID): 12623131 ● Search Scopus @ Elsevier (DOI): 10.1016/S0006-2952(02)01664-7 (DOI: 10.1016/S0006-2952(02)01664-7, PubMed: 12623131)
40.	Naoshi Yamazaki, Yasuo Shinohara, Kayo Tanida and Hiroshi Terada : Structural properties of mammalian mitochondrial ADP/ATP carriers: identification of possible amino acids that determine functional differences in its isoforms., Mitochondrion, Vol.1, No.4, 371-379, 2002. (Summary) The structural properties of isoforms of the mitochondrial ADP/ATP carrier expressed in mammals were characterized in order to understand their possible functional differences. To accomplish this, the cDNA clone of the bovine type 2 isoform was isolated and characterized. We also extensively explored the rat type 3 isoform, but it was not detected. We next compared the amino acid sequences of the ten ADP/ATP carriers, which are expressed in mammals. As a result, amino acids at positions 45, 147 and 164 were found to show strict isoform dependency regardless of species differences. Thus, they are expected to determine functional differences in the isoforms of the ADP/ATP carrier. (Link to Publication Site) ● Publication site (DOI): 10.1016/S1567-7249(01)00041-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16120291 ● Search Scopus @ Elsevier (PMID): 16120291 ● Search Scopus @ Elsevier (DOI): 10.1016/S1567-7249(01)00041-1 (DOI: 10.1016/S1567-7249(01)00041-1, PubMed: 16120291)
41.	Yasuo Shinohara, Takiko Daikoku, Kazuaki Kajimoto, Atsushi Shima, Naoshi Yamazaki and Hiroshi Terada : Expression of NAD(+)-dependent isocitrate dehydrogenase in brown adipose tissue., Biochemical and Biophysical Research Communications, Vol.281, No.3, 634-638, 2001. (Summary) cDNA clones significantly expressed in brown adipose tissue (BAT) but not in white adipose tissue (WAT) of rats were isolated by use of a PCR-select cDNA subtraction kit. Of the isolated clones, structural features of two of them, 2-58 and 2-67, were studied in detail. The results indicated that these clones were cDNAs encoding alpha- and beta-subunits of rat NAD(+)-dependent isocitrate dehydrogenase (NAD(+)-ICDH). Previous biochemical study suggested the importance of NAD(+)-ICDH in metabolism in BAT; however, transcript levels of individual subunits of this enzyme in BAT had never been analyzed. In the present study, using these newly isolated cDNAs, we clearly demonstrate that the expression of three subunits of NAD(+)-ICDH was the most remarkable in BAT among the various tissues analyzed. (Keyword) Adipose Tissue, Brown / Animals / Base Sequence / DNA, Complementary / Isocitrate Dehydrogenase / Molecular Sequence Data / NAD / Polymerase Chain Reaction / Rats / Sequence Homology, Amino Acid / Sequence Homology, Nucleic Acid (Link to Publication Site) ● Publication site (DOI): 10.1006/bbrc.2001.4351 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11237704 ● Summary page in Scopus @ Elsevier: 2-s2.0-0034816225 (DOI: 10.1006/bbrc.2001.4351, PubMed: 11237704, Elsevier: Scopus)
42.	Naoshi Yamazaki, Yasuo Shinohara, Kazuaki Kajimoto, Masayuki Shindou and Hiroshi Terada : Novel expression of equivocal messages containing both regions of choline/ethanolamine kinase and muscle type carnitine palmitoyltransferase I., The Journal of Biological Chemistry, Vol.275, No.41, 31739-31746, 2000. (Summary) For characterization of the detailed gene structure of human muscle type carnitine palmitoyltransferase I (M-CPTI), we analyzed the 5'-upstream region of the M-CPTI transcripts. As a result, we found a cDNA clone containing a nucleotide sequence unexpected from the reported M-CPTI gene structure in the upstream region of its 5' end. Comparison of this nucleotide sequence with that of genomic DNA showed that this sequence was derived from the 3'-untranslated region of the gene encoding choline/ethanolamine kinase-beta (CK/EK-beta) located upstream of the M-CPTI gene. Southern blot analysis showed that there was no other region homologous to the CK/EK-beta gene in the whole human genome. Thus, the overlapping transcript was concluded to be produced from the functional genes of CK/EK-beta and M-CPTI. Furthermore, cDNAs containing both exons of these genes were detected by the polymerase chain reaction using the cDNA of human heart M-CPTI obtained by specific reverse transcription from its 3'-untranslated region as a template. From these results, the production and organization of these overlapping transcripts are discussed. (Keyword) 3' Untranslated Regions / Amino Acid Sequence / Base Sequence / Carnitine O-Palmitoyltransferase / Choline Kinase / Cloning, Molecular / DNA, Complementary / Exons / Genes, Overlapping / Humans / Introns / Molecular Sequence Data / Muscles / Myocardium / RNA, Messenger / Reverse Transcriptase Polymerase Chain Reaction / Transcription, Genetic (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M006322200 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10918069 ● Summary page in Scopus @ Elsevier: 2-s2.0-0034644701 (DOI: 10.1074/jbc.M006322200, PubMed: 10918069, Elsevier: Scopus)
43.	Yasuo Shinohara, Taro Ishida, Mami Hino, Naoshi Yamazaki, Yoshinobu Baba and Hiroshi Terada : Characterization of porin isoforms expressed in tumor cells., European Journal of Biochemistry, Vol.267, No.19, 6067-6073, 2000. (Summary) Mitochondria from malignant tumor cell lines show a higher capability for hexokinase binding than those from normal liver. To explore possible differences in hexokinase binding sites of mitochondria between tumor cells and normal liver, we characterized porin isoforms expressed in tumor cells. Cloning experiments on the three porin isoforms, VDAC1, VDAC2 and VDAC3 from malignant tumor cell line AH130 clearly showed that their primary structures were completely identical to those of the corresponding VDACs of normal liver cells. Possible expression of the fourth porin isoform in AH130 cells was excluded by degenerate primer-based RT-PCR. However, the transcript levels of the three VDAC isoforms in AH130 cells were significantly higher than those in normal liver. These results suggest that the high hexokinase-binding capability of malignant tumor cell mitochondria was not due to any structural difference, but due to a quantitative difference in binding sites. (Keyword) Alternative Splicing / Amino Acid Sequence / Animals / Base Sequence / Carcinoma, Hepatocellular / DNA, Complementary / DNA, Neoplasm / Gene Expression Regulation, Neoplastic / Hexokinase / Humans / Liver Neoplasms / Liver Neoplasms, Experimental / Mitochondria, Liver / Mitochondrial Membrane Transport Proteins / Molecular Sequence Data / Neoplasm Proteins / Porins / Protein Isoforms / RNA, Messenger / RNA, Neoplasm / Rats / Rats, Wistar / Reverse Transcriptase Polymerase Chain Reaction / Transcription, Genetic / Tumor Cells, Cultured / Voltage-Dependent Anion Channel 1 / Voltage-Dependent Anion Channel 2 / Voltage-Dependent Anion Channels (Link to Publication Site) ● Publication site (DOI): 10.1046/j.1432-1327.2000.01687.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10998068 ● Summary page in Scopus @ Elsevier: 2-s2.0-0033798036 (DOI: 10.1046/j.1432-1327.2000.01687.x, PubMed: 10998068, Elsevier: Scopus)
44.	Takiko Daikoku, Yasuo Shinohara, Atsushi Shima, Naoshi Yamazaki and Hiroshi Terada : Specific elevation of transcript levels of particular protein subtypes induced in brown adipose tissue by cold exposure., Biochimica et Biophysica Acta (BBA) - Bioenergetics, Vol.1457, No.3, 263-272, 2000. (Summary) To understand the difference in metabolic flow in rat brown adipose tissue (BAT) from that in white adipose tissue (WAT) at the molecular level, we examined the steady-state transcript levels of 39 proteins in both adipose tissues with and without cold exposure by Northern blot analysis. In addition to the transcript levels of uncoupling protein isoforms, those of proteins involved in the transport and catabolism of fatty acids and glucose in BAT were elevated by cold exposure, suggesting the stimulation of utilization of fatty acids and glucose as fuels in BAT. As to these changes, the muscle-type subtypes were remarkable; and therefore, they were suggested to be responsible for the cold exposure-induced acceleration of energy expenditure in BAT. Furthermore, of the isoforms of beta-adrenergic receptor (beta-AR) and CCAAT enhancer binding protein (C/EBP), transcript levels of beta(1)-AR and C/EBPbeta in BAT were increased by the cold exposure. Possible roles of these proteins in energy metabolism in BAT were discussed. (Keyword) Adipose Tissue, Brown / Animals / Cold Temperature / DNA, Complementary / Fatty Acids / Glucose / Male / Mitochondria / Oxidative Phosphorylation / Proteins / Rats / Rats, Wistar / Triglycerides (Link to Publication Site) ● Publication site (DOI): 10.1016/S0005-2728(00)00107-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10773170 ● Search Scopus @ Elsevier (PMID): 10773170 ● Search Scopus @ Elsevier (DOI): 10.1016/S0005-2728(00)00107-9 (DOI: 10.1016/S0005-2728(00)00107-9, PubMed: 10773170)
45.	Chieko Aoyama, Naoshi Yamazaki, Hiroshi Terada and Kozo Ishidate : Structure and characterization of the genes for murine choline/ethanolamine kinase isozymes alpha and beta., Journal of Lipid Research, Vol.41, No.3, 452-464, 2000. (Summary) Choline/ethanolamine kinase (CK/EK) is the first enzyme in phosphatidylcholine/phosphatidylethanolamine biosynthesis in all animal cells. The highly purified CKs from mammalian sources and their recombinant gene products so far were all shown to have EK activity also, indicating that both activities reside on the same protein. CK/EK in most animal cells exists as several isoforms, for two of which (alpha and beta) their cDNAs have been cloned from both the rat and mouse, and they are found to be separate gene products. The physiological significance for the existence of more than one CK/EK enzyme, however, remains to be clarified. In this study, we isolated mouse genes encoding both types of CK/EK isozyme and determined their entire structure. The 5'-flanking promoter regions were found to have quite different features from each other, indicating that their expression could be under distinct control. Comparison of the nucleotide sequence between the corresponding coding exons showed the best homology (75%) residing on exon VIII. A search of the database resulted in the possible existence of 17 different origins of eukaryotic CK and/or EK, each of which presumably contained the entire amino acid sequence. Multialignment of their putative amino acid sequences led to an identification of the novel consensus sequence possibly required for the expression of either CK or EK activity, which corresponded to the sequence within exons VII and VIII of CK/EK-alpha and -beta genes from the mouse. This sequence was localized in close proximity to the C-terminal region of the general (Brenner's) phosphotransferase concensus sequence which was also completely conserved in all of the putative eukaryotic CK/EK proteins. The results demonstrated that, while both CK/EK-alpha and -beta genes were composed of 11 major exons, the size of their genes was quite different: 40 kb for CK/EK-alpha, whereas it was only 3.5 kb for CK/EK-beta. (Keyword) Amino Acid Sequence / Animals / Base Sequence / Choline Kinase / Consensus Sequence / DNA / DNA Primers / Exons / Humans / Isoenzymes / Mice / Molecular Sequence Data / Phosphotransferases (Alcohol Group Acceptor) / Promoter Regions, Genetic / Rats / Sequence Homology, Amino Acid (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10706593 ● Search Scopus @ Elsevier (PMID): 10706593 (PubMed: 10706593)
