{"insert":{"user_id":"B000366075","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/34602545","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=383286","label":"url"}],"paper_title":{"en":"Rap1 Small GTPase Regulates Vascular Endothelial-Cadherin-Mediated Endothelial Cell-Cell Junctions and Vascular Permeability.","ja":"Rap1 Small GTPase Regulates Vascular Endothelial-Cadherin-Mediated Endothelial Cell-Cell Junctions and Vascular Permeability."},"authors":{"en":[{"name":"Yamamoto Kiyotake"},{"name":"Takagi Yuki"},{"name":"Ando Koji"},{"name":"Fukuhara Shigetomo"}],"ja":[{"name":"山本 清威"},{"name":"Takagi Yuki"},{"name":"Ando Koji"},{"name":"Fukuhara Shigetomo"}]},"publication_date":"2021-10","publication_name":{"en":"Biological & Pharmaceutical Bulletin","ja":"Biological & Pharmaceutical Bulletin"},"volume":"44","number":"10","starting_page":"1371","ending_page":"1379","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1248/bpb.b21-00504"],"issn":["1347-5215"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
{"insert":{"user_id":"B000366075","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33870229","label":"url"},{"@id":"https://www.scopus.com/pages/publications/85103400102","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=376846","label":"url"}],"paper_title":{"en":"Protocol for analysis of integrin-mediated cell adhesion of lateral plate mesoderm cells isolated from zebrafish embryos","ja":"Protocol for analysis of integrin-mediated cell adhesion of lateral plate mesoderm cells isolated from zebrafish embryos"},"authors":{"en":[{"name":"Rho Seung-Sik"},{"name":"Oguri-Nakamura Eri"},{"name":"Ando Koji"},{"name":"Yamamoto Kiyotake"},{"name":"Takagi Yuki"},{"name":"Fukuhara Shigetomo"}],"ja":[{"name":"Rho Seung-Sik"},{"name":"Oguri-Nakamura Eri"},{"name":"Ando Koji"},{"name":"山本 清威"},{"name":"Takagi Yuki"},{"name":"Fukuhara Shigetomo"}]},"description":{"en":"Lateral plate mesoderm (LPM) cells differentiate into various cell types including endothelial and hematopoietic cells. In zebrafish embryos, LPM cells migrate toward the midline along the ventral surfaces of somites during which their cell fate specification depends upon efficient integrin-mediated cell adhesion and migration. Herein, we present a protocol for analysis of integrin-mediated cell adhesion of LPM cells isolated from zebrafish embryos. This allows the study of the molecular mechanisms underlying integrin activation required for LPM cell fate specification. For complete details on the use and execution of this protocol, please refer to Rho et al. (2019).","ja":"Lateral plate mesoderm (LPM) cells differentiate into various cell types including endothelial and hematopoietic cells. In zebrafish embryos, LPM cells migrate toward the midline along the ventral surfaces of somites during which their cell fate specification depends upon efficient integrin-mediated cell adhesion and migration. Herein, we present a protocol for analysis of integrin-mediated cell adhesion of LPM cells isolated from zebrafish embryos. This allows the study of the molecular mechanisms underlying integrin activation required for LPM cell fate specification. For complete details on the use and execution of this protocol, please refer to Rho et al. (2019)."},"publication_date":"2021-06-18","publication_name":{"en":"STAR Protocols","ja":"STAR Protocols"},"volume":"2","number":"2","starting_page":"100428","ending_page":"100428","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.xpro.2021.100428"],"issn":["2666-1667"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
