The Role of Activin Type I Receptors in Activin A-Induced Growth Arrest and Apoptosis in Mouse B-Cell Hybridoma Cells |
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| Authors: | Osamu Hashimoto Kenji Yamato Takeyoshi Koseki Masahiro Ohguchi Akira Ishisaki Hiroki Shoji Takanori Nakamura Yoshihiro Hayashi Hiromu Sugino Tatsuji Nishihara |
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| Institution: | †Department of Oral Science, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162, Japan;‡Institute for Enzyme Research, The University of Tokushima, 3-18-15 Kuramoto, Tokushima 770, Japan;§Department of Veterinary Anatomy, Faculty of Agriculture, The University of Tokyo, Yayoi, Bunkyo- ku, Tokyo 113, Japan;∥Department of Molecular Cellular Oncology/Microbiology, Faculty of Dentistry, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113, Japan |
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| 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 p21CIP1/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. |
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| Keywords: | Activin A ActRI ActRIB Apoptosis G1 arrest B cell hybridoma |
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