Tokushima University / Educator and Researcher Directory --- Horiguchi, Taigo

Personal Web Page

https://researchmap.jp/jjzg48kalw (researchmap)

Field of Study

○	Biochemistry, Molecular Biology

Subject of Study

○	Study on the Inhibition Mechanism of Glycyrrhizin against Phospholipase A2 Activity (carbon tetrachloride, glycyrrhizin, phospholipase) (Carbontetrachloride induces liver cell injury. The fact, this injury is inhibited by phospholipase A2 inhibitor, indicates that phospholipase A2 is included in this process. Because glycyrrhizin inhibits cell injury induced by carbon tetrachloride, it is possible that glycyrrhizin interfere with activity of phospholipase A2. To clarify the inhibition mechanism of glycyrrhizin against cell injury induced by carbontetrachloride, I am studying on the interaction between phospholipase A2 and glycyrrhizin, and gene expression pattern of liver cell treated with carbontetrachloride and/or glycyrrhizin using RT-PCR and microarray method.)

Book / Paper

Book:

1.	Taigo Horiguchi, Keiko Miyoshi and Takafumi Noma : 生化学実習書 (第14版1刷), 徳島大学大学院医歯薬学研究部分子医化学分野, Tokushima, May 2020.
2.	Taigo Horiguchi, Keiko Miyoshi and Takafumi Noma : 生化学実習書 (第13版1刷), 徳島大学大学院医歯薬学研究部分子医化学分野, Tokushima, May 2019.
3.	Taigo Horiguchi, Keiko Miyoshi and Takafumi Noma : 生化学実習書 (第12版1刷), 徳島大学大学院医歯薬学研究部分子医化学分野, Tokushima, May 2018.
4.	Taigo Horiguchi, Keiko Miyoshi, Ayako Tanimura and Takafumi Noma : 生化学実習書 (第11版1刷), 徳島大学大学院医歯薬学研究部分子医化学分野, Tokushima, May 2017.
5.	Taigo Horiguchi, Keiko Miyoshi, Ayako Tanimura and Takafumi Noma : 生化学実習書 (第10版1刷), 徳島大学大学院医歯薬学研究部分子医化学分野, Tokushima, May 2016.
6.	Taigo Horiguchi, Keiko Miyoshi, Ayako Tanimura and Takafumi Noma : 生化学実習書 (第9版1刷), 徳島大学大学院医歯薬学研究部分子医化学分野, Tokushima, May 2015.
7.	Taigo Horiguchi, Keiko Miyoshi, Ayako Tanimura and Takafumi Noma : 生化学実習書 (第8版1刷), 徳島大学大学院ヘルスバイオサイエンス研究部分子医化学分野, Tokushima, May 2014.
8.	Taigo Horiguchi, Keiko Miyoshi, Ayako Tanimura and Takafumi Noma : 生化学実習書 (第7版1刷), 徳島大学大学院ヘルスバイオサイエンス研究部分子医化学分野, Tokushima, May 2013.
9.	Taigo Horiguchi, Keiko Miyoshi, Ayako Tanimura and Takafumi Noma : 生化学実習書 (第6版1刷), 徳島大学大学院ヘルスバイオサイエンス研究部分子医化学分野, Tokushima, May 2012.
10.	Taigo Horiguchi, Keiko Miyoshi, Ayako Tanimura and Takafumi Noma : 生化学実習書 (第5版2刷), 徳島大学大学院ヘルスバイオサイエンス研究部分子医化学分野, Tokushima, May 2011.
11.	Taigo Horiguchi, Keiko Miyoshi, Taro Muto and Takafumi Noma : 生化学実習書 (第5版1刷), 徳島大学大学院ヘルスバイオサイエンス研究部分子医化学分野, Tokushima, May 2010.
12.	Taigo Horiguchi, Keiko Miyoshi, Taro Muto and Takafumi Noma : 生化学実習書 (第4版10刷), 徳島大学大学院ヘルスバイオサイエンス研究部分子医化学分野, Tokushima, May 2009.
13.	Taigo Horiguchi, Keiko Miyoshi, Taro Muto and Takafumi Noma : 生化学実習書 (第3版10刷), 徳島大学大学院ヘルスバイオサイエンス研究部分子医化学分野, Tokushima, May 2008.
14.	Taigo Horiguchi, Keiko Miyoshi, Taro Muto and Takafumi Noma : 生化学実習書 (第3版9刷), 徳島大学大学院ヘルスバイオサイエンス研究部分子医化学分野, Tokushima, May 2007.
15.	Taigo Horiguchi, Keiko Miyoshi, Taro Muto and Takafumi Noma : 生化学実習書 (第3版8刷), 徳島大学大学院ヘルスバイオサイエンス研究部分子医化学分野, Tokushima, May 2006.
16.	Taigo Horiguchi, Keiko Miyoshi, Taro Muto and Takafumi Noma : 生化学実習書 (第3版7刷), 徳島大学大学院ヘルスバイオサイエンス研究部分子医化学分野, Tokushima, May 2005.
17.	Taigo Horiguchi, Akemichi Ueno, Keiko Miyoshi and Takafumi Noma : 生化学実習書 (第3版6刷), 徳島大学大学院ヘルスバイオサイエンス研究部分子医化学分野, Tokushima, May 2004.
18.	Taigo Horiguchi, Akemichi Ueno, Keiko Miyoshi and Takafumi Noma : 生化学実習書 (第3版5刷), 徳島大学歯学部口腔生化学講座, Tokushima, May 2003.
19.	Taigo Horiguchi, Akemichi Ueno and Keiko Miyoshi : 生化学実習書 (第3版4刷), 徳島大学歯学部口腔生化学講座, Tokushima, May 2002.

Academic Paper (Judged Full Paper):

