pubmed-article:17873911 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17873911 | lifeskim:mentions | umls-concept:C0024265 | lld:lifeskim |
pubmed-article:17873911 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
pubmed-article:17873911 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
pubmed-article:17873911 | lifeskim:mentions | umls-concept:C0376515 | lld:lifeskim |
pubmed-article:17873911 | lifeskim:mentions | umls-concept:C1332411 | lld:lifeskim |
pubmed-article:17873911 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:17873911 | lifeskim:mentions | umls-concept:C2348519 | lld:lifeskim |
pubmed-article:17873911 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:17873911 | pubmed:dateCreated | 2008-2-28 | lld:pubmed |
pubmed-article:17873911 | pubmed:abstractText | The BH3-only protein BIK normally induces apoptotic cell death. Here, we have investigated the role of BCL-2 in BIK-induced cell death using Bcl-2+/+ and Bcl-2-/- mouse embryo fibroblasts. Ectopic expression of BIK in Bcl-2-/- cells resulted in enhanced cell death compared to Bcl-2+/+ cells. In these cells, while caspase-8 was activated, there was no significant activation of caspase-9 and 3. There was no detectable mitochondrial to cytosolic release of cytochrome-c. However, there was significant redistribution of AIF from mitochondria to the nucleus. The extent of BIK-induced cell death was augmented by treatment with the pancaspase inhibitor, zVAD-fmk. The Bcl-2 null cells expressing BIK exhibited autophagic features such as cytosolic vacuoles, punctate distribution of LC3 and enhanced expression of Beclin-1. The survival of BIK-expressing Bcl-2-/- cells was enhanced in the presence of PI3 kinase inhibitors 3-methyladenine and Wortmannin and also by depletion of Atg5 and Beclin-1. Death of BIK-expressing Bcl-2-/- cells treated with zVAD-fmk was increased under caspase-8 depletion. Our results suggest enhanced expression of BIK in the Bcl-2 deficient cells leads to cell death with autophagic features and the extent of such cell death could be increased by inhibition of caspases. | lld:pubmed |
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pubmed-article:17873911 | pubmed:language | eng | lld:pubmed |
pubmed-article:17873911 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17873911 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:17873911 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17873911 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:17873911 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17873911 | pubmed:month | Feb | lld:pubmed |
pubmed-article:17873911 | pubmed:issn | 1476-5594 | lld:pubmed |
pubmed-article:17873911 | pubmed:author | pubmed-author:ChinnaduraiGG | lld:pubmed |
pubmed-article:17873911 | pubmed:author | pubmed-author:RyerseJJ | lld:pubmed |
pubmed-article:17873911 | pubmed:author | pubmed-author:VijayalingamS... | lld:pubmed |
pubmed-article:17873911 | pubmed:author | pubmed-author:RashmiRR | lld:pubmed |
pubmed-article:17873911 | pubmed:author | pubmed-author:PillaiS GSG | lld:pubmed |
pubmed-article:17873911 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:17873911 | pubmed:day | 28 | lld:pubmed |
pubmed-article:17873911 | pubmed:volume | 27 | lld:pubmed |
pubmed-article:17873911 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17873911 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17873911 | pubmed:pagination | 1366-75 | lld:pubmed |
pubmed-article:17873911 | pubmed:dateRevised | 2010-9-14 | lld:pubmed |
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pubmed-article:17873911 | pubmed:meshHeading | pubmed-meshheading:17873911... | lld:pubmed |
pubmed-article:17873911 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:17873911 | pubmed:articleTitle | BH3-only protein BIK induces caspase-independent cell death with autophagic features in Bcl-2 null cells. | lld:pubmed |
pubmed-article:17873911 | pubmed:affiliation | Institute for Molecular Virology, Saint Louis University Health Sciences Center, St Louis, MO 63110, USA. | lld:pubmed |
pubmed-article:17873911 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17873911 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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