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Sharp‐1 modulates the cellular response to DNA damage
Author(s) -
Liu Jian-Jun,
Chung Teng-Kai,
Li Jiali,
Taneja Reshma
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.12.011
Subject(s) - dna damage , cell cycle checkpoint , microbiology and biotechnology , apoptosis , carcinogenesis , cell cycle , downregulation and upregulation , gadd45 , dna repair , biology , endogeny , dna , transcription factor , transcription (linguistics) , genome instability , chemistry , gene , genetics , biochemistry , linguistics , philosophy
DNA damage checkpoints are essential for maintenance of genome integrity. We report here that inducible overexpression of the transcription factor Sharp‐1 results in an S and G2/M cell cycle arrest, concomitant with the upregulation of Brca1 and GADD45α expression. In addition, we show that endogenous Sharp‐1 mRNA is increased by DNA‐damaging agents. Consistently, Sharp‐1 overexpressing cells exhibit reduced apoptosis in response to chemotherapeutic drugs along with lower p53 expression and activity. Our studies identify a novel function for Sharp‐1 in cell cycle arrest and DNA damage‐induced apoptosis. Inappropriate Sharp‐1 expression may therefore be associated with tumorigenesis.