A new Aven-ue to DNA-damage checkpoints

作者:Gross Atan*
来源:Trends in Biochemical Sciences, 2008, 33(11): 514-516.
DOI:10.1016/j.tibs.2008.08.005

摘要

Cells frequently arrest or die in response to DNA damage to reduce the likelihood of progression to malignancy. A recent study sheds new light on the Aven protein, a known apoptotic regulator. After DNA damage, Aven induces cell-cycle arrest via ataxia-telangiectasia-mutated (ATM) kinase activation. These findings add Aven to a growing list of apopototic regulators that function as double agents in the DNA-damage response.

  • 出版日期2008-11

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