1.	Shengjian Jin, Takaaki Tsunematsu, Taigo Horiguchi, Yasuhiro Mouri, Wenhua Shao, Keiko Miyoshi, Hiroko Hagita, Motoharu Sarubo, Natsumi Fujiwara, Qi Guangying, Naozumi Ishimaru and Yasusei Kudo : Involvement of the OTUB1-YAP1 axis in driving malignant behaviors of head and neck squamous cell carcinoma., Cancer Medicine, Vol.12, No.24, 22156-22169, 2023. (Summary) This study highlights the critical role of OTUB1 in HNSCC progression via modulating YAP1. Targeting the OTUB1-YAP1 axis holds promise as a potential therapeutic strategy for HNSCC treatment. (Keyword) deubiquitinating enzyme (DUB) / head and neck squamous cell carcinoma / invasion / OTUB1 / YAP (Tokushima University Institutional Repository) ● Metadata: 118778 (Link to Publication Site) ● Publication site (DOI): 10.1002/cam4.6735 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37986681 ● CiNii @ National Institute of Informatics (CRID): 1050017113070808192 ● Summary page in Scopus @ Elsevier: 2-s2.0-85177448617 (Tokushima University Institutional Repository: 118778, DOI: 10.1002/cam4.6735, PubMed: 37986681, CiNii: 1050017113070808192, Elsevier: Scopus)
2.	Shengjian Jin, Taigo Horiguchi, Xiaolong Ma, Shichao Yuan and Qingguo Liu : Metallic foreign bodies ingestion by schizophrenic patient: a case report, Annals of Medicine and Surgery, Vol.85, No.4, 1270-1272, 2023. (Summary) The ingestion of foreign objects is a widespread health issue, with a higher occurrence in adults with psychosis. The authors present the case of a 39-year-old man who arrived at the hospital with symptoms of abdominal distension and occasional black stools for a week. The patient was known to have schizophrenia but had not received regular hospital follow-up or treatment for the past 5 years. He had a history of exogenous stimulation, which led him to surreptitiously swallow metallic objects. Upon physical examination, he displayed abdominal distension and mild tenderness in the upper abdomen. Radiographs revealed multiple foreign objects in his stomach, leading to the decision for laparotomy, gastric opening, and removal of the foreign objects under general anesthesia. Mental illnesses, including schizophrenia, bipolar disorder, major depression, and multiple substance abuse, are recognized as being significant risk factors for ingesting foreign bodies. In such cases, it is crucial to intervene quickly. For patients presenting with psychiatric symptoms, the involvement of family caregivers is of even greater importance than endoscopic or surgical treatments. Foreign body ingestion is more prevalent in individuals with psychosis, highlighting the importance of ongoing care and follow-up for patients with mental illness. (Keyword) case report / foreign body ingestion / metal / schizophrenia (Link to Publication Site) ● Publication site (DOI): 10.1097/MS9.0000000000000497 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37113887 ● Search Scopus @ Elsevier (PMID): 37113887 ● Search Scopus @ Elsevier (DOI): 10.1097/MS9.0000000000000497 (DOI: 10.1097/MS9.0000000000000497, PubMed: 37113887)
3.	Jin Shengjian, Yasusei Kudo and Taigo Horiguchi : The Role of Deubiquitinating Enzyme in Head and Neck Squamous Cell Carcinoma, International Journal of Molecular Sciences, Vol.24, 552, 2022. (Summary) Ubiquitination and deubiquitination are two popular ways for the post-translational modification of proteins. These two modifications affect intracellular localization, stability, and function of target proteins. The process of deubiquitination is involved in histone modification, cell cycle regulation, cell differentiation, apoptosis, endocytosis, autophagy, and DNA repair after damage. Moreover, it is involved in the processes of carcinogenesis and cancer development. In this review, we discuss these issues in understanding deubiquitinating enzyme (DUB) function in head and neck squamous cell carcinoma (HNSCC), and their potential therapeutic strategies for HNSCC patients are also discussed. (Keyword) head and neck squamous cell carcinoma / deubiquitination / ubiquitination (Tokushima University Institutional Repository) ● Metadata: 117925 (Link to Publication Site) ● Publication site (DOI): 10.3390/ijms24010552 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36613989 ● Summary page in Scopus @ Elsevier: 2-s2.0-85145924629 (Tokushima University Institutional Repository: 117925, DOI: 10.3390/ijms24010552, PubMed: 36613989, Elsevier: Scopus)
4.	Taigo Horiguchi, Ayako Tanimura, Keiko Miyoshi, Hiroko Hagita, Hisanori Minami and Takafumi Noma : The Effect of Heterozygous Mutation of Adenylate Kinase 2 Gene on Neutrophil Differentiation., International Journal of Molecular Sciences, Vol.23, 16089, 2022. (Summary) Mitochondrial ATP production plays an important role in most cellular activities, including growth and differentiation. Previously we reported that Adenylate kinase 2 (AK2) is the main ADP supplier in the mitochondrial intermembrane space in hematopoietic cells, especially in the bone marrow. AK2 is crucial for the production of neutrophils and T cells, and its deficiency causes reticular dysgenesis. However, the relationship between ADP supply by AK2 and neutrophil differentiation remains unclear. In this study, we used CRISPR/Cas9 technology to establish two heterozygous AK2 knock-out HL-60 clones as models for reticular dysgenesis. Their AK2 activities were about half that in the wild-type (WT). Furthermore, neutrophil differentiation was impaired in one of the clones. In silico analysis predicted that the obtained mutations might cause a structural change in AK2. Time course microarray analysis of the WT and mutants revealed that similar gene clusters responded to all-trans retinoic acid treatment, but their expression was lower in the mutants than in WT. Application of fructose partially restored neutrophil differentiation in the heterozygous knock-out HL-60 clone after all-trans retinoic acid treatment. Collectively, our study suggests that the mutation of N-terminal region in AK2 might play a role in AK2-dependent neutrophil differentiation and fructose could be used to treat AK2 deficiency. (Keyword) Neutrophils / Adenylate Kinase / cell proliferation and differentiation / Mutation / Tretinoin (Tokushima University Institutional Repository) ● Metadata: 117929 (Link to Publication Site) ● Publication site (DOI): 10.3390/ijms232416089 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36555730 ● Search Scopus @ Elsevier (PMID): 36555730 ● Search Scopus @ Elsevier (DOI): 10.3390/ijms232416089 (Tokushima University Institutional Repository: 117929, DOI: 10.3390/ijms232416089, PubMed: 36555730)
5.	Taigo Horiguchi, Yumiko Miyake, Keiko Miyoshi, Ayako Tanimura, Hiroko Hagita, Hiroshi Sakaue and Takafumi Noma : Gene-expression profile reveals the genetic and acquired phenotypes of hyperactive mutant SPORTS rad, The Journal of Medical Investigation : JMI, Vol.VOL67, No.NO1,2, 51-61, 2020. (Summary) Spontaneously Running Tokushima Shikoku (SPORTS) rat is a hyperactive rat strain. However, the causative mutation of this phenotype has not yet been identified. To investigate the molecular basis for the unique phenotype of SPORTS rats, we examined gene-expression profiles by microarray analyses. Among adenylate kinase isozymes that maintain the homeostasis of cellular adenine nucleotide composition in the cell, only adenylate kinase 1 is highly up-regulated in both exercised and sedentary SPORTS rats compared with wild-type (WT) rats, 5.5-fold and 3.3-fold, respectively. Further comparative analyses revealed that genes involved in glucose metabolism were up-regulated in skeletal muscle tissue of exercised SPORTS rats compared with sedentary mutants, whereas genes related to extracellular matrix or region were down-regulated compared with WT rats. In brain tissue of sedentary SPORTS rats, genes associated with defense and catecholamine metabolism were highly expressed compared with WT rats. These findings suggest that genetic mutation(s) in SPORTS rat remodels metabolic demands through differentially regulating gene expression regardless of exercise. Therefore, the SPORTS rats are useful animal model not only for further examining the effects of exercise on metabolism but also for deeply studying the molecular basis how mutation affect the psychological motivation with spontaneous voluntary exercise phenotype. J. Med. Invest. 67 : 51-61, February, 2020. (Tokushima University Institutional Repository) ● Metadata: 114556 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.67.51 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32378618 ● Search Scopus @ Elsevier (PMID): 32378618 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.67.51 (Tokushima University Institutional Repository: 114556, DOI: 10.2152/jmi.67.51, PubMed: 32378618)
6.	Ayako Tanimura, Keiko Miyoshi, Taigo Horiguchi, Hiroko Hagita, Koichi Fujisawa and Takafumi Noma : Mitochondrial Activity and Unfolded Protein Response are Required for Neutrophil Differentiation., Cellular Physiology and Biochemistry, Vol.47, No.5, 1936-1950, 2018. (Summary) In this study, we demonstrated that neutrophil differentiation is regulated by ER stress/UPR that is supported by mitochondrial ATP supply, in which IRE1-XBP1 activation is essential. Our findings provide the evidence that mitochondrial energy metabolism may play a critical role in neutrophil differentiation. (Tokushima University Institutional Repository) ● Metadata: 112955 (Link to Publication Site) ● Publication site (DOI): 10.1159/000491464 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29972819 ● Search Scopus @ Elsevier (PMID): 29972819 ● Search Scopus @ Elsevier (DOI): 10.1159/000491464 (Tokushima University Institutional Repository: 112955, DOI: 10.1159/000491464, PubMed: 29972819)
