DNA Damage, Deamidation, and Death

15 November 2002

journal article
perspective
Published by American Association for the Advancement of Science (AAAS) in Science

Vol. 298 (5597) , 1346-1347
https://doi.org/10.1126/science.1079168

Abstract

DNA-damaging agents are adept at killing tumor cells by inducing them to undergo programmed cell death even though they are normally resistant to apoptosis. In their Perspective, Li and Thompson discuss new work published elsewhere that provides an explanation for this paradox. DNA damage induces deamidation of a crucial antiapoptotic protein, which overcomes the apoptotic block and allows the tumor cells to die.

Keywords

This publication has 10 references indexed in Scilit:

Bcl-xL Deamidation Is a Critical Switch in the Regulation of the Response to DNA Damage
Cell, 2002
The Bcl2 family: regulators of the cellular life-or-death switch
Nature Reviews Cancer, 2002
The RB and p53 pathways in cancer
Cancer Cell, 2002
Protein deamidation
Proceedings of the National Academy of Sciences, 2002
Age-dependent deamidation of asparagine residues in proteins
Experimental Gerontology, 2001
BH3-only proteins that bind pro-survival Bcl-2 family members fail to induce apoptosis in the absence of Bax and Bak
Genes & Development, 2001
Proliferation, cell cycle and apoptosis in cancer
Nature, 2001
Molecular clocks
Proceedings of the National Academy of Sciences, 2001
Apoptosis and therapy
The Journal of Pathology, 1999
Bordetella bronchiseptica dermonecrotizing toxin induces reorganization of actin stress fibers through deamidation of Gln-63 of the GTP-binding protein Rho
Proceedings of the National Academy of Sciences, 1997