Article abstract
Nature Cell Biology 4, 865 - 870 (2002)
Published online: 28 October 2002 | doi:10.1038/ncb869
PML-dependent apoptosis after DNA damage is regulated by the checkpoint kinase hCds1/Chk2
Shutong Yang1, Christin Kuo1, John E. Bisi2 & Myung K. Kim1
Abstract
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 
irradiation-induced apoptosis. The DNA damage checkpoint kinase hCds1/Chk2 is necessary for p53-dependent apoptosis after irradiation. In addition, irradiation-induced apoptosis also occurs through p53-independent mechanisms, although the molecular mechanism remains largely unknown. Here, we report that hCds1/Chk2 mediates 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 irradiation-induced apoptosis.
- Laboratory of Biochemical Genetics, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
- Department of Cellular Genomics, GlaxoSmithKline Inc., Research Triangle Park, NC 27709, USA
Correspondence to: Myung K. Kim1 e-mail: KimM@nhlbi.nih.gov
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