7.	Yosi Dian Arinawati, Keiko Miyoshi, Ayako Tanimura, Taigo Horiguchi, Hiroko Hagita and Takafumi Noma : Deciphering defective amelogenesis using invitro culture systems., Journal of Bioscience and Bioengineering, Vol.125, No.Issue 4, 365-496, 2018. (Summary) The conventional two-dimensional (2D) in vitro culture system is frequently used to analyze the gene expression with or without extracellular signals. However, the cells derived from primary culture and cell lines frequently deviate the gene expression profile compared to the corresponding in vivo samples, which sometimes misleads the actual gene regulation in vivo. To overcome this gap, we developed the comparative 2D and 3D in vitro culture systems and applied them to the genetic study of amelogenesis imperfecta (AI) as a model. Recently, we found specificity protein 6 (Sp6) mutation in an autosomal-recessive AI rat that was previously named AMI. We constructed 3D structure of ARE-B30 cells (AMI-derived rat dental epithelial cells) or G5 (control wild type cells) combined with RPC-C2A cells (rat pulp cell line) separated by the collagen membrane, while in 2D structure, ARE-B30 or G5 was cultured with or without the collagen membrane. Comparative analysis of amelogenesis-related gene expression in ARE-B30 and G5 using our 2D and 3D in vitro systems revealed distinct expression profiles, showing the causative outcomes. Bone morphogenetic protein 2 and follistatin were reciprocally expressed in G5, but not in ARE-B30 cells. All-or-none expression of amelotin, kallikrein-related peptidase 4, and nerve growth factor receptor was observed in both cell types. In conclusion, our in vitro culture systems detected the phenotypical differences in the expression of the stage-specific amelogenesis-related genes. Parallel analysis with 2D and 3D culture systems may provide a platform to understand the molecular basis for defective amelogenesis caused by Sp6 mutation. (Tokushima University Institutional Repository) ● Metadata: 112952 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jbiosc.2017.11.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29397320 ● Search Scopus @ Elsevier (PMID): 29397320 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jbiosc.2017.11.009 (Tokushima University Institutional Repository: 112952, DOI: 10.1016/j.jbiosc.2017.11.009, PubMed: 29397320)
8.	A Adiningrat, Ayako Tanimura, Keiko Miyoshi, Hiroko Hagita, RD Yanuaryska, Arinawati Yosi Dian, Taigo Horiguchi and Takafumi Noma : Isolation and characterization of dental epithelial cells derived from amelogenesis imperfecta rat., Oral Diseases, Vol.22, No.2, 132-139, 2016. (Summary) OBJECTIVE:Disruption of the third zinc finger domain of specificity protein 6 (SP6) presents an enamel-specific defect in a rat model of amelogenesis imperfecta (AMI rats). To understand the molecular basis of amelogenesis imperfecta caused by the Sp6 mutation, we established and characterized AMI-derived rat dental epithelial (ARE) cells.MATERIALS AND METHODS:ARE cell clones were isolated from the mandibular incisors of AMI rats, and amelogenesis-related gene expression was analyzed by reverse transcription polymerase chain reaction (RT-PCR). Localization of wild-type SP6 (SP6WT) and mutant-type SP6 (SP6AMI) was analyzed by immunocytochemistry. SP6 transcriptional activity was monitored by rho-associated protein kinase 1 (Rock1) promoter activity with its specific binding to the promoter region in dental (G5 and ARE) and non-dental (COS-7) epithelial cells.RESULTS:Isolated ARE cells were varied in morphology and gene expression. Both SP6WT and SP6AMI were mainly detected in nuclei. The promoter analysis revealed that SP6WT and SP6AMI enhanced Rock1 promoter activity in G5 cells but that enhancement by SP6AMI was weaker, whereas no enhancement was observed in the ARE and COS-7 cells, even though SP6WT and SP6AMI bound to the promoter in all instances.CONCLUSION:ARE cell clones can provide a useful in vitro model to study the mechanism of SP6-mediated amelogenesis imperfecta. (Keyword) Sp6 mutation / amelogenesis imperfecta / in vitro disease model / tooth phenotype (Link to Publication Site) ● Publication site (DOI): 10.1111/odi.12396 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26582753 ● Summary page in Scopus @ Elsevier: 2-s2.0-84958530661 (DOI: 10.1111/odi.12396, PubMed: 26582753, Elsevier: Scopus)
9.	Keiko Miyoshi, Taigo Horiguchi, Ayako Tanimura, Hiroko Hagita and Takafumi Noma : Gene Signature of Human Oral Mucosa Fibroblasts: Comparison with Dermal Fibroblasts and Induced Pluripotent Stem Cells., BioMed Research International, Vol.2015, 121575, 2015. (Summary) Oral mucosa is a useful material for regeneration therapy with the advantages of its accessibility and versatility regardless of age and gender. However, little is known about the molecular characteristics of oral mucosa. Here we report the first comparative profiles of the gene signatures of human oral mucosa fibroblasts (hOFs), human dermal fibroblasts (hDFs), and hOF-derived induced pluripotent stem cells (hOF-iPSCs), linking these with biological roles by functional annotation and pathway analyses. As a common feature of fibroblasts, both hOFs and hDFs expressed glycolipid metabolism-related genes at higher levels compared with hOF-iPSCs. Distinct characteristics of hOFs compared with hDFs included a high expression of glycoprotein genes, involved in signaling, extracellular matrix, membrane, and receptor proteins, besides a low expression of HOX genes, the hDFs-markers. The results of the pathway analyses indicated that tissue-reconstructive, proliferative, and signaling pathways are active, whereas senescence-related genes in p53 pathway are inactive in hOFs. Furthermore, more than half of hOF-specific genes were similarly expressed to those of hOF-iPSC genes and might be controlled by WNT signaling. Our findings demonstrated that hOFs have unique cellular characteristics in specificity and plasticity. These data may provide useful insight into application of oral fibroblasts for direct reprograming. (Tokushima University Institutional Repository) ● Metadata: 114177 (Link to Publication Site) ● Publication site (DOI): 10.1155/2015/121575 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26339586 ● Summary page in Scopus @ Elsevier: 2-s2.0-84939816295 (Tokushima University Institutional Repository: 114177, DOI: 10.1155/2015/121575, PubMed: 26339586, Elsevier: Scopus)
10.	Ryna Dwi Yanuaryska, Keiko Miyoshi, Arya Adiningrat, Taigo Horiguchi, Ayako Tanimura, Hiroko Hagita and Takafumi Noma : Sp6 regulation of Rock1 promoter activity in dental epithelial cells, The Journal of Medical Investigation : JMI, Vol.VOL61, No.(NO 3,4), 306-317, 2014. (Summary) Sp6 is a transcription factor of the SP/KLF family and an indispensable regulator of the morphological dynamics of ameloblast differentiation during tooth development. However, the underlying molecular mechanisms remain unclear. We have previously identified one of the Sp6 downstream genes, Rock1, which is involved in ameloblast polarization. In this study, we investigated the transcriptional regulatory mechanisms of Rock1 by Sp6. First, we identified the transcription start sites (TSS) and cloned the 5'-flanking region of Rock1. Serial deletion analyses identified a critical region for Rock1 promoter activity within the 249-bp upstream region of TSS, and chromatin immunoprecipitation assays revealed Sp6-binding to this region. Subsequent transient transfection experiments showed that Rock1 promoter activity is enhanced by Sp6, but reduced by Sp1. Treatment of dental epithelial cells with the GC-selective DNA binding inhibitor, mithramycin A, affected Rock1 promoter activity in loss of enhancement by Sp6, but not repression by Sp1. Further site-directed mutagenesis indicated that the region from -206 to -150 contains responsive elements for Sp6. Taken together, we conclude that Sp6 positively regulates Rock1 transcription by direct binding to the Rock1 promoter region from -206 to -150, which functionally distinct from Sp1. (Tokushima University Institutional Repository) ● Metadata: 109578 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.61.306 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25264049 ● Summary page in Scopus @ Elsevier: 2-s2.0-84907504213 (Tokushima University Institutional Repository: 109578, DOI: 10.2152/jmi.61.306, PubMed: 25264049, Elsevier: Scopus)
11.	Ayako Tanimura, Taigo Horiguchi, Keiko Miyoshi, Hiroko Hagita and Takafumi Noma : Differential expression of adenine nucleotide converting enzymes in mitochondrial intermembrane space: a potential role of adenylate kinase isozyme 2 in neutrophil differentiation., PLoS ONE, Vol.9, No.2, e89916, 2014. (Summary) Adenine nucleotide dynamics in the mitochondrial intermembrane space (IMS) play a key role in oxidative phosphorylation. In a previous study, Drosophila adenylate kinase isozyme 2 (Dak2) knockout was reported to cause developmental lethality at the larval stage in Drosophila melanogaster. In addition, two other studies reported that AK2 is a responsible gene for reticular dysgenesis (RD), a human disease that is characterized by severe combined immunodeficiency and deafness. Therefore, mitochondrial AK2 may play an important role in hematopoietic differentiation and ontogenesis. Three additional adenine nucleotide metabolizing enzymes, including mitochondrial creatine kinases (CKMT1 and CKMT2) and nucleoside diphosphate kinase isoform D (NDPK-D), have been found in IMS. Although these kinases generate ADP for ATP synthesis, their involvement in RD remains unclear and still an open question. In this study, mRNA and protein expressions of these mitochondrial kinases were firstly examined in mouse ES cells, day 8 embryos, and 7-week-old adult mice. It was found that their expressions are spatiotemporally regulated, and Ak2 is exclusively expressed in bone marrow, which is a major hematopoietic tissue in adults. In subsequent experiments, we identified increased expression of both AK2 and CKMT1 during macrophage differentiation and exclusive production of AK2 during neutrophil differentiation using HL-60 cells as an in vitro model of hematopoietic differentiation. Furthermore, AK2 knockdown specifically inhibited neutrophil differentiation without affecting macrophage differentiation. These data suggest that AK2 is indispensable for neutrophil differentiation and indicate a possible causative link between AK2 deficiency and neutropenia in RD. (Tokushima University Institutional Repository) ● Metadata: 114179 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0089916 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24587121 ● Summary page in Scopus @ Elsevier: 2-s2.0-84897832127 (Tokushima University Institutional Repository: 114179, DOI: 10.1371/journal.pone.0089916, PubMed: 24587121, Elsevier: Scopus)