46.	Mitsuru Hashimoto, Yasuo Shinohara, Eiji Majima, Takashi Hatanaka, Naoshi Yamazaki and Hiroshi Terada : Expression of the bovine heart mitochondrial ADP/ATP carrier in yeast mitochondria: significantly enhanced expression by replacement of the N-terminal region of the bovine carrier by the corresponding regions of the yeast carriers., Biochimica et Biophysica Acta (BBA) - Bioenergetics, Vol.1409, No.3, 113-124, 1999. (Summary) To characterize the transport mechanism mediated by the mammalian mitochondrial ADP/ATP carrier (AAC), we tried to express bovine heart mitochondrial AAC (bhAAC) in Saccharomyces cerevisiae. The open reading frame of the bhAAC was introduced into the haploid strain WB-12, in which intrinsic AAC genes were disrupted. Growth of the transformant was very low in glycerol medium, and a little amount of bhAAC was detected in the mitochondrial membrane. For improvement of bhAAC expression in WB-12, we introduced DNA fragments encoding chimeric bhAACs, in which the N-terminal region of the bhAAC extending into the cytosol was replaced by the corresponding regions of the type 1 and type 2 yeast AAC isoforms (yAAC1 and yAAC2). These transformants grew well, and the amounts of the chimeric bhAACs in their mitochondria were as high as that of yAAC2. The carriers expressed showed essentially the same ADP transport activities as that of AAC in bovine heart mitochondria. (Keyword) Amino Acid Sequence / Animals / Biological Transport / Cattle / Mitochondria / Mitochondria, Heart / Mitochondrial ADP, ATP Translocases / Molecular Sequence Data / Mutation / Oxidative Phosphorylation / Plasmids / Saccharomyces cerevisiae (Link to Publication Site) ● Publication site (DOI): 10.1016/S0005-2728(98)00155-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9878703 ● Search Scopus @ Elsevier (PMID): 9878703 ● Search Scopus @ Elsevier (DOI): 10.1016/S0005-2728(98)00155-8 (DOI: 10.1016/S0005-2728(98)00155-8, PubMed: 9878703)
47.	Yasuo Shinohara, Kenji Yamamoto, Katsuyuki Inoo, Naoshi Yamazaki and Hiroshi Terada : Quantitative determinations of the steady state transcript levels of hexokinase isozymes and glucose transporter isoforms in normal rat tissues and the malignant tumor cell line AH130., Biochimica et Biophysica Acta (BBA) - Biomembranes, Vol.1368, No.1, 129-136, 1998. (Summary) The steady state transcript levels of the four hexokinase (HK) isozymes and four glucose transporter (GLUT) isoforms were determined quantitatively by Northern analysis of RNA samples from rat tissues using synthetic fragments of the RNAs encoding the HK isozymes and GLUT isoforms. Results showed that the levels of HK isozyme transcripts were low in rat tissues, the level of that most highly expressed, the type I isozyme (HKI), in the brain being 0.025% of the total poly(A)+ RNA. A good correlation was found between the reported HK activities and the total amounts of transcripts encoding all HK isozymes in various tissues, showing that the HK activities in tissues can be estimated from the total amount of transcripts encoding HK isozymes. The proposed associated expressions of HK isozymes and GLUT isoforms in particular tissues were confirmed at their transcript levels. The steady state transcript levels of type II HK and the type 1 GLUT isoform in the malignant tumor cell line AH130 were also determined quantitatively. (Keyword) Animals / Electrophoresis, Agar Gel / Hexokinase / Isoenzymes / Monosaccharide Transport Proteins / RNA, Messenger / Rats / Tumor Cells, Cultured (Link to Publication Site) ● Publication site (DOI): 10.1016/S0005-2736(97)00189-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9459591 ● Search Scopus @ Elsevier (PMID): 9459591 ● Search Scopus @ Elsevier (DOI): 10.1016/S0005-2736(97)00189-2 (DOI: 10.1016/S0005-2736(97)00189-2, PubMed: 9459591)
48.	Takiko Daikoku, Yasuo Shinohara, Atsushi Shima, Naoshi Yamazaki and Hiroshi Terada : Dramatic enhancement of the specific expression of the heart-type fatty acid binding protein in rat brown adipose tissue by cold exposure., FEBS Letters, Vol.410, No.2-3, 383-386, 1997.
49.	Naoshi Yamazaki, Yasuhisa Yamanaka, Yoshiko Hashimoto, Yasuo Shinohara, Atsushi Shima and Hiroshi Terada : Structural features of the gene encoding human muscle type carnitine palmitoyltransferase I., FEBS Letters, Vol.409, No.3, 401-406, 1997.
50.	Naoshi Yamazaki, Yasuo Shinohara, Atsushi Shima, Yasuhisa Yamanaka and Hiroshi Terada : Isolation and characterization of cDNA and genomic clones encoding human muscle type carnitine palmitoyltransferase I., Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression, Vol.1307, No.2, 157-161, 1996. (Summary) With a cDNA probe encoding rat muscle type carnitine palmitoyltransferase I (CPTI), we isolated cDNA and genomic clones encoding the human homologue and deduced the primary structure of human muscle type CPTI. By Northern analysis, we confirmed the dominant expression of this isoform in heart and skeletal muscle. (Keyword) Amino Acid Sequence / Animals / Base Sequence / Carnitine O-Palmitoyltransferase / DNA, Complementary / Humans / Isoenzymes / Molecular Sequence Data / Muscle, Skeletal / Myocardium / Rats / Sequence Homology, Amino Acid (Link to Publication Site) ● Publication site (DOI): 10.1016/0167-4781(96)00069-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 8679700 ● Search Scopus @ Elsevier (PMID): 8679700 ● Search Scopus @ Elsevier (DOI): 10.1016/0167-4781(96)00069-3 (DOI: 10.1016/0167-4781(96)00069-3, PubMed: 8679700)
51.	Naoshi Yamazaki, Yasuo Shinohara, Atsushi Shima and Hiroshi Terada : High expression of a novel carnitine palmitoyltransferase I like protein in rat brown adipose tissue and heart: isolation and characterization of its cDNA clone., FEBS Letters, Vol.363, No.1-2, 41-45, 1995.
52.	Yasuo Shinohara, Makio Kamida, Naoshi Yamazaki and Hiroshi Terada : Isolation and characterization of cDNA clones and a genomic clone encoding rat mitochondrial adenine nucleotide translocator., Biochimica et Biophysica Acta (BBA) - Biomembranes, Vol.1152, No.1, 192-196, 1993. (Summary) Two cDNA clones encoding rat mitochondrial adenine nucleotide translocator were isolated from libraries constructed from mRNAs of heart and liver. These two clones corresponded to the heart-skeletal muscle type (ANT1) and fibroblast type (ANT2), respectively. A genomic clone encoding rat ANT1 was also isolated and characterized. (Keyword) Amino Acid Sequence / Animals / Cloning, Molecular / DNA / Gene Library / Isoenzymes / Male / Mitochondria, Heart / Mitochondria, Liver / Mitochondrial ADP, ATP Translocases / Molecular Sequence Data / RNA, Messenger / Rats / Rats, Sprague-Dawley / Rats, Wistar (Link to Publication Site) ● Publication site (DOI): 10.1016/0005-2736(93)90248-X (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 8399300 ● Search Scopus @ Elsevier (PMID): 8399300 ● Search Scopus @ Elsevier (DOI): 10.1016/0005-2736(93)90248-X (DOI: 10.1016/0005-2736(93)90248-X, PubMed: 8399300)

Review, Commentary:

1.	Masahiro Watanabe, Takenori Yamamoto, Chihiro Mori, Naoto Okada, Naoshi Yamazaki, Kazuaki Kajimoto, Masatoshi Kataoka and Yasuo Shinohara : Cold-induced changes in gene expression in brown adipose tissue: implications for the activation of thermogenesis., Biological & Pharmaceutical Bulletin, Vol.31, No.5, 775-784, May 2008. (Summary) Brown adipose tissue (BAT) is the site of heat production (thermogenesis). This unique function is performed by uncoupling protein 1 (UCP1) specifically expressed in mitochondria of BAT. UCP1 dissipates the driving force of ATP synthesis, and thus causes heat production followed by energy expenditure. The thermogenic function of BAT has the role of maintaining body temperature under cold conditions. When animals are exposed to cold, the expression of UCP1 gene is increased to activate thermogenesis. To date, functional analysis of BAT has been focused on UCP1, because it plays an indispensable role in thermogenesis. However, the gene expression of not only UCP1 but also that of other genes in BAT is expected to be regulated to achieve effective thermogenesis. Our previous investigations showed increased expression of genes that encode several energy metabolic enzymes in the BAT of rats kept in the cold. These changes in gene expression imply that the enhancement of energy metabolism is needed to activate thermogenesis. Furthermore, various reports from studies focused on genes whose expression is changed in response to cold stimulation have provided new insights into the function of BAT. In this review, to understand the thermogenic function of BAT systematically, we have provided an overview of previous findings on changes in the expression of genes thought to be related to the activation of thermogenesis in BAT. (Keyword) brown adipose tissue / Animals / Cold Temperature / gene expression / Humans / Thermogenesis (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.31.775 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18451493 ● CiNii @ National Institute of Informatics (CRID): 1390001204626091008 ● Search Scopus @ Elsevier (PMID): 18451493 ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.31.775 (DOI: 10.1248/bpb.31.775, PubMed: 18451493, CiNii: 1390001204626091008)