{"insert":{"user_id":"B000366075","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://tokushima-u.repo.nii.ac.jp/records/2004288","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28373608","label":"url"},{"@id":"https://www.scopus.com/pages/publications/85016425921","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=323288","label":"url"}],"paper_title":{"en":"Protein kinase C-δ signaling regulates glucagon secretion from pancreatic islets","ja":"Protein kinase C-δ signaling regulates glucagon secretion from pancreatic islets"},"authors":{"en":[{"name":"Yamamoto Kiyotake"},{"name":"Mizuguchi Hiroyuki"},{"name":"Tokashiki Natsumi"},{"name":"Kobayashi Makoto"},{"name":"Tamaki Motoyuki"},{"name":"Sato Youichi"},{"name":"Fukui Hiroyuki"},{"name":"Yamauchi Aiko"}],"ja":[{"name":"山本 清威"},{"name":"水口 博之"},{"name":"Tokashiki Natsumi"},{"name":"Kobayashi Makoto"},{"name":"田蒔 基行"},{"name":"佐藤 陽一"},{"name":"福井 裕行"},{"name":"山内 あい子"}]},"description":{"en":"Accumulating evidence supports the \"glucagonocentric hypothesis\", in which antecedent -cell failure and inhibition of glucagon secretion are responsible for diabetes progression. Protein kinase C (PKC) is involved in glucagon secretion from -cells, although which PKC isozyme is involved and the mechanism underlying this PKC-regulated glucagon secretion remains unknown. Here, the involvement of PKC in the onset and progression of diabetes was elucidated. Immunofluorescence studies revealed that PKC was expressed and activated in -cells of STZ-induced diabetic model mice. Phorbol 12-myristate 13-acetate (PMA) stimulation significantly augmented glucagon secretion from isolated islets. Pre-treatment with quercetin and rottlerin, PKC signaling inhibitors, significantly suppressed the PMA-induced elevation of glucagon secretion. While Go6976, a Ca(2+)-dependent PKC selective inhibitor did not suppress glucagon secretion. Quercetin suppressed PMA-induced phosphorylation of Tyr(311) of PKC in isolated islets. However, quercetin itself had no effect on either glucagon secretion or glucagon mRNA expression. Our data suggest that PKC signaling inhibitors suppressed glucagon secretion. Elucidation of detailed signaling pathways causing PKC activation in the onset and progression of diabetes followed by the augmentation of glucagon secretion could lead to the identification of novel therapeutic target molecules and the development of novel therapeutic drugs for diabetes. J. Med. Invest. 64: 122-128, February, 2017.","ja":"Accumulating evidence supports the \"glucagonocentric hypothesis\", in which antecedent -cell failure and inhibition of glucagon secretion are responsible for diabetes progression. Protein kinase C (PKC) is involved in glucagon secretion from -cells, although which PKC isozyme is involved and the mechanism underlying this PKC-regulated glucagon secretion remains unknown. Here, the involvement of PKC in the onset and progression of diabetes was elucidated. Immunofluorescence studies revealed that PKC was expressed and activated in -cells of STZ-induced diabetic model mice. Phorbol 12-myristate 13-acetate (PMA) stimulation significantly augmented glucagon secretion from isolated islets. Pre-treatment with quercetin and rottlerin, PKC signaling inhibitors, significantly suppressed the PMA-induced elevation of glucagon secretion. While Go6976, a Ca(2+)-dependent PKC selective inhibitor did not suppress glucagon secretion. Quercetin suppressed PMA-induced phosphorylation of Tyr(311) of PKC in isolated islets. However, quercetin itself had no effect on either glucagon secretion or glucagon mRNA expression. Our data suggest that PKC signaling inhibitors suppressed glucagon secretion. Elucidation of detailed signaling pathways causing PKC activation in the onset and progression of diabetes followed by the augmentation of glucagon secretion could lead to the identification of novel therapeutic target molecules and the development of novel therapeutic drugs for diabetes. J. Med. Invest. 64: 122-128, February, 2017."},"publication_date":"2017-02","publication_name":{"en":"The Journal of Medical Investigation : JMI","ja":"The Journal of Medical Investigation : JMI"},"volume":"64","number":"1,2","starting_page":"122","ending_page":"128","languages":["eng"],"referee":true,"identifiers":{"doi":["10.2152/jmi.64.122"],"issn":["1349-6867"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}