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An amidation a day keeps apoptosis away

An amidation a day keeps apoptosis away <h2>An amidation a day keeps apoptosis away</h2> Bcl-x L modification by cisplatin is blocked by Rb. Weintraub/Elsevier Rapidly dividing cells such as tumor cells are susceptible to DNA damage that then induces apoptosis. As a result, DNA-damaging chemicals such as cisplatin are used as anticancer treatments. How the majority of nontumor cells survive chemotherapy has been mysterious. The trivial explanation is that the cells are growth-arrested and thus less susceptible to DNA-damaging agents. But a more precise explanation is put forth in a new article by Benjamin Deverman, Steven Weintraub (Washington University, St. Louis, MO), and colleagues, who have identified an antiapoptotic activity necessary to keep damaged but nondividing cells alive. The proapoptotic activity that allows tumor cells to die is an unusual modification of the antiapoptotic protein Bcl-x L caused by DNA-damaging agents. This modification, deamidation of two asparagine residues, inactivated Bcl-x L , thereby allowing cell death to proceed. Growth-arrested cells escaped apoptosis by blocking deamidation. To prevent deamidation, cells needed Rb, a tumor suppressor protein that inhibits cell cycle progression. Because tumor cells lack Rb, and cycling cells down-regulate Rb, they are more sensitive to DNA-damaging agents. “Deamidation is like a checkpoint,” says Weintraub. “If http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Cell Biology Rockefeller University Press

An amidation a day keeps apoptosis away

LeBrasseur, Nicole
The Journal of Cell Biology , Volume 159 (2): 201 – Oct 28, 2002
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References (1)

Publisher
Rockefeller University Press
Copyright
Copyright © 2002, by The Rockefeller University Press
ISSN
0021-9525
eISSN
1540-8140
DOI
10.1083/jcb1592rr4
Publisher site
See Article on Publisher Site

Abstract

<h2>An amidation a day keeps apoptosis away</h2> Bcl-x L modification by cisplatin is blocked by Rb. Weintraub/Elsevier Rapidly dividing cells such as tumor cells are susceptible to DNA damage that then induces apoptosis. As a result, DNA-damaging chemicals such as cisplatin are used as anticancer treatments. How the majority of nontumor cells survive chemotherapy has been mysterious. The trivial explanation is that the cells are growth-arrested and thus less susceptible to DNA-damaging agents. But a more precise explanation is put forth in a new article by Benjamin Deverman, Steven Weintraub (Washington University, St. Louis, MO), and colleagues, who have identified an antiapoptotic activity necessary to keep damaged but nondividing cells alive. The proapoptotic activity that allows tumor cells to die is an unusual modification of the antiapoptotic protein Bcl-x L caused by DNA-damaging agents. This modification, deamidation of two asparagine residues, inactivated Bcl-x L , thereby allowing cell death to proceed. Growth-arrested cells escaped apoptosis by blocking deamidation. To prevent deamidation, cells needed Rb, a tumor suppressor protein that inhibits cell cycle progression. Because tumor cells lack Rb, and cycling cells down-regulate Rb, they are more sensitive to DNA-damaging agents. “Deamidation is like a checkpoint,” says Weintraub. “If

Journal

The Journal of Cell Biology – Rockefeller University Press

Published: Oct 28, 2002

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