Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ

摘要: c-Abl and Atm have been implicated in cell responses to DNA damage oxidative stress. However, the molecular mechanisms by which they regulate stress response remain unclear. In this report, we show that deficiency of ATM differentially altered induction antioxidant protein peroxiredoxin I (Prx I) via Nrf2 death, both required kinase C (PKC) activation were mediated reactive oxygen species. c-abl −/− osteoblasts displayed enhanced Prx induction, elevated levels, hypersusceptibility arsenate, reinstated reconstitution c-Abl; showed opposite. These phenotypes correlated with increased PKC expression decreased cells, respectively. The could be mimicked overexpression normal cells impeded inhibition , diminished rescued overexpression, indicating effects response. Hence, our results unveiled a previously unrecognized mechanism participate