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ei24, a p53 Response Gene Involved in Growth Suppression and Apoptosis
Author(s) -
Zheng Gu,
Cathy Flemington,
Thomas Chittenden,
Gerard P. Zambetti
Publication year - 2000
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.20.1.233-241.2000
Subject(s) - biology , ectopic expression , apoptosis , cell cycle , microbiology and biotechnology , effector , tumor suppressor gene , cell growth , cell cycle checkpoint , gene , dna damage , programmed cell death , carcinogenesis , dna , genetics
DNA damage and/or hyperproliferative signals activate the wild-type p53 tumor suppressor protein, which induces a G1 cell cycle arrest or apoptosis. Although the mechanism of p53-mediated cell cycle arrest is fairly well defined, the p53-dependent pathway regulating apoptosis is poorly understood. Here we report the functional characterization of murineei24 (also known asPIG8 ), a gene directly regulated by p53, whose overexpression negatively controls cell growth and induces apoptotic cell death. Ectopicei24 expression markedly inhibits cell colony formation, induces the morphological features of apoptosis, and reduces the number of β-galactosidase-marked cells, which is efficiently blocked by coexpression of Bcl-XL . Theei24 /PIG8 gene is localized on human chromosome 11q23, a region frequently altered in human cancers. These results suggest thatei24 may play an important role in negative cell growth control by functioning as an apoptotic effector of p53 tumor suppressor activities.

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