Nuclear and mitochondrial apoptotic pathways of p53

FEBS Letters

Zaika, Alex¹  Moll, Ute M¹ 

[1] Department of Pathology, State University of New York at Stony Brook, Stony Brook, NY 11794, USA

关键词: p53;    Transcription factor;    Mitochondrial localization;    Stress-induced;    Apoptosis;    KO;    knock out mouse;    ROS;    reactive oxygen species;   

DOI  :  10.1016/S0014-5793(01)02284-0

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

In contrast to p53-mediated cell cycle arrest, the mechanisms of p53-mediated apoptosis in response to cellular stresses such as DNA damage, hypoxia and oncogenic signals still remain poorly understood. Elucidating these pathways is all the more pressing since there is good evidence that the activation of apoptosis rather than cell cycle arrest is crucial in p53 tumor suppression. Moreover, the therapeutic interest in p53 as the molecular target of anticancer intervention rests mainly on its powerful apoptotic capability. This puzzling elusiveness suggests that p53 not only engages a plethora of downstream pathways but itself might possess a biochemical flexibility that goes beyond its role as a mere transcription factor. Recent evidence of a direct pro-apoptotic role of p53 protein at mitochondria suggests a synergistic effect with its transcriptional activation function and brings an unexpected new level of complexity into p53 apoptotic pathways.

【 授权许可】

Unknown