2.	Masahiro Watanabe, Naoshi Yamazaki, Masatoshi Kataoka and Yasuo Shinohara : Exploratory Studies on Biomarkers : An Example Study on Brown Adipose Tissue, IEEJ Transactions on Electronics, Information and Systems, Vol.127, No.2, 198-203, Feb. 2007. (Summary) In mammals, two kinds of adipose tissue are known to exist, i.e., white (WAT) and brown (BAT) adipose tissue. The physiological role of WAT is storage of excess energy as fat, whereas that of BAT is the expenditure of excess energy as heat. The uncoupling protein UCP1, which is specifically expressed in brown fat mitochondria, dissipates the proton electrochemical potential across the inner mitochondrial membrane, known as a driving force of ATP synthesis, and thus it dissipates excess energy in a form of heat. Because deficiency in effective expenditure of excess energy causes accumulation of this energy in the form of fat (i.e., obesity), it is very important to understand the energy metabolism in this tissue for the development of anti-obesity drugs. In this article, in addition to providing a brief introduction to the functional properties of BAT and UCP1, the results of our exploratory studies on protein components involved in the energy-dissipating function in BAT. (Keyword) brown adipose tissue / energy metabolism / gene expression profiles / microarray (Link to Publication Site) ● Publication site (DOI): 10.1541/ieejeiss.127.198 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679583070464 ● Search Scopus @ Elsevier (DOI): 10.1541/ieejeiss.127.198 (DOI: 10.1541/ieejeiss.127.198, CiNii: 1390282679583070464)
3.	Naoshi Yamazaki : Identification of muscle-type carnitine palmitoyltransferase I and characterization of its gene structure, Journal of the Pharmaceutical Society of Japan, Vol.124, No.12, 893-908, Dec. 2004. (Summary) To characterize energy metabolism in brown adipose tissue (BAT), differential screening of a cDNA library of rat BAT with a cDNA probe of rat white adipose tissue was carried out. We isolated one novel cDNA clone encoding a protein of 88.2 kDa consisting of 772 amino acids. The deduced amino acid sequence showed the highest homology (62.6%) with that of rat liver carnitine palmitoyltransferase I (CPTI). The transcript corresponding to this cDNA was abundantly expressed not only in BAT but also in the heart and skeletal muscle. CPTI is a protein necessary for the beta-oxidation of long-chain fatty acids in mammalian mitochondria, and it has been suggested that at least two isoforms, the liver type and muscle (M-CPTI) type, exist. Based on these observations, we concluded that the novel cDNA clone isolated from rat BAT encodes M-CPTI. Isolation and characterization of a genomic DNA clone revealed that the gene for human M-CPTI consists of two 5'-noncoding exons, 18 coding exons, and one 3'-noncoding exon spanning approximately 10 kbp, and a gene encoding choline/ethanolamine kinase-beta (CK/EK-beta) was located about 300 bp upstream from the M-CPTI gene with the same strand direction. Furthermore, we found atypical transcripts containing exons of both CK/EK-beta and M-CPTI genes in humans and rodents. The physiologic role(s) of these transcripts is still unknown. However, it is interesting that such transcripts are produced from two tightly arranged and functionally unrelated genes in mammalian tissues. (Keyword) Adipose Tissue, Brown / Animals / Carnitine O-Palmitoyltransferase / Exons / Fatty Acids / Gene Library / Genes, Overlapping / Humans / Liver / Muscle, Skeletal / Myocardium / Oxidation-Reduction / RNA, Messenger / Rats / Sequence Homology, Amino Acid (Link to Publication Site) ● Publication site (DOI): 10.1248/yakushi.124.893 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15577262 ● Search Scopus @ Elsevier (PMID): 15577262 ● Search Scopus @ Elsevier (DOI): 10.1248/yakushi.124.893 (DOI: 10.1248/yakushi.124.893, PubMed: 15577262)
4.	Naoshi Yamazaki : Identification of Muscle-Type Carnitine Palmitoyltransferase I and Characterization of Its Atypical Gene Structure, Biological & Pharmaceutical Bulletin, Vol.27, No.11, 1707-1716, Nov. 2004. (Summary) To characterize energy metabolism in rat brown adipose tissue (BAT), we carried out differential screening of a cDNA library of BAT with a cDNA probe of white adipose tissue and isolated one novel cDNA clone. It contained a single open-reading frame of 2316 bases, which encodes a protein of 88.2 kDa. The predicted amino acid sequence showed the highest homology (62.6%) with that of carnitine palmitoyltransferase I (CPTI) from rat liver. The transcript corresponding to this cDNA was found to be abundantly expressed not only in BAT but also in heart and skeletal muscle. CPTI is known to be a protein necessary for the beta-oxidation of long-chain fatty acids in mammalian mitochondria, and it has been suggested that at least two isoforms, the liver type and muscle type, exist. From these observations, a cDNA clone isolated from rat BAT was concluded to be encoding muscle-type CPTI (M-CPTI). Characterization of a genomic DNA clone revealed that the gene for human M-CPTI consists of two 5'-noncoding exons, 18 coding exons, and one 3'-noncoding exon spanning approximately 10 kbp, and a gene encoding choline/ethanolamine kinase-beta (CK/EK-beta) was located only about 300 bp upstream from the M-CPTI gene with the same strand direction. Furthermore, we found that unordinary transcripts containing exons of both CK/EK-beta and M-CPTI genes exist in human and rodent tissues. Although the physiologic role(s) of these transcripts is still unknown, it is interesting that such transcripts are produced from two tightly arranged and functionally unrelated genes. (Keyword) Adipose Tissue, Brown / Amino Acid Sequence / Animals / Carnitine O-Palmitoyltransferase / Energy Metabolism / Humans / Isoenzymes / Liver / Molecular Sequence Data / Muscle, Skeletal / Muscle, Smooth / Myocardium / Organ Specificity / Rats (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.27.1707 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15516711 ● Search Scopus @ Elsevier (PMID): 15516711 ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.27.1707 (DOI: 10.1248/bpb.27.1707, PubMed: 15516711)
5.	Kazuaki Kajimoto, Naoshi Yamazaki, Masatoshi Kataoka, Hiroshi Terada and Yasuo Shinohara : Identification of possible protein machinery involved in the thermogenic function of brown adipose tissue., The Journal of Medical Investigation : JMI, Vol.51, No.1-2, 20-28, Feb. 2004. (Summary) Brown adipose tissue (BAT) is believed to function by dissipating excess energy in mammals. It is very important to understand the energy metabolism held in BAT since disorder of its energy-dissipating function may cause obesity or lifestyle-related diseases such as hypertension and diabetes. This function in BAT is mainly attributable to uncoupling protein (UCP), specifically expressed in its mitochondria. This protein consumes excess energy as heat by dissipating the H+ gradient across the inner mitochondrial membrane that is utilized as a driving force for ATP synthesis. In this review article, in addition to providing a brief introduction to the functional properties of BAT and UCP, we also describe and discuss properties of cultured brown adipocytes and the results of our exploratory studies on protein components involved in the energy-dissipating function in BAT. (Keyword) Adipose Tissue, Brown / Animals / Calcium Channels / Carrier Proteins / Energy Metabolism / Gene Expression Profiling / Humans / Inositol 1,4,5-Trisphosphate Receptors / Ion Channels / Membrane Proteins / Mitochondrial Proteins / Oligonucleotide Array Sequence Analysis / Polymerase Chain Reaction / Proteins / Receptors, Cytoplasmic and Nuclear / Thermogenesis (Tokushima University Institutional Repository) ● Metadata: 110710 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.51.20 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15000252 ● Search Scopus @ Elsevier (PMID): 15000252 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.51.20 (Tokushima University Institutional Repository: 110710, DOI: 10.2152/jmi.51.20, PubMed: 15000252)
6.	Yasuo Shinohara, Kazuaki Kajimoto, Takiko Daikoku, Atsushi Shima, Naoshi Yamazaki and Hiroshi Terada : Bioenergetics in brown adipose tissue., Recent Res. Devel.Bioener., Vol.2, 1-14, 2002.
7.	Naoshi Yamazaki, Yasuo Shinohara and Hiroshi Terada : ミトコンドリア輸送タンパクスーパーファミリー, 生体の科学, Vol.46, No.5, 605-607, Oct. 1995.

Proceeding of International Conference:

1.	Seigi Yamamoto, Noriko Saito-Tarashima, Naoshi Yamazaki, Tatsuya Fukuta, Kentaro Kogure and Noriaki Minakawa : Development and Evaluation of Photoresponsive DNA Prism with Nucleic Acid Medicine., The 45th International Symposium on Nucleic Acids Chemistry (ISNAC 2018), Nov. 2018.
2.	Naoshi Yamazaki, Makiko Shinomiya, Hironobu Ike, Yasuo Shinohara, Noriaki Minakawa, Kouji Itou and Yoshiharu Takiguchi : Use of modified U1 small nuclear RNA for improved formation of properly spliced mRNA encoding human cathepsin A from the gene having an IVS7 +3a>g mutation, The 43rd FEBS Congress, Praha, Jul. 2018.
3.	Naoshi Yamazaki, Yasuo Shinohara, Kouji Itou, Noriaki Minakawa and Yoshiharu Takiguchi : Rescue of mutation-induced exon 7 skipping in human Cathepsin A by using modified U1 small nuclear RNA, 2016 ASCB Annual Meeting, San Francisco, Dec. 2016.
4.	Tarashima Noriko, Naoshi Yamazaki, Kazuhiro Furukawa and Noriaki Minakawa : Enzymatic incorporation of unnatural ImNN:NaOO base pair consisting of four hydrogen bonds, The 40th International Symposium on Nucleic Acids Chemistry, 神奈川大学(神奈川県), Nov. 2013.
5.	Noriko Saito-Tarashima, Kojima Takamitsu, Hashimoto Yosuke, Kazuhiro Furukawa, Naoshi Yamazaki, Hiroshi Kiwada, Tatsuhiro Ishida, Noriaki Minakawa and Yoshiharu Takiguchi : A novel approach of gene suppression using an intelligent shRNA expressing device (iRed), 9th Annual Meeting of the Oligonucleotide Therapeutics Society, Naples(Italy), Oct. 2013.
6.	Takuya Hada, Yumiko Kato, Eriko Obana, Naoshi Yamazaki, Takenori Yamamoto and Yasuo Shinohara : Comparison of two expression systems using COS7 Cells and yeast cells for expression of heart/muscle-type carnitine palmitoyltransferase 1, American Society for Cell Biology 2012 Annual Meeting, San Francisco, Dec. 2012.
7.	Y. Kikuchi, Naoshi Yamazaki, Yoshiharu Takiguchi and Noriaki Minakawa : Gene silencing by 2'-modified-4'-thio oligonucleotides via U1i machinery, 第39回国際核酸化学シンポジウム, Nov. 2012.
8.	Taisuke Matsuo, Takenori Yamamoto, Katsuda Chie, Naoshi Yamazaki, Yasuo Shinohara and Masatoshi Kataoka : Substitution of Certain Amino Acids in a Short Peptide Causes a Significant Difference in Their Immunoreactivities with Antibodies Against Different Epitopes: Evidence for Possible Folding of the Peptide on Nitrocellulose or PVDF Membrane, International symposium on system cell engineering by multi-scale manipulation, Nagoya, Nov. 2008.
9.	Taisuke Matsuo, Naoshi Yamazaki, Tatsuhiro Ishida, Hiroshi Kiwada, Yasuo Shinohara and Masatoshi Kataoka : Design, preparation and directional insertion of peptides into lipid bilayer membrane and heir application for the preparation of liposome of which surface could be coated by externally added antibody, International symposium on system cell engineering by multi-scale manipulation, Nagoya, Nov. 2007.
