PML-dependent apoptosis after DNA damage is regulated by the checkpoint kinase hCds1/Chk2

被引：192

作者：

Yang, ST

Kuo, C

Bisi, JE

Kim, MK

机构：

[1] NHLBI, Lab Biochem Genet, NIH, Bethesda, MD 20892 USA

[2] GlaxoSmithKline Inc, Dept Cellular Genom, Res Triangle Pk, NC 27709 USA

来源：

NATURE CELL BIOLOGY | 2002年 / 4卷 / 11期

关键词：

D O I：

10.1038/ncb869

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The promyelocytic leukaemia (PML) gene is translocated in most acute promyelocytic leukaemias and encodes a tumour suppressor protein. PML is involved in multiple apoptotic pathways and is thought to be pivotal in gamma irradiation-induced apoptosis. The DNA damage checkpoint kinase hCds1/Chk2 is necessary for p53-dependent apoptosis after gamma irradiation. In addition, gamma irradiation-induced apoptosis also occurs through p53-independent mechanisms, although the molecular mechanism remains largely unknown. Here, we report that hCds1/Chk2 mediates gamma irradiation-induced apoptosis in a p53-independent manner through an ataxia telangiectasia-mutated (ATM)-hCds1/Chk2-PML pathway. Our results provide the first evidence of a functional relationship between PML and a checkpoint kinase in gamma irradiation-induced apoptosis.

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页码：865 / 870

页数：6

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