12.	Arya Adiningrat, Ayako Tanimura, Keiko Miyoshi, Ryna Yanuaryska Dwi, Hiroko Hagita, Taigo Horiguchi and Takafumi Noma : Ctip2-mediated Sp6 transcriptional regulation in dental epithelium-derived cells., The Journal of Medical Investigation : JMI, Vol.61, No.1.2, 126-136, 2014. (Summary) Tooth development relies on the interaction between the oral ectoderm and underlying mesenchyme, and is regulated by a complex genetic cascade. This transcriptional cascade is regulated by the spatiotemporal activation and deactivation of transcription factors. The specificity proteins 6 (Sp6) and chicken ovalbumin upstream promoter transcription factor-interacting protein 2 (Ctip2) were identified in loss-of-function studies as key transcription factors required for tooth development. Ctip2 binds to the Sp6 promoter in vivo; however, its role in Sp6 expression remains unclear. In this study, we investigated Sp6 transcriptional regulation by Ctip2. Immunohistochemical analysis revealed that Sp6 and Ctip2 colocalize in the rat incisor during tooth development. We examined whether Ctip2 regulates Sp6 promoter activity in dental epithelial cells. Cotransfection experiments using serial Sp6 promoter-luciferase constructs and Ctip2 expression plasmids showed that Ctip2 significantly suppressed the Sp6 second promoter activity, although the Sp6 first promoter activity was unaffected. Ctip2 was able to bind to the proximal region of the Sp6 first promoter, as previously demonstrated, and also to the novel distal region of the first, and second promoter regions. Our findings indicate that Ctip2 regulates Sp6 gene expression through direct binding to the Sp6 second promoter region. J. Med. Invest. 61: 126-136, February, 2014. (Keyword) ameloblast differentiation / Ctip2 / Sp6 / tooth development / transcriptional regulation (Tokushima University Institutional Repository) ● Metadata: 109529 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.61.126 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24705758 ● CiNii @ National Institute of Informatics (CRID): 1390001204245161216 ● Summary page in Scopus @ Elsevier: 2-s2.0-84897946413 (Tokushima University Institutional Repository: 109529, DOI: 10.2152/jmi.61.126, PubMed: 24705758, CiNii: 1390001204245161216, Elsevier: Scopus)
13.	Taigo Horiguchi, Miyuki Fuka, Koichi Fujisawa, Ayako Tanimura, Keiko Miyoshi, Ryutaro Murakami and Takafumi Noma : Adenylate kinase 2 deficiency limits survival and regulates various genes during larval stages of Drosophila melanogaster., The Journal of Medical Investigation : JMI, Vol.61, No.1.2, 137-150, 2014. (Summary) Adenylate kinase isozyme 2 (AK2) is located in mitochondrial intermembrane space and regulates energy metabolism by reversibly converting ATP and AMP to 2 ADPs. We previously demonstrated that disruption of the Drosophila melanogaster AK2 gene (Dak2) resulted in growth arrest during the larval stage and subsequent death. Two other groups found that human AK2 mutations cause reticular dysgenesis, a form of severe combined immunodeficiency (SCID) that is associated with severe hematopoietic defects and sensorineural deafness. However, the mechanisms underlying differential outcomes of AK2 deficiency in Drosophila and human systems remain unknown. In this study, effects of tissue-specific inactivation of the Dak2 gene on Drosophila development were analyzed using RNAi-mediated gene knockdown. In addition, to investigate the roles of AK2 in the regulation of gene expression during development, microarray analysis was performed using RNA from first and second instar larvae of Dak2-deficient mutant and wild-type D. melanogaster. Knockdown of Dak2 in all germ layers caused cessation of growth and subsequent death of flies. Microarray analysis revealed that Dak2 deficiency downregulates various genes, particularly those involved in the proteasomal function and in mitochondrial translation machinery. These data indicate that adenine nucleotide interconversion by Dak2 is crucial for developmental processes of Drosophila melanogaster. J. Med. Invest. 61: 137-150, February, 2014. (Keyword) Dak2 / gene expression / in silico analysis / microarray / mitochondria (Tokushima University Institutional Repository) ● Metadata: 109541 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.61.137 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24705759 ● CiNii @ National Institute of Informatics (CRID): 1390282679221871744 ● Summary page in Scopus @ Elsevier: 2-s2.0-84897905492 (Tokushima University Institutional Repository: 109541, DOI: 10.2152/jmi.61.137, PubMed: 24705759, CiNii: 1390282679221871744, Elsevier: Scopus)
14.	Taro Muto, Keiko Miyoshi, Taigo Horiguchi, Hiroko Hagita and Takafumi Noma : Novel genetic linkage of rat Sp6 mutation to Amelogenesis imperfecta, Orphanet Journal of Rare Diseases, Vol.7, No.1, 2012. (Summary) ABSTRACT: BACKGROUND: Amelogenesis imperfecta (AI) is an inherited disorder characterized by incomplete formation of tooth enamel. Although several genes responsible for AI have been reported, not all causative genes for human AI have been identified to date. AMI rat has been reported as an autosomal recessive mutant with hypoplastic AI isolated from a colony of stroke-prone spontaneously hypertensive rat strain, but the causative gene has not yet been clarified. Through a genetic screen, we identified the causative gene of autosomal recessive AI in AMI and analyzed its role in amelogenesis. METHODS: cDNA sequencing of possible AI-candidate genes so far identified using total RNA of day 6 AMI rat molars identified a novel responsible mutation in specificity protein 6 (Sp6). Genetic linkage analysis was performed between Sp6 and AI phenotype in AMI. To understand a role of SP6 in AI, we generated the transgenic rats harboring Sp6 transgene in AMI (Ami/Ami + Tg). Histological analyses were performed using the thin sections of control rats, AMI, and Ami/Ami + Tg incisors in maxillae, respectively. RESULTS: We found the novel genetic linkage between a 2-bp insertional mutation of Sp6 gene and the AI phenotype in AMI rats. The position of mutation was located in the coding region of Sp6, which caused frameshift mutation and disruption of the third zinc finger domain of SP6 with 11 cryptic amino acid residues and a stop codon. Transfection studies showed that the mutant protein can be translated and localized in the nucleus in the same manner as the wild-type SP6 protein. When we introduced the CMV promoter-driven wild-type Sp6 transgene into AMI rats, the SP6 protein was ectopically expressed in the maturation stage of ameloblasts associated with the extended maturation stage and the shortened reduced stage without any other phenotypical changes. CONCLUSION: We propose the addition of Sp6 mutation as a new molecular diagnostic criterion for the autosomal recessive AI pateints. Our findings expand the spectrum of genetic causes of autosomal recessive AI and sheds light on the molecular diagnosis for the classification of AI. Furthermore, tight regulation of the temporospatial expression of SP6 may have critical roles in completing amelogenesis. . (Tokushima University Institutional Repository) ● Metadata: 114180 (Link to Publication Site) ● Publication site (DOI): 10.1186/1750-1172-7-34 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22676574 ● Search Scopus @ Elsevier (PMID): 22676574 ● Search Scopus @ Elsevier (DOI): 10.1186/1750-1172-7-34 (Tokushima University Institutional Repository: 114180, DOI: 10.1186/1750-1172-7-34, PubMed: 22676574)
15.	Taro Muto, Keiko Miyoshi, Taigo Horiguchi and Takafumi Noma : Dissection of morphological and metabolic differentiation of amelobrasts via ectopic SP6 expression, The Journal of Medical Investigation : JMI, Vol.59, No.1-2, 59-68, 2012. (Summary) Tooth enamel is the hardest organ in the body. In rodent incisor, the enamel is exclusively produced by ameloblasts with yellowish-brown pigmentation, indicating normal enamel formation. However, the molecular mechanisms of ameloblast differentiation and amelogenesis are not fully understood. Specificity protein (Sp) 6 has been reported as one of the critical factors for tooth development. To explore SP6 function, we generated Sp6 transgenic (Tg) rats. Unexpectedly, the enamel surfaces of the incisors in Tg rats were discolored, even though enamel formation and serum iron concentrations were normal. Histological analysis of incisors from 6-week-old Tg rats demonstrated that the ameloblast layer at the pigmentation stage was elongated up to the gingival margin with ectopic SP6 expression in longitudinal incisor sections. In contrast, the incisors from 10-week-old Tg rats revealed that the pigmented ameloblasts were morphologically changed to those of the reduced stage, concomitant with the sporadic disappearance of ectopic SP6 expression. Here we report that morphological differentiation and metabolism of the iron-containing pigment in ameloblasts are independently regulated during amelogenesis by means of ectopic SP6 expression. (Keyword) Ameloblasts / Animals / cell differentiation / Dental Enamel / Dissection / Kruppel-Like Transcription Factors / Molar / Rats / Rats, Transgenic (Tokushima University Institutional Repository) ● Metadata: 85239 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.59.59 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22449994 ● Search Scopus @ Elsevier (PMID): 22449994 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.59.59 (Tokushima University Institutional Repository: 85239, DOI: 10.2152/jmi.59.59, PubMed: 22449994)
