Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 422, Issue 1, Pages 133-138Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2012.04.121
Keywords
Apoptosis; Etoposide; Mitochondria; p53; Pin1
Categories
Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- Center for Interdisciplinary Research Tohoku University for Specially Promoted Research
- Open Research Center
- Showa University
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We studied the effects of Pin1, a regulatory molecule of the oncosuppressor p53, on both cell cycle arrest and apoptosis by treating primary mouse embryonic fibroblasts (MEFs) with etoposide. Etoposide induced Cl arrest in both wild-type and Pin1 null (pin1(-/-))MEFs, and G2/M arrest and apoptotic cell death in MEFs lacking either p53 only (p53(-/-)) or both Pint and p53 (pin1(-/-)p53(-/-)). Both pin1(-/-) and pin1(-/-)p53(-/-) MEFs were enhanced the release of cytochrome c from the mitochondria, which might induce apoptosis. In response to etoposide treatment, apoptotic cell death was displayed in pin1(-/-)p53(-/-) MEFs but not in pin1(-/-) MEFs. These results suggest that p53 retards growth and suppresses etoposide-induced apoptosis in pin1(-/-) MEFs. (C) 2012 Elsevier Inc. All rights reserved.
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