10.	Tatsuhiro Ishida, Tatsuaki Tagami, Barichello M. Jose, Kiyomi Hirose, Naoshi Yamazaki, Tomohiro Asai, Naoto Oku and Hiroshi Kiwada : Argonaute2 (Ago2) gene silencing by liposomal transfection with siRNA for Ago2 induces apoptosis on HT1080 cells and HUVECs., American Society of Gene Therapy's 10th annual Meeting, Seattle USA, May 2007.
11.	Taisuke Matsuo, Naoshi Yamazaki, Tatsuhiro Ishida, Hiroshi Kiwada, Yasuo Shinohara and Masatoshi Kataoka : Mutant coat proteins of Pf3 bacteriophage as models of membrane proteins and their interactions with lipid bilayer membrane, Pre-Satellite Meeting of the 3rd Pharmaceutical Sciences World Congress (PSWC 2007) for and by Ph.D. students and postdoctoral fellows, Amsterdam, Apr. 2007.
12.	Akihiro Iwahasi, Naoshi Yamazaki, Hiroshi Terada and Yasuo Shinohara : Structural analysis of C-terminal region of mitochondrial ADP/ATP carrier by site-directed mutagenesis and chemical modifications, Pre-Satellite Meeting of the 3rd Pharmaceutical Sciences World Congress (PSWC 2007) for and by Ph.D. students and postdoctoral fellows, Amsterdam, Apr. 2007.
13.	Masahiro Watanabe, Takenori Yamamoto, Rei Kakuhata, Kazuaki Kajimoto, Fumiyo Kita, Naoshi Yamazaki, Yoshinobu Baba and Yasuo Shinohara : Synchronized changes in the transcript levels of the genes towards activated thermogenesis in brown adipose tissue induced by cold exposure of experimental animals, Pre-Satellite Meeting of the 3rd Pharmaceutical Sciences World Congress (PSWC 2007) for and by Ph.D. students and postdoctoral fellows, Amsterdam, Apr. 2007.
14.	Rei Kakuhata, Takenori Yamamoto, Masahiro Watanabe, Naoshi Yamazaki, Masatoshi Kataoka, Yoshinobu Baba and Yasuo Shinohara : Possible utilization of synthetic mRNAs as standards for microarray analysis, Pre-Satellite Meeting of the 3rd Pharmaceutical Sciences World Congress (PSWC 2007) for and by Ph.D. students and postdoctoral fellows, Amsterdam, Apr. 2007.
15.	Taisuke Matsuo, Naoshi Yamazaki, Tatsuhiro Ishida, Hiroshi Kiwada, Yasuo Shinohara and Masatoshi Kataoka : Mutant coat proteins of Pf3 bacteriophage as models of membrane proteins and their interactions with lipid bilayer membrane, International symposium on system cell engineering by multi-scale manipulation, Nagoya, Nov. 2006.
16.	Naoshi Yamazaki, Saki Imamura, Hirokazu Sato, Arisa Hironaga, Takenori Yamamoto, Yasuo Shinohara and Hiroshi Terada : cDNA from Rat Brown Adipose Tissue Codes a Novel Protein Containing DH, BAR, and SH3 Domains, 20th IUBMB International Congress of Biochemistry and Molecular Biology and 11th FAOBMB Congress, Kyoto, Jun. 2006.
17.	Takenori Yamamoto, Naoshi Yamazaki, Masatoshi Kataoka, Hiroshi Terada and Yasuo Shinohara : Two critical factors affecting the release of mitochondrial cytochrome c as revealed by studies using N,N'-dicyclohexylcarbodiimide as an inducer of permeability transition, The 11th Korea-Japan Joint Symposium on Drug Design and Development, Cheju, May 2006.
18.	Kazuaki Kajimoto, Takiko Daikoku, Naoshi Yamazaki, Yasuo Shinohara and Hiroshi Terada : Dominant Expression of NAD+-dependent Isocitrate Dehydrogenase in Brown Adipose Tissue, 42nd American Society for Cell Biology Annual Meeting, San Francisco, Dec. 2002.
19.	Naoshi Yamazaki, Yasuo Shinohara and Hiroshi Terada : High Expression of a Novel Carnitine Palmitoyltransferase I in Brown Adipose Tissue and Muscle: Isolation and Characterization of its cDNA and Genomic Clones, The 9th Korea-Japan Joint Symposium on Drug Design and Development, Seoul, May 2002.
20.	Naoshi Yamazaki, Yasuo Shinohara and Hiroshi Terada : Isolation and characterization of cDNA and genomic clones encoding human muscle type carnitine palmitoyltransferase I, 12th International Symposium of Federation of Asian and Oceanian Biochemists and Molecular Biologist, Tokushima, Jul. 1996.

Proceeding of Domestic Conference:

1.	松田あすか, Naoshi Yamazaki and Kentaro Kogure : カルニチンパルミトイルトランスフェラーゼ1Bの翻訳後修飾の可能性, 第63回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2024.
2.	KAZUTO Takegawa, 伊藤剛, Yuka Nagasaki, Naoshi Yamazaki, 新藤充 and Yasuo Shinohara : ボンクレキン酸がミトコンドリアのADP/ATP輸送体を阻害する際に重要となる部分構造, ダイバーシティ推進研究交流発表会オンライン2023, Mar. 2024.
3.	Kiri Akieda, KAZUTO Takegawa, 伊藤剛, NAGAYAMA Gaku, Naoshi Yamazaki, Yuka Nagasaki, 西野耕平, Hidetaka Kosako and Yasuo Shinohara : 大腸菌発現系を用いた哺乳類脂質代謝酵素の特性解析と機能評価, ダイバーシティ推進研究交流発表会オンライン2023, Mar. 2024.
4.	Kentaro Kogure, Chiho Ohtsuka, Mizune Ohzono and Naoshi Yamazaki : 微弱電流により誘起されるエンドサイトーシスのユニークな特性, 日本膜学会「第45年会」・「膜シンポジウム2023」合同大会, Nov. 2023.
5.	堤敏彦, 川畑公平, Naoshi Yamazaki, 月川健士, 西博行 and Akira Tokumura : NRK52E細胞内外でのリゾホスファチジン酸と環状ホスファチジン酸の産生, 第96回日本生化学会大会, Oct. 2023.
6.	Naoshi Yamazaki, Airi Ohkawa, Shiori Yamamoto, Arisa Biwatani, Jun Tsukimoto, Kouji Itou and Kentaro Kogure : 塩基改変U1 snRNAを用いたカテプシンAスプライス異常の修復, 第62回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2023.
7.	Airi Ohkawa, Shiori Yamamoto, Arisa Biwatani, Jun Tsukimoto, Kouji Itou, Kentaro Kogure and Naoshi Yamazaki : 改変 U1 snRNA を用いたカテプシン A スプライス異常の修復, 第64回日本生化学会中国四国支部例会, May 2023.
8.	KAZUTO Takegawa, Takeshi Ito, Naoshi Yamazaki, Mitsuru Shindo and Yasuo Shinohara : ボンクレキン酸誘導体 KH-17はミトコンドリアのADP/ATP輸送体を膜の外側からも弱く阻害する, 第95回日本生化学大会(一般講演), Nov. 2022.
9.	堤敏彦, 川畑公平, 西博行, Naoshi Yamazaki, 月川健 and Akira Tokumura : 腎臓由来NRK52E細胞のリゾホスホリパーゼD活性の分泌―グリセロホスホジエステラーゼ7関与の可能性, 第95回日本生化学会大会, Nov. 2022.
10.	Ryosuke Kotoh, Asuka Matsuda, Chika Sugahara, Yasuo Shinohara and Naoshi Yamazaki : カルニチンパルミトイルトランスフェラーゼ1Bの翻訳段階以降の過程での発現調節の可能性, 第61回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2022.
11.	Megumi Naka, Atsumi Toiyama, Takeshi Ito, Yoshinobu Fujiwara, Takenori Yamamoto, Naoshi Yamazaki and Yasuo Shinohara : Inhibitor resistant ADP/ATP carrier by combination of mutations weakening its sensitivity, 日本薬学会第142年会(一般ポスター発表), Mar. 2022.
12.	Takeshi Ito, Yoshinobu Fujiwara, Atsumi Toiyama, Takenori Yamamoto, Naoshi Yamazaki, Mitsuru Shindo and Yasuo Shinohara : スラミンはミトコンドリアADP/ATP 輸送体を膜の両側から阻害する, 第42 回生体膜と薬物の相互作用シンポジウム(一般講演), Oct. 2021.
13.	Mao Kawai, Momoka Ueta, Naoshi Yamazaki and Yoshiharu Takiguchi : ヒトCPT1a mRNAの3'非翻訳領域におけるA-to-I RNA編集部位, 第60回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2021.
14.	Sakura Miyagi, Naoshi Yamazaki, Ryosuke Kotoh, Yasuo Shinohara and Yoshiharu Takiguchi : A-to-I RNA編集によるヒトCPT1a発現量の変化, 第59回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2020.
15.	堤敏彦, Naoshi Yamazaki and Akira Tokumura : グリセロホスホジエステラーゼによるリゾホスファチジン酸産生と腎障害, 令和2年度日本生化学会九州支部例会, 32, May 2020.
16.	Rina Takahashi, Momoka Ueta, Kanae Koide, Mao Kawai, Naoshi Yamazaki, Jun Tsukimoto, Kouji Itou and Yoshiharu Takiguchi : イントロンやエクソン内の配列と結合する改変U1 snRNAによるCTSAエクソン7スプライス異常の修復, 第58回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2019.
17.	Toshiki Okumura, Naoshi Yamazaki, Seitaroh Takaishi, Sakura Miyagi and Yoshiharu Takiguchi : ヒトCPT1A mRNAにおけるA-to-I RNA編集の意義の解明, 第58回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2019.
18.	堤敏彦, Risa Matsuda, Katsuya Morito, Miho Yokota, Miki Nikawadori, 川島聡, 藤原愛美, Takenori Yamamoto, Naoshi Yamazaki, Tamotsu Tanaka, Yasuo Shinohara and Akira Tokumura : 動物培養細胞においてグリセロホスホジエステラーゼ3はリゾホスファチジルイノシトールをモノアシルグリセロールに分解するエクト型リゾホスホリパーゼCとして機能する, 第92回日本生化学会大会, Sep. 2019.
19.	徳橋尚紀, Yuka Kawaguchi, Naoshi Yamazaki, 宮城さくら, Yasuo Shinohara and Yoshiharu Takiguchi : ヒトCPT1A mRNAの3'-UTRにおけるA-to-I RNA編集, 第57回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2018.
20.	四宮槙子, 小出華永, Rina Takahashi, Naoshi Yamazaki, Jun Tsukimoto, Kouji Itou and Yoshiharu Takiguchi : Exon specific U1 snRNAによる CTSAエクソン7スプライス異常の修復, 第57回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2018.