16.	W Trianna Utami, Keiko Miyoshi, Hiroko Hagita, Dwi Ryna Yanuaryska, Taigo Horiguchi and Takafumi Noma : Possible Linkage of SP6 Transcriptional Activity with Amelogenesis by Protein Stabilization., Journal of Biomedicine & Biotechnology, Vol.2011, 2011. (Summary) Ameloblasts produce enamel matrix proteins such as amelogenin, ameloblastin, and amelotin during tooth development. The molecular mechanisms of ameloblast differentiation (amelogenesis) are currently not well understood. SP6 is a transcription factor of the Sp/KLF family that was recently found to regulate cell proliferation in a cell-type-specific manner. Sp6-deficient mice demonstrate characteristic tooth anomalies such as delayed eruption of the incisors and supernumerary teeth with disorganized amelogenesis. However, it remains unclear how Sp6 controls amelogenesis. In this study, we used SP6 high producer cells to identify SP6 target genes. Based on the observations that long-term culture of SP6 high producer cells reduced SP6 protein expression but not Sp6 mRNA expression, we found that SP6 is short lived and specifically degraded through a proteasome pathway. We established an in vitro inducible SP6 expression system coupled with siRNA knockdown and found a possible linkage between SP6 and amelogenesis through the regulation of amelotin and Rock1 gene expression by microarray analysis. Our findings suggest that the regulation of SP6 protein stability is one of the crucial steps in amelogenesis. (Tokushima University Institutional Repository) ● Metadata: 114183 (Link to Publication Site) ● Publication site (DOI): 10.1155/2011/320987 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22046099 ● Search Scopus @ Elsevier (PMID): 22046099 ● Search Scopus @ Elsevier (DOI): 10.1155/2011/320987 (Tokushima University Institutional Repository: 114183, DOI: 10.1155/2011/320987, PubMed: 22046099)
17.	Trianna W Utami, Keiko Miyoshi, Hiroko Hagita, Ryna D. Yanuaryska, Taigo Horiguchi and Takafumi Noma : Dynamic changes of Sp6 Transgene Expression in Dental Epithelial Cells during Long-term Culture, The Indonesian Journal of Dental Research, Vol.1, No.3, 2011. (Tokushima University Institutional Repository) ● Metadata: 114181 (Link to Publication Site) ● Publication site (DOI): 10.22146/theindjdentres.10009 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.22146/theindjdentres.10009 (Tokushima University Institutional Repository: 114181, DOI: 10.22146/theindjdentres.10009)
18.	Ivan Arie Wahyudi, Taigo Horiguchi, Keiko Miyoshi, Taro Muto, Trianna Wahyu Utami, Hiroko Hagita and Takafumi Noma : Isolation and Characterization of Mouse Specificity Protein 6 Promoter, The Indonesian Journal of Dental Research, Vol.2010, Volume 1, No.1, 21-34, 2010. (Summary) Specificity protein 6 (SP6) is a member of the SP/Krüppel-like transcription factor family and plays key roles in tooth development. To study its biological roles, it is important to understand the spatiotemporal regulation of Sp6 gene expression. For this purpose, we first identified two separate 5' ends of the Sp6 cDNA by 5' RACE analysis using mouse mandibular RNA. Next, we isolated mouse genomic DNA fragments covering the Sp6 gene including two putative mouse Sp6 promoter regions and generated a series of luciferase reporter constructs. We confirmed the activity of both promoters by a luciferase assay and found strong second promoter activity in dental epithelial cells. Unexpectedly, we also detected potential third promoter activity in the intron 2 of the Sp6 gene. Last, we also found that bone morphogenetic protein and wingless signals could enhance Sp6 promoter activity in dental epithelial cells, suggesting the regulatory roles of two cytokines in Sp6 gene expression during tooth development. Our findings may shed new light on the regulatory mechanisms of Sp6 gene expression and provide a possible linkage between cytokine regulation of Sp6 expression and inductive epithelial and mesenchymal interactions. (Keyword) promoter activity / gene expression / luciferase assay (Tokushima University Institutional Repository) ● Metadata: 114182 (Link to Publication Site) ● Publication site (DOI): 10.22146/theindjdentres.9984 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.22146/theindjdentres.9984 (Tokushima University Institutional Repository: 114182, DOI: 10.22146/theindjdentres.9984)
19.	Keiko Miyoshi, Yuki Akazawa, Taigo Horiguchi and Takafumi Noma : Localization of adenylate kinase 4 in mouse tissues., Acta Histochemica et Cytochemica, Vol.42, No.2, 55-64, 2009. (Tokushima University Institutional Repository) ● Metadata: 114185 (Link to Publication Site) ● Publication site (DOI): 10.1267/ahc.08012 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19492028 ● Summary page in Scopus @ Elsevier: 2-s2.0-66149122562 (Tokushima University Institutional Repository: 114185, DOI: 10.1267/ahc.08012, PubMed: 19492028, Elsevier: Scopus)
20.	Koichi Fujisawa, Ryutaro Murakami, Taigo Horiguchi and Takafumi Noma : Adenylate kinase isozyme 2 is essential for growth and development of Drosophila melanogaster., Comparative Biochemistry and Physiology. Part B, Biochemistry & Molecular Biology, Vol.153, No.1, 29-38, 2009. (Summary) Adenylate kinases are phylogenetically widespread, highly conserved, and involved in energy metabolism and energy transfer. Of these, adenylate kinase (AK) isozyme 2 is uniquely localized in the mitochondrial intermembrane space and its physiological role remains largely unknown. In this study, we selected Drosophila melanogaster to analyze its role in vivo. AK isozyme cDNAs were cloned and their gene expressions were characterized in D. melanogaster. The deduced amino acid sequences contain highly conserved motifs for P-loop, NMP binding, and LID domains of AKs. In addition, the effects of AK2 gene knockout on phenotype of AK2 mutants were examined using P-element technology. Although homozygous AK2 mutated embryos developed without any visible defects, their growth ceased and they died before reaching the third instar larval stage. Maternally provided AK2 mRNA was detected in fertilized eggs, and weak AK2 activity was observed in first and second instar larvae of the homozygous AK2 mutants, suggesting that maternally provided AK2 is sufficient for embryonic development. Disappearance of AK2 activity during larval stages resulted in growth arrest and eventual death. These results demonstrate that AK2 plays a critical role in adenine nucleotide metabolism in the mitochondrial intermembrane space and is essential for growth in D. melanogaster. (Keyword) Adenine Nucleotides / Adenylate Kinase / Amino Acid Sequence / Animals / Blotting, Northern / Blotting, Western / Cloning, Molecular / Drosophila Proteins / Drosophila melanogaster / Enzyme Assays / female / Gene Expression Profiling / Gene Expression Regulation, Developmental / Gene Expression Regulation, Enzymologic / Kinetics / male / Molecular Sequence Data / Mutation / Phylogeny / Sequence Homology, Amino Acid (Link to Publication Site) ● Publication site (DOI): 10.1016/j.cbpb.2009.01.006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19416704 ● Summary page in Scopus @ Elsevier: 2-s2.0-63249086236 (DOI: 10.1016/j.cbpb.2009.01.006, PubMed: 19416704, Elsevier: Scopus)
21.	Keiko Miyoshi, Hideya Nagata, Taigo Horiguchi, Kaori Abe, Ivan Wahyudi Arie, Yoshinobu Baba, Hidemitsu Harada and Takafumi Noma : BMP2-induced gene profiling in dental epithelial cell line., The Journal of Medical Investigation : JMI, Vol.55, No.3-4, 216-226, 2008. (Summary) Tooth development is regulated by epithelial-mesenchymal interactions and their reciprocal molecular signaling. Bone morphogenetic protein 2 (BMP2) is known as one of the inducers for tooth development. To analyze the molecular mechanisms of BMP2 on ameloblast differentiation (amelogenesis), we performed microarray analyses using rat dental epithelial cell line, HAT-7. After confirming that BMP2 could activate the canonical BMP-Smads signaling in HAT-7 cells, we analyzed the effects of BMP2 on 14,815 gene expressions and profiled them. Seventy-three genes were up-regulated and 28 genes were down-regulated by BMP2 treatment for 24 hours in HAT-7 cells. Functional classification revealed that 18% of up-regulated genes were ECM/adhesion molecules present in the enamel organ. Furthermore, we examined the expression of several differentiation markers in dental epithelial four cell-lineages including inner enamel epithelium (ameloblasts), stratum intermedium, stratum reticulum, and outer enamel epithelium. The results indicated that BMP2 might induce at least two different cell-lineage markers including a BMP antagonist expressed in HAT-7 cells, suggesting that BMP2 could accelerate amelogenesis via BMP signaling. (Keyword) Ameloblasts / Amelogenesis / Animals / Base Sequence / Bone Morphogenetic Protein 2 / Cell Line / DNA Primers / Down-Regulation / Epithelial Cells / Gene Expression Profiling / Oligonucleotide Array Sequence Analysis / Rats / Reverse Transcriptase Polymerase Chain Reaction / Signal Transduction / Smad Proteins / Up-Regulation (Tokushima University Institutional Repository) ● Metadata: 110862 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.55.216 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18797134 ● Search Scopus @ Elsevier (PMID): 18797134 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.55.216 (Tokushima University Institutional Repository: 110862, DOI: 10.2152/jmi.55.216, PubMed: 18797134)
