| pubmed-article:11931670 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11931670 | lifeskim:mentions | umls-concept:C0242606 | lld:lifeskim |
| pubmed-article:11931670 | lifeskim:mentions | umls-concept:C0007620 | lld:lifeskim |
| pubmed-article:11931670 | lifeskim:mentions | umls-concept:C0031671 | lld:lifeskim |
| pubmed-article:11931670 | lifeskim:mentions | umls-concept:C0033634 | lld:lifeskim |
| pubmed-article:11931670 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:11931670 | lifeskim:mentions | umls-concept:C1556066 | lld:lifeskim |
| pubmed-article:11931670 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
| pubmed-article:11931670 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
| pubmed-article:11931670 | pubmed:issue | Pt 2 | lld:pubmed |
| pubmed-article:11931670 | pubmed:dateCreated | 2002-4-4 | lld:pubmed |
| pubmed-article:11931670 | pubmed:abstractText | Phospholipase C-gamma1 (PLC-gamma1) activation has been reported to enhance cell survival during the cellular response to oxidative stress. We studied the role of protein kinase C (PKC) pathways in mediating PLC-gamma1 survival signalling in oxidative stress by using mouse embryonic fibroblasts genetically deficient in PLC-gamma1 (Plcg1(-/-)) and its wild type (Plcg1(+/+)). PLC-gamma1 was activated by H(2)O(2) treatment in a dose- and time-dependent manner. Activation of PKC was also markedly increased in both cell lines treated with H(2)O(2) (1-5 mM), but with low doses (50-200 microM), PKC activation was considerably decreased in Plcg1(-/-) cells. After treatment with H(2)O(2), PKC-dependent phosphorylation of Bcl-2 and cell viability of Plcg1(-/-) cells decreased dramatically and caspase-3-like activity increased significantly compared with that of the wild-type cells. Furthermore, pretreatment of Plcg1(+/+) cells with PKC-specific inhibitor decreased levels of PKC-dependent Bcl-2 phosphorylation, enhanced caspase-3 activity and their sensitivity to H(2)O(2). On the contrary, treatment of Plcg1(-/-) cells with PKC-specific activator increased the Bcl-2 phosphorylation, decreased caspase-3 activity and improved their survival. These results suggest that PLC-gamma1 mediates survival signalling in oxidative-stress response by PKC-dependent phosphorylation of Bcl-2 and inhibition of caspase-3. | lld:pubmed |
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| pubmed-article:11931670 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11931670 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11931670 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11931670 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11931670 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11931670 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:11931670 | pubmed:issn | 0264-6021 | lld:pubmed |
| pubmed-article:11931670 | pubmed:author | pubmed-author:WangYuY | lld:pubmed |
| pubmed-article:11931670 | pubmed:author | pubmed-author:DengFanF | lld:pubmed |
| pubmed-article:11931670 | pubmed:author | pubmed-author:BaiXiao-ChunX... | lld:pubmed |
| pubmed-article:11931670 | pubmed:author | pubmed-author:LiuAn-LingAL | lld:pubmed |
| pubmed-article:11931670 | pubmed:author | pubmed-author:ZouZhi-PengZP | lld:pubmed |
| pubmed-article:11931670 | pubmed:author | pubmed-author:KeZhi-YongZY | lld:pubmed |
| pubmed-article:11931670 | pubmed:author | pubmed-author:JiQun-ShengQS | lld:pubmed |
| pubmed-article:11931670 | pubmed:author | pubmed-author:LuoShen-QiuSQ | lld:pubmed |
| pubmed-article:11931670 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11931670 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:11931670 | pubmed:volume | 363 | lld:pubmed |
| pubmed-article:11931670 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11931670 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11931670 | pubmed:pagination | 395-401 | lld:pubmed |
| pubmed-article:11931670 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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