21.	高田元太, 橋本晴香, Naoshi Yamazaki and Yoshiharu Takiguchi : トランススプライシングを用いたヒトカテプシンAエクソンスキップ修復の試み, 第57回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2018.
22.	四宮槙子, 小出華永, Rina Takahashi, Naoshi Yamazaki, 月本準, Kouji Itou and Yoshiharu Takiguchi : Exon specific U1 snRNAs correct CTSA exon7 skipping caused by the 5-splice site mutation, 第91回日本生化学会大会, Sep. 2018.
23.	徳橋尚紀, Yuka Kawaguchi, Naoshi Yamazaki, 宮城さくら, Yasuo Shinohara and Yoshiharu Takiguchi : 3'-UTR inverted repeat Alu elements of human carnitine palmitoyltransferase 1A mRNA undergo RNA editing by ADAR, 第91回日本生化学会大会, Sep. 2018.
24.	高田元太, 橋本晴香, Naoshi Yamazaki and Yoshiharu Takiguchi : Repair of human cathepsin A exon 7 skipping by trans-splicing, 第91回日本生化学会大会, Sep. 2018.
25.	四宮槙子, 小出華永, Rina Takahashi, Jun Tsukimoto, Naoshi Yamazaki, Kouji Itou and Yoshiharu Takiguchi : 改変U1 snRNAによるカテプシンAスプライス異常修復効果の検討, 第59回日本生化学会中国四国支部例会, May 2018.
26.	Yuka Kawaguchi, Naoki Tokuhashi, Naoshi Yamazaki, Yasuo Shinohara and Yoshiharu Takiguchi : ヒトCPT1a mRNA 3'-UTR中の逆向きAlu配列はA-to-I RNA編集を受ける, ConBio2017, Dec. 2017.
27.	Yuka Kawaguchi, Naoki Tokuhashi, Naoshi Yamazaki, Yasuo Shinohara and Yoshiharu Takiguchi : ヒトCPT1a mRNAの3 '-UTRに存在する逆向きAlu配列とRNA編集, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
28.	Akari Saitoh, Makiko Shinomiya, Rina Takahashi, Naoshi Yamazaki and Yoshiharu Takiguchi : ヒトカテプシンAエクソン7スキッピングにおける3 'スプライスサイトの関与, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
29.	Momoko Yamamura, Genta Takada, Kazuya Tominaga, Naoshi Yamazaki and Yoshiharu Takiguchi : ヒトカテプシンAスプライス異常修復を目指したトランススプライシング法の確立, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
30.	Mao Inoue, Genta Takada, Naoshi Yamazaki and Yoshiharu Takiguchi : トランススプライシングを用いたヒトカテプシンAスプライシング異常修復の検討, 第55回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2016.
31.	Maria Kimura, Makiko Shinomiya, Hironobu Ike, Akari Saitoh, Naoshi Yamazaki, Kouji Itou, Noriaki Minakawa and Yoshiharu Takiguchi : カテプシンAスプライシング異常の修復を目指した改変U1 snRNA発現系の構築, 第55回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2016.
32.	坪井一人, Iffat Sonia Ara Rahman, 岡本蓉子, 宇山徹, Naoshi Yamazaki, Tamotsu Tanaka, Akira Tokumura and 上田夏生 : GDE7はリゾホスホリパーゼD型酵素としてN-アシルエタノールアミンとLPAを生成する, 第89回日本生化学会大会, Sep. 2016.
33.	松田璃沙, 坪井一人, 岡本蓉子, 山下量平, Rahman Ara Sonia Iffat, 日高麻由美, Naoshi Yamazaki, 上田夏生, Tamotsu Tanaka and Akira Tokumura : 口腔粘膜上皮細胞に存在する膜結合型リゾホスホリパーゼD, 第58回日本脂質生化学会, Jun. 2016.
34.	Iffat Sonia Ara Rahman, Kazuhito Tsuboi, Yoko Okamoto, Toru Uyama, Naoshi Yamazaki, Tamotsu Tanaka, Akira Tokumura and Natsuo Ueda : Glycerophosphodiesterases, GDE4 and GDE7, are novel lysophospholipase D-type enzymes generating N-acylethanolamine and LPA, 第57回日本生化学会中国四国支部例会, May 2016.
35.	Maria Kimura, Hironobu Ike, Akari Saitoh, Naoshi Yamazaki, Kouji Itou, Noriaki Minakawa and Yoshiharu Takiguchi : 塩基改変したU1 snRNAによるカテプシンAスプライス異常修復効果の検討, 第57回日本生化学会中国四国支部例会, May 2016.
36.	上田夏瑞, Noriko Saito-Tarashima, 三木和也, 山村桃子, Naoshi Yamazaki and Noriaki Minakawa : iRedを利用した持続的microRNA補充法の開発, 日本薬学会第136年会, Mar. 2016.
37.	池啓伸, Naoshi Yamazaki, 金澤慶祐, 木村麻里安, Noriaki Minakawa, Daisuke Tsuji and Kouji Itou : 改変型U1 snRNAを用いたヒトカテプシンAの遺伝子発現におけるスプライシング異常の是正, 日本薬学会第136年会(横浜), Mar. 2016.
38.	池啓伸, Naoshi Yamazaki, 金澤慶祐, 木村麻里安, Noriaki Minakawa, Daisuke Tsuji and Kouji Itou : 改変型低分子RNAを用いたヒトカテプシンAの遺伝子発現におけるスプライシング異常の是正, BMB2015 第38回日本分子生物学会年会・第88回日本生化学会大会合同大会, Dec. 2015.
39.	Kazuya Miki, Momoko Yamamura, Noriko Saito-Tarashima, Naoshi Yamazaki, Noriaki Minakawa and Yoshiharu Takiguchi : 新規機能性RNA発現デバイスiRedを用いたmiRNA産生による遺伝子発現抑制効果の検討, BMB2015 第38回日本分子生物学会年会・第88回日本生化学会大会合同大会, Dec. 2015.
40.	Maria Kimura, Keisuke Kanazawa, Akari Saitoh, Naoshi Yamazaki, Hironobu Ike, Kouji Itou, Noriaki Minakawa and Yoshiharu Takiguchi : 改変U1 snRNAを用いた変異カテプシンAスプライス異常の修復, BMB2015 第38回日本分子生物学会年会・第88回日本生化学会大会合同大会, Dec. 2015.
41.	松田璃沙, 坪井一人, 岡本蓉子, Rahman Ara Iffat Sonia, Naoshi Yamazaki, 上田夏生, Tamotsu Tanaka and Akira Tokumura : 消化管上皮細胞に存在する新規膜結合型リゾホスホリパーゼD, 第54回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2015.
42.	Keisuke Kanazawa, Maria Kimura, Akari Saitoh, Naoshi Yamazaki, Hironobu Ike, Kouji Itou, Noriaki Minakawa and Yoshiharu Takiguchi : 改変U1 snRNAを用いたヒトカテプシンAエクソンスキッピングの修復, 第54回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2015.
43.	Yuki Itoh, Naoshi Yamazaki and Yoshiharu Takiguchi : Carnitine palmitoyltransferase 1アイソフォームのSDS-PAGE移動度に違いをもたらす領域の同定, 第54回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2015.
44.	金澤慶佑, Naoshi Yamazaki, Hironobu Ike, Kouji Itou, Noriaki Minakawa and Yoshiharu Takiguchi : 改変U1 snRNAによるヒトカテプシンAスプライス異常修復, 遺伝子・デリバリー研究会第15回シンポジウム, May 2015.
45.	Yuki Itoh, Mao Inoue, Naoshi Yamazaki and Yoshiharu Takiguchi : CPTⅠタンパク質のアイソフォーム間におけるSDS-PAGE移動度の違い, 第36回生体膜と薬物の相互作用シンポジウム, Nov. 2014.
46.	Shoko Tanaka, Keisuke Kanazawa, Naoshi Yamazaki, Hironobu Ike, Kouji Itou, Noriaki Minakawa and Yoshiharu Takiguchi : 改変U1 snRNAによるヒトカテプシンAスプライス異常修復の試み, 第53回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2014.
47.	Kazuya Miki, Naoshi Yamazaki, Hirotaka Kira, Noriko Saito-Tarashima, Kazuhiro Furukawa, Noriaki Minakawa and Yoshiharu Takiguchi : ナノ核酸デバイスを用いたsiRNAオフターゲット効果の抑制, 第53回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2014.
48.	Yuki Asakura, Kazuya Miki, Maria Kimura, Naoshi Yamazaki and Yoshiharu Takiguchi : 改変U1 snRNAによる遺伝子発現抑制効果の検討, 第53回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2014.
49.	池啓伸, Naoshi Yamazaki, 田中翔子, 金澤慶祐, Yoshiharu Takiguchi, Noriaki Minakawa and Kouji Itou : 改変U1 snRNAによるヒトカテプシンAの遺伝子発現におけるスプライシング異常の修復, 第87回日本生化学会, Oct. 2014.
50.	Noriko Saito-Tarashima, 吉良太孝, Naoshi Yamazaki, Kazuhiro Furukawa and Noriaki Minakawa : ナノ核酸デバイスを利用したsiRNA-タンパク質相互作用における分子認識機構の解明, 創薬懇話会2014in岐阜, Jul. 2014.
51.	Naoshi Yamazaki, Shoko Tanaka, Keisuke Kanazawa, Kouji Itou, Noriaki Minakawa and Yoshiharu Takiguchi : 改変U1snRNAによるヒトカテプシンAスプライス異常修復の試み, 第55回日本生化学会中国・四国支部例会, Jun. 2014.
52.	智子中西, Keisuke Ishizawa, Shinji Abe, Mari Nakase, Hirofumi Shibata, Chiemi Sato, Naokatu Arakaki, Youichi Sato, Naoshi Yamazaki, Jiro Kasahara, Mami Azuma, Tetsuo Yamazaki, Aiko Yamauchi, Yoshiharu Takiguchi and Koichiro Tsuchiya : Study of the method for development of case-problem solving abilities through advanced practice and the results that have been achieved, 日本薬学会第134年会, Mar. 2014.
53.	Noriko Saito-Tarashima, Naoshi Yamazaki, Kazuhiro Furukawa and Noriaki Minakawa : 人工塩基対ImNN :NaO0 のPCR増幅とRNAi創薬への応用, 日本薬学会第134年回, Mar. 2014.
54.	Keita Kageyama, Yasuo Shinohara, Takenori Yamamoto, Naoshi Yamazaki and Yoshiharu Takiguchi : ミトコンドリア透過性遷移におけるシクロフィリンDの挙動解析, 第87回日本薬理学会年会, Mar. 2014.
55.	Naoshi Yamazaki, 阿萬明, Yuki Asakura, Yuji Fujiwara, Noriaki Minakawa and Yoshiharu Takiguchi : 改変U1 snRNAによる遺伝子発現抑制効果の検討, 第23回アンチセンスシンポジウム, Nov. 2013.
