The role of activin type I receptors in activin A-induced growth arrest and apoptosis in mouse B-cell hybridoma cells

Osamu Hashimoto, Kenji Yamato, Takeyoshi Koseki, Masahiro Ohguchi, Akira Ishisaki, Hiroki Shoji, Takanori Nakamura, Yoshihiro Hayashi, Hiromu Sugino, Tatsuji Nishihara

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)

Abstract

Activins transduce their signals by binding to activin type I receptors and activin type II receptors, both of which contain a serine/threonine kinase domain. In this study, we established stable transfectants expressing two types of activin receptors, ActRI and ActRIB, to clarify the role of these receptors in activin signalling for growth inhibition in HS-72 mouse B-cell hybridoma cells. Over-expression of ActRI suppressed activin A-induced cell-cycle arrest in the G1 phase caused by inhibition of retinoblastoma protein phosphorylation through induction of p21(CIP1/WAF1), a cyclin-dependent kinase inhibitor, and subsequent apoptosis. In contrast, HS-72 clones that over-expressed ActRIB significantly facilitated activin A-induced apoptosis. These results indicate that ActRI and ActRIB are distinct from each other and that the ActRI/ActRIB expression ratio could regulate cell-cycle arrest in the G1 phase and subsequent apoptosis in HS-72 cells induced by activin A. Copyright (C) 1998 Elsevier Science Inc.

Original languageEnglish
Pages (from-to)743-749
Number of pages7
JournalCellular Signalling
Volume10
Issue number10
DOIs
Publication statusPublished - 1998 Nov
Externally publishedYes

Keywords

  • ActRI
  • ActRIB
  • Activin A
  • Apoptosis
  • B cell hybridoma
  • G1 arrest

ASJC Scopus subject areas

  • Cell Biology

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