The roads to ferroptosis under homeostatic versus pathological conditions

被引:4
|
作者
Chen, Vincent [1 ,2 ,3 ]
Bo, Chu [1 ,2 ,3 ]
Gu, Wei [1 ,2 ,3 ]
机构
[1] Columbia Univ, Vagelos Coll Phys & Surg, Inst Canc Genet, 1130 Nicholas Ave, New York, NY 10032 USA
[2] Columbia Univ, Vagelos Coll Phys & Surg, Dept Pathol & Cell Biol, 1130 Nicholas Ave, New York, NY 10032 USA
[3] Columbia Univ, Vagelos Coll Phys & Surg, Herbert Irving Comprehens Canc Ctr, 1130 Nicholas Ave, New York, NY 10032 USA
基金
美国国家卫生研究院;
关键词
Ferroptosis; iPLA2; beta; p53; lipid peroxidation; DEATH;
D O I
10.1080/23723556.2021.1970477
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The calcium-independent phospholipase iPLA2 beta has been identified as a transcriptional target of the tumor suppressor TP53 (or p53). Unlike GPX4 (glutathione peroxidase 4), iPLA2 beta is not required for normal homeostasis but critical for ferroptosis during stress responses. Our results implicate iPLA2 beta as an essential regulator in a noncanonical ferroptosis pathway.
引用
收藏
页数:2
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