22.	Intan Ruspita, Keiko Miyoshi, Taro Muto, Kaori Abe, Taigo Horiguchi and Takafumi Noma : Sp6 downregulation of follistatin gene expression in ameloblasts., The Journal of Medical Investigation : JMI, Vol.55, No.1-2, 87-98, 2008. (Summary) Sp6 is a member of the Sp family of transcription factors that regulate a wide range of cellular functions, such as cell growth and differentiation. Sp6, also called epiprofin, is specifically expressed in tooth germ, limb bud, and hair follicle, but there is little information on its function.To investigate the possible role of Sp6 in tooth development, first we established an Sp6-overproducing clone, CHA9, and analyzed the features of the cell, including cell proliferation and gene expression. The parental cells of CHA9 are the ameloblast-lineage G5 cells that we previously established from rat dental epithelia of lower incisor. Sp6 overproduction accelerated cell proliferation and induced the expression of ameloblastin mRNA, a marker of ameloblast differentiation. Second, we performed genome-wide screening of Sp6 target genes by microarray analysis. Out of a total 20,450 genes, 448 genes were up-regulated and 500 genes were down-regulated by Sp6. We found the expression of follistatin, a BMP antagonist, to be 22.4-fold lower in CHA9 than in control cells. Transfection of the Sp6-antisense construct into CHA9 cells restored follistatin expression back to equivalent levels seen in control cells, indicating that Sp6 regulates follistatin gene expression in ameloblasts.Our findings demonstrate that the follistatin gene is one of the Sp6 target genes in ameloblasts and suggest that Sp6 promotes amelogenesis through inhibition of follistatin gene expression. (Keyword) Ameloblasts / Amelogenesis / Animals / COS Cells / Cell Differentiation / Cercopithecus aethiops / Clone Cells / Dental Enamel Proteins / Down-Regulation / Follistatin / Gene Expression Regulation, Developmental / Kruppel-Like Transcription Factors / Oligonucleotide Array Sequence Analysis / Rabbits / Rats / Transfection (Tokushima University Institutional Repository) ● Metadata: 110844 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.55.87 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18319550 ● Search Scopus @ Elsevier (PMID): 18319550 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.55.87 (Tokushima University Institutional Repository: 110844, DOI: 10.2152/jmi.55.87, PubMed: 18319550)
23.	Kaori Abe, Keiko Miyoshi, Taro Muto, Ruspita Intan, Taigo Horiguchi, Toshihiko Nagata and Takafumi Noma : Establishment and characterization of rat dental epithelial derived ameloblast-lineage clones., Journal of Bioscience and Bioengineering, Vol.103, No.5, 479-485, 2007. (Summary) Teeth are the hardest tissues covered with enamel produced by ameloblasts. The ameloblast differentiation is controlled by sequential epithelial-mesenchymal interactions during tooth morphogenesis. However, the molecular mechanism of ameloblast differentiation remains unclear. To address this question, we developed an in vitro assay system to evaluate the molecular mechanism of amelogenesis. First, we established dental epithelium-derived clones from 6-day-old rat incisors and established that cells of the clone SRE-G5 were the largest producers of amelogenin mRNA. Next, we analyzed the effects of several chemicals on the amelogenin expression in SRE-G5 cells. Only mitogen-activated protein kinase (MAPK) activators enhanced amelogenin mRNA expression. This finding corresponded to the immunohistochemical data showing the presence of phosphorylated forms of p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) during ameloblast differentiation. To examine the roles of MAPK signals, we compared the effects of anisomycin and sodium salicylate on the expression of tooth-related differentiation markers. Both anisomycin and sodium salicylate induced amelogenin, Abcg2, and Bmp4 mRNA and down-regulated p75NGFR mRNA. On the other hand, ALP, ectodin, Bmp2 and Fgf8 mRNA were up-regulated only by anisomycin. These results indicate that MAPK signaling functions, at least in part, as the inducer of ameloblast differentiation. (Keyword) Ameloblasts / Amelogenesis / Amelogenin / Animals / cell differentiation / Cells, Cultured / Cloning, Molecular / Epithelial Cells / Incisor / Rats (Link to Publication Site) ● Publication site (DOI): 10.1263/jbb.103.479 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17609165 ● Summary page in Scopus @ Elsevier: 2-s2.0-34250827878 (DOI: 10.1263/jbb.103.479, PubMed: 17609165, Elsevier: Scopus)
24.	Akemichi Ueno, Yoshihiro Miwa, Keiko Miyoshi, Taigo Horiguchi, Hideo Inoue, Intan Ruspita, Kaori Abe, Kikuji Yamashita, Eiji Hayashi and Takafumi Noma : Constitutive expression of thrombospondin 1 in MC3T3-E1 osteoblastic cells inhibits mineralization, Journal of Cellular Physiology, Vol.209, No.2, 322-332, 2006. (Summary) Thrombospondin 1 (TSP1) is a multifunctional extracellular glycoprotein present mainly in the fetal and adult skeleton. Although an inhibitory effect of TSP1 against pathological mineralization in cultured vascular pericytes has been shown, its involvement in physiological mineralization by osteoblasts is still unknown. To determine the role of TSP1 in biomineralization, mouse osteoblastic MC3T3-E1 cells were cultured in the presence of antisense phosphorothioate oligodeoxynucleotides complementary to the TSP1 sequence. The 18- and 24-mer antisense oligonucleotides caused concentration-dependent increases in the number of mineralized nodules, acid-soluble calcium deposition in the cell/matrix layer, and alkaline phosphatase activity within 9 days, without affecting cell proliferation. The corresponding sense or scrambled oligonucleotides did not affect these parameters. In the antisense oligonucleotide-treated MC3T3-E1 cells, thickened extracellular matrix, well-developed cell processes, increased intracellular organelles, and collagen fibril bundles were observed. On the other hand, the addition of TSP1 to the culture decreased the production of a mineralized matrix by MC3T3-E1 cells. Furthermore, MC3T3-E1 clones overexpressing mouse TSP1 were established and assayed for TSP1 protein and their capacity to mineralize. TSP1 dose-dependently inhibited mineralization by these cells both in vitro and in vivo. These results indicate that TSP1 functions as an inhibitory regulator of bone mineralization and matrix production by osteoblasts to sustain bone homeostasis. (Keyword) Alkaline Phosphatase / Animals / Antibodies, Monoclonal / Bone Matrix / Calcification, Physiologic / Cell Differentiation / Cell Line / Cell Proliferation / Cell Transplantation / Cells, Cultured / Down-Regulation / Female / Gene Expression / Mice / Oligonucleotides, Antisense / Osteoblasts / Osteocalcin / RNA, Messenger / Recombinant Proteins / Thrombospondin 1 (Link to Publication Site) ● Publication site (DOI): 10.1002/jcp.20735 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16883596 ● Search Scopus @ Elsevier (PMID): 16883596 ● Search Scopus @ Elsevier (DOI): 10.1002/jcp.20735 (DOI: 10.1002/jcp.20735, PubMed: 16883596)
25.	Akemichi Ueno, Kikuji Yamashita, Keiko Miyoshi, Taigo Horiguchi, Intan Ruspita, Kaori Abe and Takafumi Noma : Soluble matrix from osteoblastic cells induces mineralization by dental pulp cells, The Journal of Medical Investigation : JMI, Vol.53, No.3-4, 297-302, 2006. (Summary) Dental pulp cells have a capacity to differentiate into mineralization-inducing cells. To clarify the molecular mechanism, we established an in vitro mineralization-inducing system by rat clonal dental pulp cell line, RPC-C2A, and tried to purify a mineralization-inducing factor in conditioned medium (CM) from pre-osteoblastic MC3T3-E1 cells. The active factor was impermeable to an ultrafiltration membrane, and sedimented by ultracentrifugation. The sedimented factor was found as a needle-like structure about 1.3 microm in average length as observed by transmission electron microscopy. The factor contained type I collagen, suggesting not a matrix vesicle, but a soluble matrix. The mineralization-inducing activity was also detected in CM from primary culture of rat calvaria (RC) cells. These results suggested that the soluble matrices from osteoblastic cells serve, at least in part, as differentiation-inducing agents. (Keyword) Animals / Calcification, Physiologic / Cell Line / Collagen Type I / Dental Pulp / extracellular matrix / Extracellular Matrix Proteins / Osteoblasts / Osteogenesis / Rats / Skull (Tokushima University Institutional Repository) ● Metadata: 110826 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.53.297 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16953068 ● Summary page in Scopus @ Elsevier: 2-s2.0-33750334069 (Tokushima University Institutional Repository: 110826, DOI: 10.2152/jmi.53.297, PubMed: 16953068, Elsevier: Scopus)
26.	Nishikawa Hiroyuki, Akemichi Ueno, Taigo Horiguchi, Kikuji Yamashita, Inoue Hideo and Toshihiko Nagata : Effects of TGF-beta1 on Extracellular Matrix Formation in Rat Clonal Dental Pulp Cells, Dentistry in Japan, Vol.38, 44-50, 2002. (Keyword) TGF-beta1 / RPC-C2A cell / Dental pulp cell
27.	Xiong Yu, Taigo Horiguchi, Katsuya Shigesada and Edward Egelman : Three-dimensional Reconstruction of Transcription Termination Factor rho: Orientation of the N-terminal Domain and Visualization of an RNA-binding Site, Journal of Molecular Biology, Vol.299, No.5, 1279-1287, 2000. (Summary) The Escherichia coli rho transcription termination protein is a hexameric helicase, and is believed to function by separating an RNA-DNA hybrid. Unlike hexameric DNA helicases, where a single strand of DNA passes through the central channel, it has been proposed that the RNA wraps around the outside of the ring. We have generated a three-dimensional reconstruction of rho, and localized a tRNA molecule bound to the primary RNA-binding site to the outside of the ring. An atomic structure of the N-terminal domain of rho fits into our reconstruction uniquely, with the residues involved in RNA-binding on the outside of the ring. Although rho shares a common structural core with the F1-ATPase and other hexameric helicases, there has been a divergence in function due to rho's N-terminal domain, which has no homology to other helicases. (Keyword) Binding Sites / Escherichia coli / Microscopy, Electron / Models, Biological / Models, Molecular / Protein Structure, Quaternary / Protein Structure, Secondary / Proton-Translocating ATPases / RNA, Bacterial / RNA, Transfer / RNA-Binding Proteins / Rho Factor / Transcription, Genetic (Link to Publication Site) ● Publication site (DOI): 10.1006/jmbi.2000.3810 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10873452 ● Summary page in Scopus @ Elsevier: 2-s2.0-0034705329 (DOI: 10.1006/jmbi.2000.3810, PubMed: 10873452, Elsevier: Scopus)
28.	Taigo Horiguchi, Yoshihiro Miwa and Katsuya Shigesada : The Quaternary Geometry of Transcription Termination Factor rho: Assignment by Chemical Cross-linking, Journal of Molecular Biology, Vol.269, No.4, 514-528, 1997.
29.	Yoshihiro Miwa, Taigo Horiguchi and Katsuya Shigesada : Structural and Functional Dissections of Transcription Termination Factor Rho by Random Mutagenesis, Journal of Molecular Biology, Vol.254, No.5, 815-837, 1995.

