DNA damage-induced G2–M checkpoint activation by histone H2AX and 53BP1 View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2002-12

AUTHORS

Oscar Fernandez-Capetillo, Hua-Tang Chen, Arkady Celeste, Irene Ward, Peter J Romanienko, Julio C Morales, Kazuhito Naka, Zhenfang Xia, R Daniel Camerini-Otero, Noboru Motoyama, Phillip B Carpenter, William M Bonner, Junjie Chen, André Nussenzweig

ABSTRACT

Activation of the ataxia telangiectasia mutated (ATM) kinase triggers diverse cellular responses to ionizing radiation (IR), including the initiation of cell cycle checkpoints. Histone H2AX, p53 binding-protein 1 (53BP1) and Chk2 are targets of ATM-mediated phosphorylation, but little is known about their roles in signalling the presence of DNA damage. Here, we show that mice lacking either H2AX or 53BP1, but not Chk2, manifest a G2-M checkpoint defect close to that observed in ATM(-/-) cells after exposure to low, but not high, doses of IR. Moreover, H2AX regulates the ability of 53BP1 to efficiently accumulate into IR-induced foci. We propose that at threshold levels of DNA damage, H2AX-mediated concentration of 53BP1 at double-strand breaks is essential for the amplification of signals that might otherwise be insufficient to prevent entry of damaged cells into mitosis. More... »

PAGES

993-997

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncb884

DOI

http://dx.doi.org/10.1038/ncb884

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1039958608

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/12447390


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