| pubmed-article:15665818 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15665818 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:15665818 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
| pubmed-article:15665818 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:15665818 | lifeskim:mentions | umls-concept:C1413357 | lld:lifeskim |
| pubmed-article:15665818 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:15665818 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:15665818 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:15665818 | pubmed:dateCreated | 2005-2-15 | lld:pubmed |
| pubmed-article:15665818 | pubmed:abstractText | In T lymphocytes, the role of Akt in regulating Fas/Fas ligand (FasL)-mediated apoptotic signaling and death is not clearly understood. In this study, we observed that inhibition of Akt causes enhanced expression of FasL mRNA and protein and increased death-inducing signaling complex (DISC) formation with Fas-associated death domain (FADD) and procaspase-8 recruitment. Also, caspase-8 was activated at the DISC with accompanying decrease in c-FLIPs expression. FasL neutralizing antibody significantly decreased apoptotic death in the Akt-inhibited T cells. Additionally, Akt inhibition-induced Fas signaling was observed to link to the mitochondrial pathway via Bid cleavage. Further, inhibition of caspase-8 activity effectively blocked the loss of mitochondrial membrane potential and DNA fragmentation, suggesting that DISC formation and subsequent caspase-8 activation are critical initiating events in Akt inhibition-induced apoptotic death in T lymphocytes. These data demonstrate yet another important survival function governed by Akt kinase in T lymphocytes, which involves the regulation of FasL expression and consequent apoptotic signaling. | lld:pubmed |
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| pubmed-article:15665818 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:15665818 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15665818 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:15665818 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15665818 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15665818 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:15665818 | pubmed:issn | 1350-9047 | lld:pubmed |
| pubmed-article:15665818 | pubmed:author | pubmed-author:McClainCC | lld:pubmed |
| pubmed-article:15665818 | pubmed:author | pubmed-author:SongZZ | lld:pubmed |
| pubmed-article:15665818 | pubmed:author | pubmed-author:Joshi-BarveSS | lld:pubmed |
| pubmed-article:15665818 | pubmed:author | pubmed-author:HaribabuBB | lld:pubmed |
| pubmed-article:15665818 | pubmed:author | pubmed-author:GobejishviliL... | lld:pubmed |
| pubmed-article:15665818 | pubmed:author | pubmed-author:SahooRR | lld:pubmed |
| pubmed-article:15665818 | pubmed:author | pubmed-author:BarveSS | lld:pubmed |
| pubmed-article:15665818 | pubmed:author | pubmed-author:IMRESS | lld:pubmed |
| pubmed-article:15665818 | pubmed:author | pubmed-author:UriarteS MSM | lld:pubmed |
| pubmed-article:15665818 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15665818 | pubmed:volume | 12 | lld:pubmed |
| pubmed-article:15665818 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15665818 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15665818 | pubmed:pagination | 233-42 | lld:pubmed |
| pubmed-article:15665818 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:15665818 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15665818 | pubmed:articleTitle | Akt inhibition upregulates FasL, downregulates c-FLIPs and induces caspase-8-dependent cell death in Jurkat T lymphocytes. | lld:pubmed |
| pubmed-article:15665818 | pubmed:affiliation | Department of Internal Medicine, University of Louisville Medical Center, Louisville, KY 40292, USA. | lld:pubmed |
| pubmed-article:15665818 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15665818 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15665818 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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