Academic Paper (Unrefereed Paper):

1.	Taigo Horiguchi : Microarray Data Analysis Mainly on a Functional Analysis using DAVID, Journal of Oral Health and Biosciences, Vol.29, No.2, 55-62, 2017. (Keyword) Microarray / Cluster Analysis / DAVID / GO Analysis (Tokushima University Institutional Repository) ● Metadata: 111060 (Link to Publication Site) ● Publication site (DOI): 10.20738/johb.29.2_55 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282680799299840 ● Search Scopus @ Elsevier (DOI): 10.20738/johb.29.2_55 (Tokushima University Institutional Repository: 111060, DOI: 10.20738/johb.29.2_55, CiNii: 1390282680799299840)

Proceeding of International Conference:

1.	Keiko Miyoshi, Arinawati Yosi Dian, Hagita Hiroko, Taigo Horiguchi and Takafumi Noma : Possible roles of Sp6 in ameloblast differentiation, The 6th International Conference on Biology and Pathobiology of KLF/Sp Transcription Factors, Oct. 2018.
2.	Ayako Tanimura, Keiko Miyoshi, Taigo Horiguchi, Hagita Hiroko, Koichi Fujisawa and Takafumi Noma : A role of ER stress and UPR on hematopoietic differentiation, 51st Miami Winter Symposium, Stem Cells Todays Research Tomorrows Therapies, Miami, Jan. 2018.
3.	Arinawati Yosi Dian, Keiko Miyoshi, Ayako Tanimura, Taigo Horiguchi and Takafumi Noma : Comparative study of gene profiling using 2D and 3D culture as an in vitro amelogenesis imperfecta model, Internationl Joint meeting 4th ASEAN plus Tokushima Joint International Conference, Dec. 2017.
4.	Ayako Tanimura, Keiko Miyoshi, Taigo Horiguchi, Hagita Hiroko, Koichi Fujisawa and Takafumi Noma : Impact of mitochondrial ATP production on neutrophil differentiation, Gordon Research Conference(From Molecular Structures and Mechanisms to Cellular Bioenergetics in Health and Disease), Jun. 2017.
5.	Keiko Miyoshi, Hagita Hiroko, Arinawati Yosi Dian, Ayako Tanimura, Taigo Horiguchi and Takafumi Noma : Regulation of SP6 protein expression in stably transformed dental epithelial cells, 12th International Conference on Tooth Morphogenesis and Differentiation, Porvoo,Finland, Jun. 2016.
6.	Keiko Miyoshi, Adiningrat Arya, Ayako Tanimura, Yanuaryska Dwi Ryna, Arinawati Yosi Dian, Taigo Horiguchi and Takafumi Noma : Establishment of an in Vitro amelogenesis imperfecta model, Challenge to Intractable Oral Diseases International Symposium 2015 which takes place at Yumikura Hall,Osaka University Graduate School of Dentistry in Japan from 10-11 December 2015, Dec. 2015. (Keyword) amelogenesis imperfecta / ARE / in vitro model / SP6 / structure-activity relationship
7.	Taigo Horiguchi, Keiko Miyoshi, Ayako Tanimura, H. Hagita, Y. Miyatake, Hiroshi Sakaue and Takafumi Noma : Gene expression analysis of hyperactive mutant SPORTS rat, Cell Symposia:Exercise and Metabolism which takes place at NH Grand Krasnapolsky Hotel Amsterdam from 12-14 July 2015, Amsterdam, Jul. 2015.
8.	Hiroko Hagita, Keiko Miyoshi, Taigo Horiguchi, Ayako Tanimura, Arya Adiningrat, Dian Yosi Arinawati and Takafumi Noma : Analysis of GBA1 gene structure and expression, The 11th International workshop on Advanced Genomics, Tokyo, May 2015.
9.	Keiko Miyoshi, Taigo Horiguchi, Ayako Tanimura, Hiroko Hagita, Yoshihiro Touda, Shoji Kagami, Kenji Mori, Daisuke Tsuji, Kouji Itou and Takafumi Noma : Gaucher disease caused by possible atypical mechanism, Gordon Research Conference, USA,Texas,Galveston(Hotel Galvez), Mar. 2015.
10.	Ayako Tanimura, Taigo Horiguchi, Keiko Miyoshi, Hiroko Hagita and Takafumi Noma : Adenylate Kinase 2 Regulates Neutrophil Differentiation Via Mitochondrial, The 3rd ASEAN Plus and Tokushima Joint International Conference, Makassar,Indonesia, Dec. 2014.
11.	Arya Adinigrat, Ayako Tanimura, Keiko Miyoshi, Ryna Dwi Yanuaryska, Hiroko Hagita, Taigo Horiguchi and Takafumi Noma : Ctip2 Regulation Of Tooth Development Via Sp6 Gene Expression, The 3rd ASEAN Plus and Tokushima Joint International Conference, Makassar,Indonesia, Dec. 2014.
12.	Ayako Tanimura, Taigo Horiguchi, Keiko Miyoshi, Hiroko Hagita and Takafumi Noma : A role of adenine nucleotide converting enzymes in the mitochondrial intermembrane space on the hematopoietic cell differentiation, Keystone meeting Mitochondrial Dynamics and Physiology, SantaFe, New Mexico, USA, Feb. 2014.
13.	Taigo Horiguchi, Miyuki Fuka, Koichi Fujisawa, Ayako Tanimura, Keiko Miyoshi, Ryutaro Murakami and Takafumi Noma : A Role of AK2 during Development of Drosohila melanogaster, The 4th International Symposium on Dynamics of Mitochondria, Oct. 2013.
14.	Arya Adiningrat, Keiko Miyoshi, Hiroko Hagita, Taigo Horiguchi, Ayako Tanimura, Ryna Dwi Yanuaryska and Takafumi Noma : Role of Bcl11b/Ctip2 on Sp6 Gene Expression in Dental Epithelial Cell, ASEAN PLUS and TOKUSHIMA JOINT INTERNATIONAL CONFERENCE, Dec. 2012.
15.	Ryna Dwi Yanuaryska, Keiko Miyoshi, Taigo Horiguchi, Ayako Tanimura, Hiroko Hagita, Arya Adiningrat and Takafumi Noma : SP6 Regulation of Rock1 Expression in Dental Epithelial Cells, ASEAN PLUS and TOKUSHIMA JOINT INTERNATIONAL CONFERENCE, Tokushima, Dec. 2012.
16.	Keiko Miyoshi, Taro Muto, Taigo Horiguchi, Hiroko Hagita and Takafumi Noma : A frameshift mutation in Sp6 linked to Amelogenesis imperfecta, ASEAN PLUS and TOKUSHIMA JOINT INTERNATIONAL CONFERENCE, Tokushima, Dec. 2012.
17.	Trianna W Utami, Keiko Miyoshi, Hiroko Hagita, Ryna D Yanuaryska, Taigo Horiguchi and Takafumi Noma : REGULATION OF SP6 GENE EXPRESSION AND CELL TYPE SPECIFIC FUNCTION OF SP6 IN DENTAL EPITHELIAL CELLS, The 2nd International Joint Sypmosium on Oral and Dental Sciences In Conjuction with Dental Specialists Seminar, Mar. 2012.
18.	Utami Wahyu Trianna, Keiko Miyoshi, Taigo Horiguchi, Taro Muto, Wahyudi Arie Ivan, Hiroko Hagita and Takafumi Noma : Differential regulation of Sp6 silencing in dental epithelial cells, Inter national Joint Symposium on Oral Science, Dec. 2010.
19.	Ivan Arie Wahyudi, Taigo Horiguchi, Keiko Miyoshi, Taro Muto, Trianna Wahyu Utami, Hagita Hiroko and Takafumi Noma : Caracterization of Specificity Protein 6 promoter Activity, International Joint Symposium on Oral Science, Dec. 2010.
20.	Takafumi Noma, Taro Muto, Keiko Miyoshi, Taigo Horiguchi, Hiroko Hagita, Wahyudi Arie Ivan and Utami Wahyu Trianna : From a study of tooth morphology and development to a perspective for the future regeneration therapy, ガジャマダ大学創立62年記念講演会, Feb. 2010.
21.	Ruspita Intan, Keiko Miyoshi, Taro Muto, Kaori Abe, Taigo Horiguchi and Takafumi Noma : Identification of Sp6 target gene in dental epithelial cells, Gordon Research Conferences, Feb. 2008.
22.	Keiko Miyoshi, Taigo Horiguchi, Kazuki Abe, Inoue Hideo and Takafumi Noma : Effects of glycyrrhizin on the gene expression in CC14-induced hepatitis, 8th World Congress on Inflammation, Jun. 2007.
23.	Takafumi Noma, Keiko Miyoshi, Yuki Akazawa and Taigo Horiguchi : Tissue-ditribution and possible functional roles of AK4, Mitchondrial Medicine 2007: Riding the Wave of the Future, Jun. 2007.
24.	Takafumi Noma, Keiko Miyoshi, Yuki Akazawa and Taigo Horiguchi : Tissue-distribution and possible functional roles of AK4, Mitochondrial Medicine Meeting, San Diego, Jun. 2007. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.mito.2007.08.016 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.mito.2007.08.016 (DOI: 10.1016/j.mito.2007.08.016)
25.	Kaori Abe, Keiko Miyoshi, Taro Muto, Intan Ruspita, Taigo Horiguchi, Toshihiko Nagata and Takafumi Noma : Establishment and charactarization of rat ameloblast-lineage clones, The 19th Annual and International Meeting of the Japanese Association for Animal Cell Technology, Kyoto, Sep. 2006.
26.	Keiko Miyoshi, Taigo Horiguchi, Kaori Abe, Akemichi Ueno, Hideya Nagata, Yoshinobu Baba, Hidemitsu Harada and Takafumi Noma : Effects of BMP2 on Gene Expression in Dental Epithelial Cell Line, Eight International Conference on Tooth Morphogenesis and Differentiation, York, UK, Jul. 2004.