56.	Yuji Fujiwara, Naoshi Yamazaki, Noriaki Minakawa and Yoshiharu Takiguchi : 複数の改変U1 snRNAを用いた遺伝子発現抑制, 第23回アンチセンスシンポジウム, Nov. 2013.
57.	Yuji Fujiwara, Naoshi Yamazaki and Yoshiharu Takiguchi : 改変U1 snRNAによる遺伝子発現制御, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
58.	智子中西, Keisuke Ishizawa, Shinji Abe, Mari Nakase, Hirofumi Shibata, Chiemi Sato, Naokatu Arakaki, Youichi Sato, Naoshi Yamazaki, Jiro Kasahara, Mami Azuma, Tetsuo Yamazaki, Aiko Yamauchi, Yoshiharu Takiguchi and Koichiro Tsuchiya : Study of the method for development of case-problem solving abilities through advanced practice and the results that have been achieved, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
59.	Mika Kadota, Naoshi Yamazaki and Yoshiharu Takiguchi : CPT1アイソフォームのSDS-PAGE移動度の違い, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
60.	Takuya Hada, 加藤弓子, Eriko Obana, 山本篤司, Naoshi Yamazaki, Takenori Yamamoto and Yasuo Shinohara : 異なる発現系において観察された筋型カルニチンパルミトイルトランスフェラーゼ1(CPT1b)の酵素活性の違い, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 23, Oct. 2013.
61.	Naoto Okada, Takenori Yamamoto, 渡邊政博, 吉村勇哉, Eriko Obana, Naoshi Yamazaki, Kazuyoshi Kawazoe, Yasuo Shinohara and Kazuo Minakuchi : 機能未知タンパク質TMEM45Bの熱凝集に関与するアミノ酸配列の同定, 第85回生化学会, Dec. 2012.
62.	Ken Ishido, Yumi Kondoh, Satoru Hashimura, Akira Tokumura, Naoshi Yamazaki and Yoshiharu Takiguchi : ラット血管肥厚形成への内因性リゾホスファチジン酸の関与, 第122回日本薬理学会近畿部会, Nov. 2012.
63.	Miki Yanagisawa, Yoshiharu Takiguchi and Naoshi Yamazaki : CPT1アイソフォームのSDS-PAGE移動度の違い, 第51回日本薬学会・日本病院薬剤師会中国四国支部学術大会, Nov. 2012.
64.	Akira Ama, Yuki Asakura, Noriaki Minakawa, Yoshiharu Takiguchi and Naoshi Yamazaki : 改変U1snRNAによる遺伝子発現抑制, 第51回日本薬学会・日本病院薬剤師会中国四国支部学術大会, Nov. 2012.
65.	Hirotaka Kira, Naoshi Yamazaki, Tatsuhiro Ishida, Hiroshi Kiwada and Noriaki Minakawa : ケミカルツールを利用したRNA干渉の発現機構解明, アンチセンス,遺伝子,デリバリーシンポジウム2012, Sep. 2012.
66.	秦拓也, 加藤弓子, Eriko Obana, Naoshi Yamazaki, Takenori Yamamoto and Yasuo Shinohara : Comparison of two expression systems using COS7 cells and yeast Cells for expression of heart/muscle-type CPT1, 第50回日本生物物理学会, Sep. 2012.
67.	Keita Kageyama, Yasuo Shinohara, Takenori Yamamoto, Naoshi Yamazaki and Yoshiharu Takiguchi : 透過性遷移を誘起したミトコンドリアにおけるシクロフィリンDの挙動の解析, 第121回日本薬理学会近畿部会, Jun. 2012.
68.	菊地優作, Naoshi Yamazaki, Yoshiharu Takiguchi and Noriaki Minakawa : 2'-F-4'-チオヌクレオシドを含むキメラ型オリゴマーの合成と性質, 日本薬学会第132年会(札幌), Mar. 2012.
69.	Takuya Hada, Yumiko Kato, Eriko Obana, Atsushi Yamamoto, Naoshi Yamazaki, Mitsuru Hashimoto, Takenori Yamamoto and Yasuo Shinohara : COS細胞および酵母で発現させた筋型カルニチンパルミトイル基転移酵素(Cpt1b)の性質の比較, 日本薬学会第132年会, Mar. 2012. (Keyword) mitochondria
70.	Takamitsu Kojima, Naoto Moriyoshi, Naoshi Yamazaki, Tatsuhiro Ishida, Hiroshi Kiwada and Noriaki Minakawa : 4'-チオDNAを利用した遺伝子発現抑制法の開発, 日本薬学会第132年会, Mar. 2012.
71.	石戸健, 中本淳子, 淺木千佳, Akira Tokumura, Naoshi Yamazaki and Yoshiharu Takiguchi : リゾフォスファチジン酸の血管肥厚形成への関与, 第85回日本薬理学会年会, Mar. 2012.
72.	Tomomi Ishido, Naoshi Yamazaki, Mitsuru Ishikawa and Ken Hirano : Characterization of DNA polymerase b from model fish organisms Medaka and Zebrafish., 第34回日本分子生物学会年会, Dec. 2011.
73.	Naoto Okada, Takenori Yamamoto, 渡邊政博, 吉村勇哉, Eriko Obana, Naoshi Yamazaki, Kazuyoshi Kawazoe, Kazuo Minakuchi and Yasuo Shinohara : 機能未同定のタンパク質TMEM45Bに見られた熱凝集と熱凝集を引き起こすアミノ酸領域の同定, 第33回生体膜と薬物の相互作用シンポジウム, Nov. 2011.
74.	新田芳久, 塩田祐子, 下川義彦, Naoshi Yamazaki and Yoshiharu Takiguchi : 毛髪を用いた肝CYP3A4代謝活性評価に関する基礎的検討, 第50回日本薬学会・日本病院薬剤師会中国四国支部学術大会, Nov. 2011.
75.	中本淳子, 板東由佳, 淺木千佳, Akira Tokumura, Naoshi Yamazaki and Yoshiharu Takiguchi : ラット血管肥厚形成への内因性リゾホスファチジン酸の関与, 第50回日本薬学会・日本病院薬剤師会中国四国支部学術大会, Nov. 2011.
76.	小島孝充, 丸山豪斗, 田良島典子, Naoshi Yamazaki, Yoshiharu Takiguchi, 松田彰 and Noriaki Minakawa : PCRによる4'-チオDNAの合成, アンチセンス・遺伝子・デリバリーシンポジウム, Sep. 2011.
77.	Naoto Okada, Takenori Yamamoto, 渡邊政博, 吉村勇哉, Naoshi Yamazaki, Yasuo Shinohara and Kazuo Minakuchi : TMEM45Bのthermal aggregationに関与するアミノ酸配列の同定, 日本薬学会第131年会, Mar. 2011.
78.	平野研, 吉田雄一郎, 石堂智美, Naoshi Yamazaki, 水品善之, Yoshinobu Baba and Mitsuru Ishikawa : 蛍光標識ヌクレオチドを連続取り込み可能なDNA polymeraseβの機能解析, 第33回日本分子生物学会・第83回日本生化学会合同大会, Nov. 2010.
79.	塩田祐子, 新田芳久, 下川義彦, Naoshi Yamazaki and Yoshiharu Takiguchi : 毛髪を用いた肝CYP3A4活性評価に関する基礎的研究, 第49回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2010.
80.	梶真一朗, 中本淳子, Naoshi Yamazaki and Yoshiharu Takiguchi : PPAR-αおよびγ活性化による心筋虚血再灌流障害抑制効果の比較, 第83回日本薬理学会年会, Mar. 2010.
81.	秦拓也, Takenori Yamamoto, 森千尋, 森田結貴, 新山加菜美, Naoshi Yamazaki, Masatoshi Kataoka and Yasuo Shinohara : 初代培養した脂肪細胞と3T3-L1細胞の遺伝子発現プロファイルの違い, 第130回日本薬学会, Mar. 2010.
82.	Takenori Yamamoto, 吉村勇哉, Akiko Yamada, 合田俊一, Naoshi Yamazaki, Kikuji Yamashita, Masatoshi Kataoka, Hiroshi Terada and Yasuo Shinohara : 呼吸基質非存在下において透過性遷移を誘起したミトコンドリアに観察される特徴的なタンパク質の放出様式, 第31回生体膜と薬物の相互作用シンポジウム, Dec. 2009.
83.	梶真一朗, 中本淳子, Naoshi Yamazaki and Yoshiharu Takiguchi : 心筋虚血再灌流障害に対するPPAR-γ及びPPAR-α活性化効果の比較, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
84.	田澤綾香, 木下綾子, 森咲子, Naoshi Yamazaki and Yoshiharu Takiguchi : サリチル酸系薬物の吸収に及ぼすカルバペネム系抗生物質の影響, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
85.	Tatsuaki Tagami, Kazuya Nakamura, Taro Shimizu, Naoshi Yamazaki, Tatsuhiro Ishida and Hiroshi Kiwada : ポリエチレングリコール(PEG)を利用した核酸送達システムにおいてプラスミドDNA配列内のCpG除去が抗PEG抗体産生に与える影響, 第25回日本DDS学会, Jul. 2009.
86.	Tatsuaki Tagami, Kazuya Nakamura, Taro Shimizu, Naoshi Yamazaki, Tatsuhiro Ishida and Hiroshi Kiwada : CpG-free pDNAを使用したPEG修飾リポプレックス投与がABC現象に与える影響, 日本薬学会第129年会, Mar. 2009.
87.	新山加菜美, Takenori Yamamoto, 渡邊政博, 森千尋, Naoto Okada, 荻野真理, Naoshi Yamazaki, Masatoshi Kataoka and Yasuo Shinohara : 脂肪組織に選択的に発現した遺伝子の同定とその発現プロフィールの解析, 第129回日本薬学会, Mar. 2009.
88.	Eriko Obana, Takenori Yamamoto, 渡邊政博, 角幡玲, Naoshi Yamazaki, Masatoshi Kataoka, Toshihiko Ooie, Yoshinobu Baba, 堀友繁 and Yasuo Shinohara : マイクロアレイを用いた遺伝子発現の定量的評価におけるプローブ設計領域の重要性, 第129回日本薬学会, Mar. 2009.
89.	梶真一朗, 竹永葉月, Naoshi Yamazaki, Akira Tokumura and Yoshiharu Takiguchi : The effect of lysophosphatidic acid on myocardial ischemia-reperfusion injury, 第82回日本薬理学会年会, Mar. 2009.
90.	Takenori Yamamoto, Yuya Yoshimura, Naoshi Yamazaki, Kikuji Yamashita, Masatoshi Kataoka, Hiroshi Terada and Yasuo Shinohara : 呼吸基質非存在下でミトコンドリアに誘起される透過性遷移の解析, 日本生物物理学会第1回中国四国支部大会, May 2008.
