Journal
MOLECULAR CELL
Volume 30, Issue 1, Pages 61-72Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2008.02.030
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Funding
- NCI NIH HHS [R01-CA77274, R01 CA109355, R01 CA064140, R01 CA077274, T32 CA009582, P30 CA068485, R21 CA132010-02, R01-CA64140, R01 CA077274-10, R21 CA132010, P30-CA68485, R01 CA064140-15] Funding Source: Medline
- NIDDK NIH HHS [P30DK58404, P30 DK058404] Funding Source: Medline
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Histone deacetylases (HDACs) are enzymes that modify key residues in histones to regulate chromatin architecture, and they play a vital role in cell survival, cell-cycle progression, and tumorigenesis. To understand the function of Hdac3(-/-), a critical component of the N-CoR/SMRT repression complex, a conditional allele of Hdac3 was engineered. Cre-recombinasemediated inactivation of Hdac3 led to a delay in cell-cycle progression, cell-cycle-dependent DNA damage, and apoptosis in mouse embryonic fibroblasts (MEFs). While no overt defects in mitosis were observed in Hdac3(-/-) MEFs, including normal H3Ser10 phosphorylation, DNA damage was observed in Hdac3(-/-) interphase cells, which appears to be associated with defective DNA double-strand break repair. Moreover, we noted that Hdac3(-/-) MEFs were protected from DNA damage when quiescent, which may provide a mechanistic basis for the action of HDAC inhibitors on cycling tumor cells.
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