Proceeding of Domestic Conference:

1.	Jin Shengjian, Takaaki Tsunematsu, Taigo Horiguchi, Yasuhiro Mouri, Wenhua Shao, Keiko Miyoshi, Noriko Mizusawa, Hagita Hiroko, Sarubo Motoharu, Yoshida Kayo, Kaya Yoshida, Natsumi Fujiwara, Kazumi Ozaki, Naozumi Ishimaru and Yasusei Kudo : The role of deubiquitinating enzyme, OTUB1 in head and neck squamous cell carcinoma (HNSCC) progression, 第82回日本癌学会学術集会, Sep. 2023.
2.	Jin Shengjian, Takaaki Tsunematsu, Taigo Horiguchi, Yasuhiro Mouri, Wenhua Shao, Keiko Miyoshi, Noriko Mizusawa, Hiroko Hagita, YOSHIDA Kayo, Kaya Yoshida, Natsumi Fujiwara, Kazumi Ozaki, Naozumi Ishimaru and Yasusei Kudo : The role of Deubiquitinating enzyme, OTUB1 in head and neck squamous cell carcinoma (HNSCC) progression, 第61回四国歯学会, Mar. 2023.
3.	Keiko Miyoshi, Taigo Horiguchi and Ayako Tanimura : GBA遺伝子構造の再定義と細胞特異的発現制御機構の解析, 第64回歯科基礎医学会学術大会, Sep. 2022.
4.	shengjian jin, Takaaki Tsunematsu, Taigo Horiguchi, Naozumi Ishimaru and Yasusei Kudo : 脱ユビキチン化酵素OTUB1の頭頸部扁平上皮癌の進展における役割, 第64回歯科基礎医学会学術大会, Sep. 2022.
5.	Taigo Horiguchi, Keiko Miyoshi, 萩田浩子 and Takafumi Noma : 運動が遺伝子発現に与える影響の網羅的解析, 四国歯学会56回例会, Feb. 2020.
6.	Keiko Miyoshi, Taigo Horiguchi, 萩田浩子 and Takafumi Noma : 再生歯学戦略におけるヒト口腔粘膜由来線維芽細胞の特性, 四国歯学会56回例会, Feb. 2020.
7.	Arinawati Yosi Dian, Keiko Miyoshi, Hagita Hiroko, Taigo Horiguchi and Takafumi Noma : Perturbation of gene regulateion in an in vitro amelogenesis imperfecta model, The 91st Annual Meeting of the Japanese Biochemical Society, Sep. 2018.
8.	Arinawati Yosi Dian, Keiko Miyoshi, Taigo Horiguchi and Takafumi Noma : アメロジェネシスのステージ特異的な遺伝子制御におけるSp6の関与, 第60回歯科基礎医学会学術大会, Sep. 2018.
9.	Arinawati Yosi Dian, Keiko Miyoshi, Hagita Hiroko, Taigo Horiguchi and Takafumi Noma : Demonstration of defective amelogenesis using an in vitro amelogenesis imperfecta model, 第257回徳島医学会学術集会, Aug. 2018.
10.	Keiko Miyoshi, hagita hiroko, Ayako Tanimura, Taigo Horiguchi and Takafumi Noma : 5´end structure of GBA and expression profile of its variants, 2017年度生命科学系学会合同年次大会 ConBio 2017, Dec. 2017.
11.	Ayako Tanimura, Keiko Miyoshi, Taigo Horiguchi, hagita hiroko, Koichi Fujisawa and Takafumi Noma : ミトコンドリアがUPR活性をコントロールして免疫細胞分化の方向を決定づける, 第17回日本ミトコンドリア学会年会, Nov. 2017.
12.	Yosi Dian Arinawati, Keiko Miyoshi, Ayako Tanimura, Taigo Horiguchi and Takafumi Noma : エナメル質形成不全モデルにおけるアメロジェネシス関連遺伝子発現プロファイル, 第59回歯科基礎医学会学術大会, Sep. 2017.
13.	Ayako Tanimura, Keiko Miyoshi, Taigo Horiguchi, Koichi Fujisawa and Takafumi Noma : CRISPR/Cas9を用いたAK2の段階的欠損による細胞代謝への影響, The 2nd ANNUAL MEETING OF THE JAPANESE SOCIETY FOR GENOME EDITING, Jun. 2017.
14.	Ayako Tanimura, Taigo Horiguchi, Keiko Miyoshi, Arinawati Yosi Dian and Takafumi Noma : HL-60細胞を用いた血球分化時におけるUnfolded protein responseの解析, 第57回日本生化学会中国・四国支部例会, May 2016.
15.	Taigo Horiguchi : マイクロアレイデータ解析法 ─DAVIDによる機能解析を中心に─, 四国歯学会第48回例会, Mar. 2016.
16.	Taigo Horiguchi, Keiko Miyoshi, Ayako Tanimura, Hagita Hiroko, Miyatake Yumiko, Hiroshi Sakaue and Takafumi Noma : 運動能が亢進したSPORTSラットの遺伝子発現解析, 第38回日本分子生物学会，第88回日本生化学会合同大会, Dec. 2015.
17.	Keiko Miyoshi, Taigo Horiguchi, Ayako Tanimura, Hiroko Hagita and Takafumi Noma : ヒト口腔粘膜線維芽細胞の特性:皮膚線維芽細胞，iPS細胞との網羅的遺伝子発現の比較解析, The 14th Congress of the Japanese Society for Regenerative Medicine, Mar. 2015.
18.	青山修平, 深美由紀, Taigo Horiguchi, Takafumi Noma, 原田由美子 and 村上柳太郎 : ショウジョウバエアデニル酸キナーゼ2 (AK2) の発生時期特異的ノックダウン, 第37回日本分子生物学会年会, Nov. 2014.
19.	Arya Adiningrat, Keiko Miyoshi, Ryna Dwi Yanuaryska, Hiroko Hagita, Taigo Horiguchi, Ayako Tanimura and Takafumi Noma : Establishment and Characterization of Dental Epithelial Cells Derived from Amelogenesis Imperfecta Rat, 第87回日本生化学会大会, Oct. 2014.
20.	Arya Adiningrat, Ayako Tanimura, Keiko Miyoshi, Ryna Dwi Yanuaryska, Hiroko Hagita, Taigo Horiguchi and Takafumi Noma : Ctip2 role in Sp6 transcriptional regulation in dental epithelial-derived cells, 2014 Tokushima Bioscience Retreat, Sep. 2014.
21.	青山修平, 深美由紀, Taigo Horiguchi, Takafumi Noma, 原田由美子 and 村上柳太郎 : アデニル酸キナーゼ2の時期特異的ノックダウン, (), May 2014.
22.	Taigo Horiguchi : 2013 「ストレスと栄養クラスター」研究報告会, 「アデニル酸キナーゼ2 ノックアウトフライを用いたヒト重症免疫不全症の基礎研究」, Dec. 2013.
23.	Adiningrat Arya, Ayako Tanimura, Keiko Miyoshi, Yanuaryska Dwi Ryna, Taigo Horiguchi, 萩田浩子 and Takafumi Noma : Role of Ctip2 in Sp6 gene regulation, 第36回日本分子生物学会年会, Dec. 2013.
24.	青山修平, 深美由紀, Taigo Horiguchi, Takafumi Noma, 原田由美子 and 村上柳太郎 : ショウジョウバエアデニル酸キナーゼ(AK2)の発生時期特異的ノックダウン, 第36回日本分子生物学会年会, Dec. 2013.
25.	Yanuaryska Dwi Ryna, Keiko Miyoshi, Taigo Horiguchi, Ayako Tanimura, Adiningrat Arya and Takafumi Noma : SP6 Positiyvely Regulates Rock1 Promoter Activity in Dental Epithelial Cells, 第55回歯科基礎医学会, Sep. 2013.
26.	大本卓司, 吉谷信幸, Taigo Horiguchi and Naomi Sakashita : 皮膚腫瘍, 第111回中国四国スライドカンファレンス, Jun. 2013.
27.	Keiko Miyoshi, Yanuaryska Dwi Ryna, Adiningrat Arya, 萩田浩子, Ayako Tanimura, Taigo Horiguchi and Takafumi Noma : 転写因子SP6の構造と機能解析, 第54回日本生化学会中国・四国支部例会, Jun. 2013.
28.	Ryna Dwi Yanuaryska, Keiko Miyoshi, Taigo Horiguchi, Ayako Tanimura, Hiroko Hagita and Takafumi Noma : SP6 and AP2 regulate Rock1 expression in dental epithelial cells, 第54回日本生化学会中国・四国支部例会, May 2013.
29.	Ayako Tanimura, Taigo Horiguchi, Hiroko Hagita, Keiko Miyoshi and Takafumi Noma : アデニル酸キナーゼ2の血球系分化への影響, 第54回日本生化学会中国・四国支部例会, May 2013.
30.	Taigo Horiguchi, Ayako Tanimura, HIROKO HAGITA, Keiko Miyoshi and Takafumi Noma : SPRTSラットにおける遺伝子発現パターンとその意義, 第54回日本生化学会中国・四国支部例会, May 2013.
31.	佐藤綾, Naomi Sakashita, Taigo Horiguchi and Seiko Kagawa : 総肺静脈灌流異常修復術後性肺静脈狭窄病変におけるHic-5陽性平滑筋細胞の意義, 第102回日本病理学会, May 2013.
32.	Taigo Horiguchi, Ayako Tanimura, Keiko Miyoshi and Takafumi Noma : SPORTSラットにおけるAK isozymesの発現パターンとその意義, 平成24年度「ストレスと栄養クラスター」の研究報告会, Jan. 2013.
33.	Ayako Tanimura, Taigo Horiguchi, Keiko Miyoshi and Takafumi Noma : ミトコンドリア膜間酵素AK2の細胞分化における役割, 平成24年度「ストレスと栄養クラスター」の研究報告会, Jan. 2013.
34.	深美由紀, 阿武雅之, Taigo Horiguchi, Koichi Fujisawa, Takafumi Noma and 村上柳太郎 : Functional Analysis of the Drosophila Adenylate Kinase Genes AK1,AK2 and AK3, 第35回日本分子生物学会, Dec. 2012.
35.	Keiko Miyoshi, Taro Muto, Taigo Horiguchi, 萩田浩子 and Takafumi Noma : エナメル質形成不全症の新規変異遺伝子の発見, 日本人類遺伝学会第57回大会, Oct. 2012.
36.	Taigo Horiguchi : Investigation into Pathogenic Mechanism of Reticular Dysgenesis Using iPS Cells Derived frome Human Oral Fibroblast, 平成23年度再生工学カテゴリー研究報告会, Feb. 2012.
37.	深美由紀, 阿武雅之, Taigo Horiguchi, Koichi Fujisawa, Takafumi Noma and 村上柳太郎 : Functionla analysis of Drosophila adenylate kinase-2(Dak2), 第34回日本分子生物学会, Dec. 2011.
38.	Yanuaryska Dwi Ryna, Keiko Miyoshi, Utami Wahyu Trianna, Taigo Horiguchi and Takafumi Noma : Identification of SP6 Target Genes inRat Dental Epithelial Cell, 第53回歯科基礎医学会学術大会・総会, Oct. 2011.
39.	Utami Wahyu Trianna, Keiko Miyoshi, Hiroko Hagita, Yanuaryska Dwi Ryna, Taigo Horiguchi and Takafumi Noma : SP6 Stability and Functional Linkage during Amelogenesis, 第84回日本生化学会大会, Sep. 2011.
40.	Takafumi Noma, Taro Muto, Keiko Miyoshi and Taigo Horiguchi : Sp6トランスジェニックラットに見られた鉄代謝異常, 第35回日本鉄バイオサイエンス学会, Sep. 2011.
41.	Utami Wahyu Triannna, Keiko Miyoshi, Taigo Horiguchi, Wahyudi A Ivan, Hiroko Hagita, Yanuaryska D Ryna and Takafumi Noma : Regulation of Sp6 expression and function in C9 cells, 第52回日本生化学会中国四国支部例会, May 2011.
42.	Utami Wahyu Trianna, Keiko Miyoshi, Taigo Horiguchi, Taro Muto, Wahyudi Arie Ivan, Hiroko Hagita and Takafumi Noma : Regulation of Sp6 expression in CHA9 cells, 第33回日本分子生物学会第83回日本生化学会, Dec. 2010.
43.	Wahyudi Arie Ivan, Taigo Horiguchi, Keiko Miyoshi, Taro Muto, Utami Wahyu Trianna, Hiroko Hagita and Takafumi Noma : Isolation and Characterization of Mouse Specificity Protein 6 Promoter, 第33回日本分子生物学会第83回日本生化学会, Dec. 2010.
44.	Utami Wahyu Trianna, Keiko Miyoshi, Taigo Horiguchi, Taro Muto, Hiroko Hagita and Takafumi Noma : Regulation of Sp6 expression in CHA9 cells, 2010 Tokushima Bioscience Retreat, Sep. 2010.
45.	Wahyudi Arie Ivan, Taigo Horiguchi, Keiko Miyoshi, Taro Muto, Hiroko Hagita and Takafumi Noma : Isolation and Characterization of Mouse Specificity Protein 6 Promoter, 2010 Tokushima Bioscience Retreat, Sep. 2010.
46.	Wahyudi Arie IVAN, Taigo Horiguchi, Keiko Miyoshi, Taro Muto and Takafumi Noma : Regulation of Sp6 Expression in Dental Epthelial Cells, ミニリトリート若手研究報告会「ストレスと栄養クラスター」, Feb. 2010.
47.	Wahyudi Arie Ivan, Taigo Horiguchi, Keiko Miyoshi, Taro Muto and Takafumi Noma : Regulation of Sp6 expression in dental epithelial cells, 第51回歯科基礎医学会, Sep. 2009.
48.	Ruspita Ita, Keiko Miyoshi, Taro Muto, Taigo Horiguchi, Kaori Abe, Takafumi Noma and Toshihiko Nagata : A possible role of Sp6 in Amelogenesis, 「魅力ある大学院教育」イニシアティブ「21世紀の口腔科学が目指すべき方向性」, Dec. 2007.
49.	Ruspita Intan, Keiko Miyoshi, Taro Muto, Taigo Horiguchi, Kaori Abe and Takafumi Noma : Sp6 induced down-regulation of follistatin gene in rat dental epithelial cells, 第49回歯科基礎医学学術大会, Aug. 2007.
50.	Kaori Abe, Keiko Miyoshi, Taro Muto, Taigo Horiguchi, Ruspita Intan, Toshihiko Nagata and Takafumi Noma : Redox regulation of amelogenin gene expression, 第49回歯科基礎医学学術大会, Aug. 2007.
51.	Kaori Abe, Keiko Miyoshi, Taro Muto, Taigo Horiguchi, Ruspita Ita, Takafumi Noma and Toshihiko Nagata : MAPK activation via ROS induces amelognin expression in the ameloblast-lineage cells, 「魅力ある大学院教育」イニシアティブ「21世紀の口腔科学が目指すべき方向性」, 2007.

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

Investigation of novel oral cancer-specific molecular targets based on genetic diversity (Project/Area Number: 23K24546 )
RNA修飾による糖脂質分解酵素活性制御機構の解明とゴーシェ病克服への挑戦 (Project/Area Number: 22K09913 )
Identification of signal targets in neutrophil differentiation (Project/Area Number: 19K10090 )
Study on elucidation of the pathophysiology of rare intractable diseases (reticular dysgenesis) with severe combined immunodeficiency and development of therapeutic methods (Project/Area Number: 15K11072 )
Characterization of Gaucher disease by new gene mutation using patient-derived oral mucosa fibroblasts (Project/Area Number: 15K11041 )
Development of sensors for monitoring intracellular ATP and GTP. (Project/Area Number: 16591858 )
象牙質に特異的な非コラーゲン性蛋白質の機能に関する研究 (Project/Area Number: 13771096 )
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Assistant Professor : Horiguchi, Taigo

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