オオノ　ヒデキ   大野　秀樹    所属   医学部 医学科（附属足立医療センター）    職種   講師
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Up-regulation of JAM-1 in AR42J cells treated with activin A and betacellulin and the diabetic regenerating islets
掲載誌名	正式名：Endocr J ISSNコード：1348-4540 (Electronic) 0918-8959 (Linking
掲載区分	国外
巻・号・頁	55(4),pp.757-65
著者・共著者	Yoshikumi, Y. Ohno, H. Suzuki, J. Isshiki, M. Morishita, Y. Ohnishi, H. Yasuda, H. Omata, M. Fujita, T. Mashima, H.
担当区分	2nd著者
発行年月	2008
概要	Pancreatic AR42J cells demonstrate the pluripotency in precursor cells of the gut endoderm and also provide an excellent model system to study the differentiation of the pancreas. Using the mRNA differential display technique, we identified junctional adhesion molecule-1 (JAM-1), a component of the tight junction, was highly up-regulated during thedifferentiation of AR42J cells, although junctions were not formed. The expression level of JAM-1 showed an up-regulation in the mRNA level after 3 hours and in the protein level after 24 hours in [activin A + betacellulin]-treated AR42J cells. The expressions of its signaling molecules, PAR-3 and atypical PKC lambda, also increased after the addition of activin A + betacellulin. When JAM-1 was over-expressed in [activin A + betacellulin]-treated AR42J cells, tagged-JAM-1 was observed in cytoplasm as vesicular structures and JAM-1 was colocalized with Rab3B and Rab13, members of the Rab family expressed at tight junctions. In streptozotocin-induced regenerating islets, the expression of JAM-1 was also up-regulated in the mRNA level and the protein level. JAM-1 might therefore play an important role in the differentiation of AR42J cells and the regeneration of pancreatic islets.
文献番号	18506084