91.	Taisuke Matsuo, Naoshi Yamazaki, 新山加菜美, Takenori Yamamoto, Tatsuhiro Ishida, Hiroshi Kiwada, Masatoshi Kataoka and Yasuo Shinohara : タグを付加したPf3 coat protein変異体の調製およびリポソームとの相互作用の解析, Mar. 2008.
92.	Naoshi Yamazaki, Hirokazu Sato and Yasuo Shinohara : Characterization of a Novel Protein from Rat Brown Adipose Tissue, Containing DH, BAR, and SH3 Domains., 第30回日本分子生物学会・第80回日本生化学会合同大会, Dec. 2007.
93.	中谷極, Takenori Yamamoto, Taisuke Matsuo, Naoshi Yamazaki, Hiroshi Terada and Yasuo Shinohara : プロテオミクス解析による新規ミトコンドリア溶質輸送担体の探索, 第6回ファーマ・バイオフォーラム 2007, Dec. 2007.
94.	吉村勇哉, Takenori Yamamoto, Naoshi Yamazaki, Kikuji Yamashita, Hiroshi Terada and Yasuo Shinohara : 呼吸基質非存在下においてミトコンドリアに誘導される透過性遷移の解析, 第6回ファーマ・バイオフォーラム 2007, Dec. 2007.
95.	岩橋晶洋, Naoshi Yamazaki and Yasuo Shinohara : ミトコンドリアADP/ATP透過担体のC末端領域の構造及び機能の解析, 第6回ファーマ・バイオフォーラム 2007, Dec. 2007.
96.	渡邊政博, Takenori Yamamoto, 角幡玲, 岡田直人, 梶本和昭, Naoshi Yamazaki, Masatoshi Kataoka, Yoshinobu Baba, Toshiaki Tamaki and Yasuo Shinohara : 褐色脂肪組織の機能亢進に関与する新規因子の探索, 第6回ファーマ・バイオフォーラム 2007, Dec. 2007.
97.	森千尋, 渡邊政博, Naoto Okada, Takenori Yamamoto, Naoshi Yamazaki, Masatoshi Kataoka and Yasuo Shinohara : 脂肪組織に特異的に発現している機能未知遺伝子の同定とそのキャラクタリゼーション, 第6回ファーマ・バイオフォーラム 2007, Dec. 2007.
98.	角幡玲, 渡邊政博, Takenori Yamamoto, Naoshi Yamazaki, Masatoshi Kataoka, Toshihiko Ooie, Yoshinobu Baba, 堀友繁 and Yasuo Shinohara : マイクロアレイのデータの規格化，標準化に向けた試み(2), 第6回ファーマ・バイオフォーラム 2007, Dec. 2007.
99.	石井葵, Takenori Yamamoto, Taisuke Matsuo, Naoshi Yamazaki, Hiroshi Terada and Yasuo Shinohara : 寒冷暴露した褐色脂肪組織におけるHFABPの免疫学的解析, 第6回ファーマ・バイオフォーラム 2007, Dec. 2007.
100.	Takenori Yamamoto, Akiko Yamada, Naoshi Yamazaki, Kikuji Yamashita, Toshihiko Nagata, Hiroshi Terada and Yasuo Shinohara : シトクロムcと伴にミトコンドリアから放出されるタンパク質のプロテオーム解析, 第29回生体膜と薬物の相互作用シンポジウム, Nov. 2007.
101.	Mami Azuma, Harumi Hinode, Yoshiki Kashiwada, Masahiro Yoshida, Naoshi Yamazaki, Koichiro Tsuchiya, Aiko Yamauchi, Hirofumi Shibata, Naokatu Arakaki, Yoshiharu Takiguchi, Tsutomu Araki, Yoshiyuki Yoshimura, Toshiki Himeda, Tatsuhiro Ishida, Daisuke Tsuji and Masaru Kihara : 徳島大学薬学部OSCEトライアル実施体制の確立と検証, 第17回日本医療薬学会年会, Sep. 2007.
102.	岩橋晶洋, Naoshi Yamazaki and Yasuo Shinohara : Structural analysis of C-terminal region of mitochondrial ADP/ATP carrier by site-directed mutagenesis, 日本分子生物学会フォーラム, Dec. 2006.
103.	Akiko Yamada, Takenori Yamamoto, Naoshi Yamazaki, Toshihiko Nagata, Hiroshi Terada and Yasuo Shinohara : Differential protein release from mitochondria induced by Ca²⁺ and valinomycin as revealed by immunological and proteomics techniques, 第6回ミトコンドリア学会, Dec. 2006.
104.	Takenori Yamamoto, Akiko Yamada, masahiro watanabe, yuya yoshimura, Naoshi Yamazaki, Yoshiyuki Yoshimura, Takashi Yamauchi, Toshihiko Nagata, Hiroshi Terada and Yasuo Shinohara : Expression levels of voltage-dependent anion channel (VDAC) isoforms in mitochondrial outer membrane revealed by immunological and proteomics techniques, 第28回生体膜と薬物の相互作用シンポジウム, Nov. 2006.
105.	角幡玲, Takenori Yamamoto, Naoshi Yamazaki, Masatoshi Kataoka, Yoshinobu Baba and Yasuo Shinohara : マイクロアレイのデータの規格化，標準化に向けた試み, 第45回日本薬学会・日本病院薬剤師会中国四国支部学術大会, Oct. 2006.
106.	赤峰理恵, Takenori Yamamoto, Naoshi Yamazaki, Masatoshi Kataoka, Mitsuru Ishikawa, Yoshinobu Baba and Yasuo Shinohara : 組織間や動物種間での遺伝子発現の比較に適した標準遺伝子, 第44回日本薬学会・日本病院薬剤師会中国四国支部学術大会, Nov. 2005.
107.	Taisuke Matsuo, 鈴木真希子, 倉田美保, Naoshi Yamazaki and Yasuo Shinohara : 変異導入したM-CPTIの安定性および酵素活性の解析, 第44回日本薬学会・日本病院薬剤師会中国四国支部学術大会, Nov. 2005.
108.	Takenori Yamamoto, Akiko Yamada, 吉村勇哉, Kikuji Yamashita, Naoshi Yamazaki, Masatoshi Kataoka, Hiroshi Terada and Yasuo Shinohara : Caイオンによって誘導される酵母ミトコンドリアの透過性遷移とシトクロムc放出, 第27回生体膜と薬物の相互作用シンポジウム, Nov. 2005.
109.	渡邊政博, Takenori Yamamoto, 喜多史代, 梶本和昭, Naoshi Yamazaki, Masatoshi Kataoka, Hiroshi Terada, Yoshinobu Baba and Yasuo Shinohara : 褐色脂肪組織の機能亢進に伴う遺伝子発現変動のマイクロアレイ解析, 第26回日本肥満学会, Oct. 2005.
110.	Naoshi Yamazaki, saki imamura, hirokazu sato, Takenori Yamamoto, Yasuo Shinohara and Hiroshi Terada : Characterization of Novel cDNA from Rat Brown Adipose Tissue: It Codes a Protein Containing Dbl Homology, Bin/Amphiphysin/Rvs and Src Homology 3 Domains, 第78回日本生化学会大会, Oct. 2005.
111.	今村早喜, 佐藤裕一, Takenori Yamamoto, Naoshi Yamazaki, Masatoshi Kataoka and Yasuo Shinohara : 褐色脂肪組織から単離された新規タンパク質2-88の解析, 第6回長井長義記念シンポジウム, Jul. 2005.
112.	Taisuke Matsuo, 鈴木真希子, 倉田美保, Naoshi Yamazaki and Yasuo Shinohara : 筋型カルニチンパルミトイルトランスフェラーゼⅠ遺伝子の多型の解析, 第6回長井長義記念シンポジウム, Jul. 2005.
113.	立川愛子, Takenori Yamamoto, Masatoshi Kataoka, Naoshi Yamazaki, Yoshinobu Baba and Yasuo Shinohara : porin欠損酵母における遺伝子発現のマイクロアレイ解析, 第6回長井長義記念シンポジウム, Jul. 2005.
114.	渡邊政博, Takenori Yamamoto, 喜多史代, 梶本和昭, Naoshi Yamazaki, Masatoshi Kataoka, Hiroshi Terada, Yoshinobu Baba and Yasuo Shinohara : 褐色脂肪組織の機能亢進に伴う遺伝子発現変動のマイクロアレイ解析, 第6回長井長義記念シンポジウム, Jul. 2005.
115.	Naoshi Yamazaki : 筋型カルニチンパルミトイル転移酵素の発見とその極めて稀な遺伝子構造の解明, 日本薬学会第124年会要旨集, Mar. 2004.
116.	梶本和昭, Yasuo Shinohara, 大黒多希子, Naoshi Yamazaki and Hiroshi Terada : 褐色脂肪組織に選択的に発現したメッセージの同定とそのキャラクタリゼーション, 第24回生体膜と薬物の相互作用シンポジウム, Nov. 2002.
117.	喜多史代, 梶本和昭, Yasuo Shinohara, Naoshi Yamazaki and Hiroshi Terada : 褐色脂肪組織におけるミトコンドリアタンパク質の発現量とミトコンドリア含量との相関性に関する解析, 第75回日本生化学会大会, Oct. 2002.
118.	Naoshi Yamazaki, Takenori Yamamoto, Yasuo Shinohara and Hiroshi Terada : ラット筋型カルニチンパルミトイルトランスフェラーゼⅠ遺伝子の上流領域を含んだmRNAの解析, 日本薬学会第122年会, Mar. 2002.
119.	梶本和昭, Yasuo Shinohara, 大黒多希子, 島厚志, Naoshi Yamazaki and Hiroshi Terada : 褐色脂肪組織における心筋型脂肪酸結合タンパク質の発現とその転写調節機構, 第23回生体膜と薬物の相互作用シンポジウム, Nov. 2001.
120.	Naoshi Yamazaki, 日野真美, Takenori Yamamoto, Yasuo Shinohara and Hiroshi Terada : 上流に位置する遺伝子領域を介した筋型carnitine palmitoyltransferase I遺伝子の転写調節, 第74回日本生化学会大会, Oct. 2001.
121.	梶本和昭, 大黒多希子, Naoshi Yamazaki, Yasuo Shinohara and Hiroshi Terada : 褐色脂肪組織におけるイソクエン酸脱水素酵素の転写レベルの解析, 第74回日本生化学会大会, Oct. 2001.
122.	kayo tanida, Naoshi Yamazaki, Yasuo Shinohara and Hiroshi Terada : 哺乳類のミトコンドリアに発現したADP/ATP透過担体の構造特性, 第74回日本生化学会大会, Oct. 2001.
123.	梶本和昭, 大黒多希子, Naoshi Yamazaki, Yasuo Shinohara and Hiroshi Terada : イソクエン酸脱水素酵素の褐色脂肪組織におけるドミナントな発現, 日本薬学会第121年会, Mar. 2001.
