pubmed-article:11101524 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11101524 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
pubmed-article:11101524 | lifeskim:mentions | umls-concept:C0031678 | lld:lifeskim |
pubmed-article:11101524 | lifeskim:mentions | umls-concept:C0041625 | lld:lifeskim |
pubmed-article:11101524 | lifeskim:mentions | umls-concept:C0205160 | lld:lifeskim |
pubmed-article:11101524 | lifeskim:mentions | umls-concept:C1366876 | lld:lifeskim |
pubmed-article:11101524 | lifeskim:mentions | umls-concept:C1418816 | lld:lifeskim |
pubmed-article:11101524 | lifeskim:mentions | umls-concept:C1833235 | lld:lifeskim |
pubmed-article:11101524 | lifeskim:mentions | umls-concept:C0015744 | lld:lifeskim |
pubmed-article:11101524 | lifeskim:mentions | umls-concept:C2911691 | lld:lifeskim |
pubmed-article:11101524 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:11101524 | lifeskim:mentions | umls-concept:C1154974 | lld:lifeskim |
pubmed-article:11101524 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:11101524 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
pubmed-article:11101524 | pubmed:issue | 23 | lld:pubmed |
pubmed-article:11101524 | pubmed:dateCreated | 2000-12-26 | lld:pubmed |
pubmed-article:11101524 | pubmed:abstractText | The stress-responsive p38 MAPK, when activated by genotoxic stresses such as UV radiation, enhances p53 activity by phosphorylation and leads to cell cycle arrest or apoptosis. Here we report that a member of the protein phosphatase type 2C family, Wip1, has a role in down-regulating p38-p53 signaling during the recovery phase of the damaged cells. Wip1 was originally identified as a gene whose expression is induced following gamma or UV radiation in a p53-dependent manner. We found that Wip1 is also inducible by other environmental stresses, such as anisomycin, H(2)O(2) and methyl methane sulfonate. UV-induction of Wip1 requires p38 activity in addition to the wild-type p53. Wip1 selectively inactivates p38 by specific dephosphorylation of its conserved threonine residue. Furthermore, Wip1 expression attenuates UV-induced p53 phosphorylation at Ser33 and Ser46, residues previously reported to be phosphorylated by p38. Wip1 expression also suppresses both p53-mediated transcription and apoptosis in response to UV radiation. These results suggest that p53-dependent expression of Wip1 mediates a negative feedback regulation of p38-p53 signaling and contributes to suppression of the UV-induced apoptosis. | lld:pubmed |
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pubmed-article:11101524 | pubmed:language | eng | lld:pubmed |
pubmed-article:11101524 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11101524 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11101524 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11101524 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11101524 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:11101524 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11101524 | pubmed:month | Dec | lld:pubmed |
pubmed-article:11101524 | pubmed:issn | 0261-4189 | lld:pubmed |
pubmed-article:11101524 | pubmed:author | pubmed-author:ImaiKK | lld:pubmed |
pubmed-article:11101524 | pubmed:author | pubmed-author:NakayamaII | lld:pubmed |
pubmed-article:11101524 | pubmed:author | pubmed-author:TsukudaHH | lld:pubmed |
pubmed-article:11101524 | pubmed:author | pubmed-author:ItouSS | lld:pubmed |
pubmed-article:11101524 | pubmed:author | pubmed-author:AdachiMM | lld:pubmed |
pubmed-article:11101524 | pubmed:author | pubmed-author:TayaYY | lld:pubmed |
pubmed-article:11101524 | pubmed:author | pubmed-author:TakekawaMM | lld:pubmed |
pubmed-article:11101524 | pubmed:author | pubmed-author:NakahataAA | lld:pubmed |
pubmed-article:11101524 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11101524 | pubmed:day | 1 | lld:pubmed |
pubmed-article:11101524 | pubmed:volume | 19 | lld:pubmed |
pubmed-article:11101524 | pubmed:owner | NLM | lld:pubmed |