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