ATM-dependent activation of the gene encoding MAP kinase phosphatase 5 by radiomimetic DNA damage View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2002-01

AUTHORS

Anat Bar-Shira, Sharon Rashi-Elkeles, Liat Zlochover, Lilach Moyal, Nechama I Smorodinsky, Rony Seger, Yosef Shiloh

ABSTRACT

Cellular responses to DNA damage are mediated by an extensive network of signaling pathways. The ATM protein kinase is a master regulator of the response to double-strand breaks (DSBs), the most cytotoxic DNA lesion caused by ionizing radiation. ATM is the protein missing or inactive in patients with the pleiotropic genetic disorder ataxia-telangiectasia (A-T). A major response to DNA damage is altered expression of numerous genes. While studying gene expression in control and A-T cells following treatment with the radiomimetic chemical neocarzinostatin (NCS), we identified an expressed sequence tag that represented a gene that was induced by DSBs in an ATM-dependent manner. The corresponding cDNA encoded a dual specificity phosphatase of the MAP kinase phosphatase family, MKP-5. MKP-5 dephosphorylates and inactivates the stress-activated MAP kinases JNK and p38. The phosphorylation-dephosphorylation cycle of JNK and p38 by NCS was attenuated in A-T cells. Thus, ATM modulates this cycle in response to DSBs. These results further highlight ATM as a link between the DNA damage response and major signaling pathways involved in proliferative and apoptotic processes. More... »

PAGES

1205127

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1205127

DOI

http://dx.doi.org/10.1038/sj.onc.1205127

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1047114526

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11850813


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