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氧化应激产生的过量活性氧簇(reactive oxygen species,ROS)可通过分子毒性作用或相关信号通路影响相关病理生理学过程.p66Shc是Shc蛋白家族的重要成员之一.氧化应激下p66Shc能被蛋白激酶Cβ(protein kinase Cβ,PKCβ)、Jun氨基末端激酶(Jun N-terminal kinase,JNK)和p53等激活,促进线粒体产生ROS.本文将对氧化应激下p66Shc的作用以及调控其作用的信号转导机制做一综述.
Over-reactive oxygen species (ROS) produced by oxidative stress can affect related pathophysiological processes through molecular toxic effects or related signaling pathways.p66Shc is an important member of the Shc protein family.P66Shc can be oxidized by protein Activation of PKCβ, JunN-terminal kinase (JNK) and p53 can promote ROS production in mitochondria.In this paper, the effect of p66Shc on oxidative stress and its role in signal transduction Guide mechanism to make a review.