124.	Naoshi Yamazaki, 梶本和昭, 大黒多希子, 濱田祐二, 日野真美, Yasuo Shinohara and Hiroshi Terada : 褐色脂肪組織に優位に発現している新規cDNAクローンの解析, 日本薬学会第121年会, Mar. 2001.
125.	Naoshi Yamazaki, 新藤雅之, Yasuo Shinohara and Hiroshi Terada : ヒト筋型CPTIとCK/EKの2つの遺伝子領域を含んだmRNAのキャラクタリゼーション, 日本薬学会第120年会, Mar. 2000.
126.	Naoshi Yamazaki, 新藤雅之, 梶本和昭, Yasuo Shinohara and Hiroshi Terada : 上流に位置する遺伝子中にoverlapして存在するヒト筋型carnitine palmitoyltransferase I遺伝子, 第72回日本生化学会大会, Oct. 1999.
127.	平松隆之, Naoshi Yamazaki, Yasuo Shinohara and Hiroshi Terada : 筋型カルニチンパルミトイルトランスフェラーゼⅠをコードする遺伝子の上流領域の構造解析, 第72回日本生化学会大会, Oct. 1999.
128.	大黒多希子, Naoshi Yamazaki, Yasuo Shinohara and Hiroshi Terada : 褐色脂肪組織でのエネルギー代謝に関わるタンパク質の発現, 日本薬学会第119年会, Mar. 1999.
129.	佐野友香, 大黒多希子, Naoshi Yamazaki, Yasuo Shinohara and Hiroshi Terada : 心筋型脂肪酸結合タンパク質の遺伝子構造と転写調節機構, 日本薬学会第119年会, Mar. 1999.
130.	Naoshi Yamazaki, 中村香織, 平松隆之, Yasuo Shinohara and Hiroshi Terada : 上流に位置する遺伝子中にoverlapして存在するヒト筋型carnitine palmitoyltransferase I遺伝子エクソンの存在意義, 日本薬学会第119年会, Mar. 1999.
131.	Naoshi Yamazaki, 平松隆之, 中村香織, Yasuo Shinohara and Hiroshi Terada : ヒト，ラット，マウスの筋型carnitine palmitoyltransferase Iをコードする遺伝子の上流領域の構造的特徴, 第71回日本生化学会大会, Oct. 1998.
132.	大黒多希子, Yasuo Shinohara, Naoshi Yamazaki and Hiroshi Terada : 褐色脂肪組織で営まれているエネルギー代謝系のキャラクタリゼーション, 第3回アディポサイエンス研究会, Aug. 1998.
133.	大黒多希子, 佐野友香, Naoshi Yamazaki, 島厚志, Yasuo Shinohara and Hiroshi Terada : 褐色脂肪組織においてUCPと協調的に発現するH-FABP, 日本薬学会第118年会, Mar. 1998.
134.	橋本良子, Naoshi Yamazaki, 平松隆之, 山中靖久 and Hiroshi Terada : 筋型カルニチンパルミトイルトランスフェラーゼⅠをコードする遺伝子の上流領域の構造解析, 日本薬学会第118年会, Mar. 1998.
135.	Naoshi Yamazaki, 平松隆之, Yasuo Shinohara and Hiroshi Terada : マウス筋型carnitine palmitoyltransferase IをコードするcDNAおよびゲノムDNAの単離と構造解析, 日本薬学会第118年会, Mar. 1998.
136.	橋本良子, Naoshi Yamazaki and Hiroshi Terada : 筋型カルニチンパルミトイルトランスフェラーゼⅠ遺伝子の構造解析, 第36回日本薬学会・日本病院薬剤師会学術大会中国四国支部大会, Nov. 1997.
137.	大黒多希子, Yasuo Shinohara, 島厚志, Naoshi Yamazaki and Hiroshi Terada : 寒冷条件下で誘発される褐色脂肪細胞における筋型脂肪酸結合タンパク質の特異的転写レベルの亢進, 第70回日本生化学会大会, Sep. 1997.
138.	Naoshi Yamazaki, 山中靖久, 橋本良子, Yasuo Shinohara, 島厚志 and Hiroshi Terada : ヒトの筋型カルニチンパルミトイルトランスフェラーゼⅠをコードする遺伝子とその上流領域の構造解析, 第70回日本生化学会大会, Sep. 1997.
139.	山中靖久, 橋本良子, Naoshi Yamazaki, Yasuo Shinohara and Hiroshi Terada : ヒトの筋型カルニチンパルミトイルトランスフェラーゼⅠをコードする遺伝子の単離と構造解析, 日本薬学会第117年会, Mar. 1997.
140.	Naoshi Yamazaki, 山中靖久, 橋本良子, Yasuo Shinohara, 島厚志 and Hiroshi Terada : ヒト筋型カルニチンパルミトイルトランスフェラーゼⅠをコードする遺伝子の単離と構造解析, 第69回日本生化学会・第19回日本分子生物学会年会合同年会, Aug. 1996.
141.	大黒多希子, Yasuo Shinohara, 島厚志, Naoshi Yamazaki and Hiroshi Terada : 褐色脂肪組織と白色脂肪組織におけるエネルギー代謝機構の相違, 第69回日本生化学会・第19回日本分子生物学会年会合同年会, Aug. 1996.
142.	Naoshi Yamazaki, 山中靖久, Yasuo Shinohara, 島厚志 and Hiroshi Terada : ヒト筋型カルニチンパルミトイルトランスフェラーゼⅠをコードするcDNAの単離と構造解析, 日本薬学会第116年会, Mar. 1996.
143.	Naoshi Yamazaki, 島厚志, Yasuo Shinohara and Hiroshi Terada : 褐色脂肪組織に特異的なタンパク質をコードするcDNAの単離と構造解析, 第68会日本生化学会大会, Sep. 1995.
144.	Naoshi Yamazaki, 島厚志, Yasuo Shinohara and Hiroshi Terada : 褐色脂肪組織に特異的なタンパク質をコードするcDNAの単離と構造解析, 日本薬学会第115年会, Mar. 1995.
145.	Naoshi Yamazaki, Yasuo Shinohara and Hiroshi Terada : 褐色脂肪組織に特異的なタンパク質をコードする遺伝子の解析, 日本薬学会 114年会, Mar. 1994.
146.	紙田真喜夫, Naoshi Yamazaki, Yasuo Shinohara and Hiroshi Terada : ラットミトコンドリアADP/ATP透過担体をコードする遺伝子の転写調節機構の解析, 日本薬学会第112年会, Mar. 1992.

Et cetera, Workshop:

1.	髙橋永, 多田安里, Kentaro Kogure and Naoshi Yamazaki : カルニチンパルミトイルトランスフェラーゼ1A(CPT1A)におけるA-to-I RNA編集の意義の解明, 第45回生体膜と薬物の相互作用シンポジウム, Oct. 2024.
2.	枇杷谷有佐, Jun Tsukimoto, Kentaro Kogure and Naoshi Yamazaki : 改変U1 snRNAを用いたカテプシンAスプライス異常の修復, 第45回生体膜と薬物の相互作用シンポジウム, Oct. 2024.
3.	菅原千佳, 川合真央, 多田安里, Kentaro Kogure and Naoshi Yamazaki : CPT1A mRNAの3'非翻訳領域におけるA-to-I RNA編集部位, 第45回生体膜と薬物の相互作用シンポジウム, Oct. 2024.
4.	松田あすか, 古藤遼佑, 小西怜哉, Kentaro Kogure and Naoshi Yamazaki : 動物細胞で発現させたヒトおよびラットカルニチンパルミトイルトランスフェラーゼ1Bの解析, 第45回生体膜と薬物の相互作用シンポジウム, Oct. 2024.
5.	吉岡里紗, 橋本晴香, Jun Tsukimoto, Kentaro Kogure and Naoshi Yamazaki : トランススプライシングによるヒトカテプシンAスプライス異常の修復, 第45回生体膜と薬物の相互作用シンポジウム, Oct. 2024.
6.	Naoshi Yamazaki, Makiko Shinomiya, Hironobu Ike, Yasuo Shinohara, Noriaki Minakawa, Kouji Itou and Yoshiharu Takiguchi : Use of modified U1 small nuclear RNA for improved formation of properly spliced mRNA encoding human cathepsin A from the gene having an IVS7 +3a>g mutation, FEBS Open Bio, Vol.8, No.Supplement 1, ShT.35-1, Jul. 2018.
7.	Naoshi Yamazaki : 褐色脂肪組織に特徴的なタンパク質の探索, 国立大学法人徳島大学薬友会近畿支部総会及び大阪サテライトオフィス合同交流会, Jul. 2006.
8.	梶本和昭, Naoshi Yamazaki, 島厚志, Hiroshi Terada, Yasuo Shinohara and Yoshinobu Baba : 褐色脂肪組織におけるエネルギー代謝系のキャラクタリゼーション, 平成14年度産業技術総合研究所四国センターシンポジウム, Dec. 2002.
9.	Naoshi Yamazaki, Yasuo Shinohara and Hiroshi Terada : Novel carnitine palmitoyltransferase I isoform in rat BAT, The Joint Symposium between Seoul National University and University of Tokushima on Pharmacy (10th Anniversary of Exchange Program), Aug. 2000.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

デコイ核酸によるRNA編集阻害とこれを利用した疾病治療の可能性 (Project/Area Number: 24K09813 )
Use of modified U1 snRNA for rescue from exon skipping caused by 5' splice site mutation of human CTSA gene (Project/Area Number: 16K08235 )
Development of a novel approach toward nucleic acids-based therapeutics (Project/Area Number: 23659054 )
Characterization of a novel protein which inhibits adipocytes differentiation (Project/Area Number: 22590066 )
腫瘍内微小環境変化を利用した新規DDSの開発 (Project/Area Number: 20015033 )
脂肪細胞の分化を抑制する新規タンパク質の解析とこれを標的とした抗肥満戦略 (Project/Area Number: 16790055 )
Roles of mitochondrial proteins in regulations of energy metabolism and apoptosis (Project/Area Number: 14370746 )
上流に近接した遺伝子による筋型CPTI遺伝子の発現調節機構の解明と心筋症治療薬 (Project/Area Number: 13771413 )
極めて稀な構造をしたヒト筋型CPTI遺伝子の転写調節機構の解明 (Project/Area Number: 11771437 )
Signal transmission of carcinogenesis and tumorigenesis and formation of specific metabolic pathway in tumor cells. (Project/Area Number: 10470496 )
筋型カルニチンパルミトイルトランスフェラーゼIの異常に基づく発症機構 (Project/Area Number: 09771985 )
Design and development of anti-tumor drugs using the energy metabolism specifically held in tumor cells as potential targets (Project/Area Number: 09357020 )
Molecular characterization of the tumor specific energy metabolisms (Project/Area Number: 08457609 )
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Associate Professor : Yamazaki, Naoshi

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Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)