DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lim, Dae-Sik | ko |
dc.contributor.author | Kim, Seong-Tae | ko |
dc.contributor.author | Xu, Bo | ko |
dc.contributor.author | Maser, Richard S. | ko |
dc.contributor.author | Lin, Junyu | ko |
dc.contributor.author | Petrini, John H.J. | ko |
dc.contributor.author | Kastan, Michael B. | ko |
dc.date.accessioned | 2013-03-02T17:57:23Z | - |
dc.date.available | 2013-03-02T17:57:23Z | - |
dc.date.created | 2012-02-06 | - |
dc.date.created | 2012-02-06 | - |
dc.date.issued | 2000-04 | - |
dc.identifier.citation | NATURE, v.404, no.6778, pp.613 - 613 | - |
dc.identifier.issn | 0028-0836 | - |
dc.identifier.uri | http://hdl.handle.net/10203/74814 | - |
dc.description.abstract | The rare diseases ataxia-telangiectasia (AT), caused by mutations in the ATM gene, and Nijmegen breakage syndrome (NBS), with mutations in the p95/nbs1 gene, share a variety of phenotypic abnormalities such as chromosomal instability, radiation sensitivity and defects in cell-cycle checkpoints in response to ionizing radiation(1-4). The ATM gene encodes a protein kinase that is activated by ionizing radiation or radiomimetic drugs(5,6), whereas p95/nbs1 is part of a protein complex that is involved in responses to DNA double-strand breaks(3,7). Here, because of the similarities between AT and NBS, we evaluated the functional interactions between ATM and p95/nbs1. Activation of the ATM kinase by ionizing radiation and induction of ATM-dependent responses in NBS cells indicated that p95/nbs1 may not be required for signalling to ATM after ionizing radiation. However, p95/nbs1 was phosphorylated on serine 343 in an ATM-dependent manner in vitro and in vivo after ionizing radiation. A p95/nbs1 construct mutated at the ATM phosphorylation site abrogated an S-phase checkpoint induced by ionizing radiation in normal cells and failed to compensate for this functional deficiency in NBS cells. These observations link ATM and p95/nbs1 in a common signalling pathway and provide an explanation for phenotypic similarities in these two diseases. | - |
dc.language | English | - |
dc.publisher | MACMILLAN MAGAZINES LTD | - |
dc.subject | NIJMEGEN BREAKAGE SYNDROME | - |
dc.subject | ATAXIA-TELANGIECTASIA | - |
dc.subject | DNA-DAMAGE | - |
dc.subject | IONIZING-RADIATION | - |
dc.subject | PROTEIN-KINASE | - |
dc.subject | REPAIR | - |
dc.subject | P53 | - |
dc.subject | LINKAGE | - |
dc.title | ATM phosphorylates p95/nbs1 in an S-phase checkpoint pathway | - |
dc.type | Article | - |
dc.identifier.wosid | 000086400100056 | - |
dc.identifier.scopusid | 2-s2.0-0034611728 | - |
dc.type.rims | ART | - |
dc.citation.volume | 404 | - |
dc.citation.issue | 6778 | - |
dc.citation.beginningpage | 613 | - |
dc.citation.endingpage | 613 | - |
dc.citation.publicationname | NATURE | - |
dc.contributor.localauthor | Lim, Dae-Sik | - |
dc.contributor.nonIdAuthor | Kim, Seong-Tae | - |
dc.contributor.nonIdAuthor | Xu, Bo | - |
dc.contributor.nonIdAuthor | Maser, Richard S. | - |
dc.contributor.nonIdAuthor | Lin, Junyu | - |
dc.contributor.nonIdAuthor | Petrini, John H.J. | - |
dc.contributor.nonIdAuthor | Kastan, Michael B. | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordPlus | NIJMEGEN BREAKAGE SYNDROME | - |
dc.subject.keywordPlus | ATAXIA-TELANGIECTASIA | - |
dc.subject.keywordPlus | DNA-DAMAGE | - |
dc.subject.keywordPlus | IONIZING-RADIATION | - |
dc.subject.keywordPlus | PROTEIN-KINASE | - |
dc.subject.keywordPlus | REPAIR | - |
dc.subject.keywordPlus | P53 | - |
dc.subject.keywordPlus | LINKAGE | - |
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