Gross Atan
Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Trends Biochem Sci. 2008 Nov;33(11):514-6. doi: 10.1016/j.tibs.2008.08.005. Epub 2008 Oct 1.
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.
细胞常因DNA损伤而停滞或死亡,以降低发展为恶性肿瘤的可能性。最近一项研究为已知的凋亡调节因子Aven蛋白带来了新线索。DNA损伤后,Aven通过激活共济失调毛细血管扩张症突变(ATM)激酶诱导细胞周期停滞。这些发现使Aven加入了越来越多在DNA损伤反应中充当双重角色的凋亡调节因子行列。