Journal article
ERK Activation Mediates Cell Cycle Arrest and Apoptosis after DNA Damage Independently of p53∗
Abstract
In response to DNA damage, ataxia-telangiectasia mutant and ataxia-telangiectasia and Rad-3 activate p53, resulting in either cell cycle arrest or apoptosis. We report here that DNA damage stimuli, including etoposide (ETOP), adriamycin (ADR), ionizing irradiation (IR), and ultraviolet irradiation (UV) activate ERK1/2 (ERK) mitogen-activated protein kinase in primary (MEF and IMR90), immortalized (NIH3T3) and transformed (MCF-7) cells. ERK …
Authors
Tang D; Wu D; Hirao A; Lahti JM; Liu L; Mazza B; Kidd VJ; Mak TW; Ingram AJ
Journal
Journal of Biological Chemistry, Vol. 277, No. 15, pp. 12710–12717
Publisher
Elsevier
Publication Date
April 2002
DOI
10.1074/jbc.m111598200
ISSN
0021-9258
Fields of Research (FoR)
Medical Subject Headings (MeSH)
3T3 CellsAnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsCell CycleCell Cycle ProteinsCell Line, TransformedCyclin-Dependent Kinase Inhibitor p21CyclinsDNA DamageDNA-Binding ProteinsEnzyme ActivationEtoposideHumansMiceMitogen-Activated Protein KinasesProtein Serine-Threonine KinasesTumor Suppressor Protein p53Tumor Suppressor Proteins