Activin isoforms signal through type I receptor serine/threonine kinase ALK7

Kunihiro Tsuchida, Masashi Nakatani, Norio Yamakawa, Osamu Hashimoto, Yoshihisa Hasegawa, Hiromu Sugino

研究成果: ジャーナルへの寄稿学術論文査読

126 被引用数 (Scopus)

抄録

Activins play a fundamental role in cell differentiation and development. Activin A signaling is mediated through a combination of activin type II receptors (ActRIIs) and the activin type IB receptor, ALK4. Signaling receptors of other activin isoforms remain to be elucidated. Here, we found that activin AB and activin B are ligands for ALK7. ALK7 is an orphan receptor serine/threonine kinase expressed in neuroendocrine tissues including pancreatic islets. The combination of ActRIIA and ALK7, preferred by activin AB and activin B but not by activin A, is responsible for activin-mediated secretion of insulin from pancreatic β cell line, MIN6. In contrast, all activins activate a combination of ActRIIA and ALK4 with various levels of potency. Thus, variation in activin signaling through type I receptors is dependent upon homo- and heterodimeric assembly of activin isoforms. Thus, the differential combination of receptor heterodimers mediates variation in activin isoform signaling.

本文言語英語
ページ(範囲)59-65
ページ数7
ジャーナルMolecular and Cellular Endocrinology
220
1-2
DOI
出版ステータス出版済み - 31-05-2004
外部発表はい

All Science Journal Classification (ASJC) codes

  • 生化学
  • 分子生物学
  • 内分泌学

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