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| pubmed-article:17371867 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
| pubmed-article:17371867 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:17371867 | lifeskim:mentions | umls-concept:C0011065 | lld:lifeskim |
| pubmed-article:17371867 | lifeskim:mentions | umls-concept:C0013935 | lld:lifeskim |
| pubmed-article:17371867 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
| pubmed-article:17371867 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:17371867 | lifeskim:mentions | umls-concept:C0205102 | lld:lifeskim |
| pubmed-article:17371867 | lifeskim:mentions | umls-concept:C0014239 | lld:lifeskim |
| pubmed-article:17371867 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:17371867 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:17371867 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:17371867 | pubmed:issue | 19 | lld:pubmed |
| pubmed-article:17371867 | pubmed:dateCreated | 2007-5-7 | lld:pubmed |
| pubmed-article:17371867 | pubmed:abstractText | Members of the caspase family are essential for many apoptotic programs. We studied mouse embryonic fibroblasts (MEFs) deficient in caspases 3 and 7 and in caspase 9 to determine the role of these proteases in endoplasmic reticulum (ER) stress-induced apoptosis. Both caspase 3(-/-)/caspase 7(-/-) and caspase 9(-/-) MEFs were resistant to cytotoxicity induced via ER stress and failed to exhibit apoptotic morphology. Specifically, apoptosis induced by increased intracellular calcium was shown to depend only on caspases 3 and 9, whereas apoptosis induced by disruption of ER function depended additionally on caspase 7. Caspase 3(-/-)/caspase 7(-/-) and caspase 9(-/-) MEFs also exhibited decreased loss of mitochondrial membrane potential, which correlated with altered caspase 9 processing, increased induction of procaspase 11, and decreased processing of caspase 12 in caspase 3(-/-)/caspase 7(-/-) cells. Furthermore, disruption of ER function was sufficient to induce accumulation of cleaved caspase 3 and 7 in a heavy membrane compartment, suggesting a potential mechanism for caspase 12 processing and its role as an amplifier in the death pathway. Caspase 8(-/-) MEFs were not resistant to ER stress-induced cytotoxicity, and processing of caspase 8 was not observed upon induction of ER stress. This study thus demonstrates a requirement for caspases 3 and 9 and a key role for the intrinsic pathway in ER stress-induced apoptosis. | lld:pubmed |
| pubmed-article:17371867 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17371867 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17371867 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17371867 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17371867 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17371867 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17371867 | pubmed:month | May | lld:pubmed |
| pubmed-article:17371867 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:17371867 | pubmed:author | pubmed-author:FlavellRichar... | lld:pubmed |
| pubmed-article:17371867 | pubmed:author | pubmed-author:HakemRazqalla... | lld:pubmed |
| pubmed-article:17371867 | pubmed:author | pubmed-author:MohapatraAlex... | lld:pubmed |
| pubmed-article:17371867 | pubmed:author | pubmed-author:LakhaniSaquib... | lld:pubmed |
| pubmed-article:17371867 | pubmed:author | pubmed-author:MasudAliA | lld:pubmed |
| pubmed-article:17371867 | pubmed:author | pubmed-author:FerrandinoAnt... | lld:pubmed |
| pubmed-article:17371867 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17371867 | pubmed:day | 11 | lld:pubmed |
| pubmed-article:17371867 | pubmed:volume | 282 | lld:pubmed |
| pubmed-article:17371867 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17371867 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17371867 | pubmed:pagination | 14132-9 | lld:pubmed |
| pubmed-article:17371867 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:17371867 | pubmed:meshHeading | pubmed-meshheading:17371867... | lld:pubmed |
| pubmed-article:17371867 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17371867 | pubmed:articleTitle | Endoplasmic reticulum stress-induced death of mouse embryonic fibroblasts requires the intrinsic pathway of apoptosis. | lld:pubmed |
| pubmed-article:17371867 | pubmed:affiliation | University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA. | lld:pubmed |
| pubmed-article:17371867 | pubmed:publicationType | Journal Article | lld:pubmed |
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