DC Field | Value | Language |
---|---|---|
dc.contributor.author | Canman, Christine E. | ko |
dc.contributor.author | Lim, Dae-Sik | ko |
dc.contributor.author | Cimprich, Karlene A. | ko |
dc.contributor.author | Taya, Yoichi | ko |
dc.contributor.author | Tamai, Katsuyuki | ko |
dc.contributor.author | Sakaguchi, Kazuyasu | ko |
dc.contributor.author | Kastan, Michael B. | ko |
dc.contributor.author | Siliciano, Janet D. | ko |
dc.date.accessioned | 2013-03-02T18:17:08Z | - |
dc.date.available | 2013-03-02T18:17:08Z | - |
dc.date.created | 2012-02-06 | - |
dc.date.created | 2012-02-06 | - |
dc.date.issued | 1998-09 | - |
dc.identifier.citation | SCIENCE, v.281, no.5383, pp.1677 - 1679 | - |
dc.identifier.issn | 0036-8075 | - |
dc.identifier.uri | http://hdl.handle.net/10203/74858 | - |
dc.description.abstract | The p53 tumor suppressor protein is activated and phosphorylated on serine-15 in response to various DNA damaging agents. The gene product mutated in ataxia telangiectasia, ATM, acts upstream of p53 in a signal transduction pathway initiated by ionizing radiation. Immunoprecipitated ATM had intrinsic protein kinase activity and phosphorylated p53 on serine-15 in a manganese-dependent manner. Ionizing radiation, but not ultraviolet radiation, rapidly enhanced this p53-directed kinase activity of endogenous ATM. These observations, along with the fact that phosphorylation of p53 on serine-15 in response to ionizing radiation is reduced in ataxia telangiectasia cells, suggest that ATM is a protein kinase that phosphorylates p53 in vivo. | - |
dc.language | English | - |
dc.publisher | AMER ASSOC ADVANCEMENT SCIENCE | - |
dc.subject | CELL-CYCLE CHECKPOINT | - |
dc.subject | ATAXIA-TELANGIECTASIA CELLS | - |
dc.subject | PROTEIN-KINASE | - |
dc.subject | DNA-DAMAGE | - |
dc.subject | PATHWAYS | - |
dc.subject | RECOMBINATION | - |
dc.subject | INDUCTION | - |
dc.subject | PRODUCT | - |
dc.subject | DEFECT | - |
dc.subject | MDM2 | - |
dc.title | Activation of the ATM kinase by ionizing radiation and phosphorylation of p53 | - |
dc.type | Article | - |
dc.identifier.wosid | 000075856500048 | - |
dc.identifier.scopusid | 2-s2.0-0032508608 | - |
dc.type.rims | ART | - |
dc.citation.volume | 281 | - |
dc.citation.issue | 5383 | - |
dc.citation.beginningpage | 1677 | - |
dc.citation.endingpage | 1679 | - |
dc.citation.publicationname | SCIENCE | - |
dc.identifier.doi | 10.1126/science.281.5383.1677 | - |
dc.contributor.localauthor | Lim, Dae-Sik | - |
dc.contributor.nonIdAuthor | Canman, Christine E. | - |
dc.contributor.nonIdAuthor | Cimprich, Karlene A. | - |
dc.contributor.nonIdAuthor | Taya, Yoichi | - |
dc.contributor.nonIdAuthor | Tamai, Katsuyuki | - |
dc.contributor.nonIdAuthor | Sakaguchi, Kazuyasu | - |
dc.contributor.nonIdAuthor | Kastan, Michael B. | - |
dc.contributor.nonIdAuthor | Siliciano, Janet D. | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordPlus | CELL-CYCLE CHECKPOINT | - |
dc.subject.keywordPlus | ATAXIA-TELANGIECTASIA CELLS | - |
dc.subject.keywordPlus | PROTEIN-KINASE | - |
dc.subject.keywordPlus | DNA-DAMAGE | - |
dc.subject.keywordPlus | PATHWAYS | - |
dc.subject.keywordPlus | RECOMBINATION | - |
dc.subject.keywordPlus | INDUCTION | - |
dc.subject.keywordPlus | PRODUCT | - |
dc.subject.keywordPlus | DEFECT | - |
dc.subject.keywordPlus | MDM2 | - |
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