| pubmed-article:16954146 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16954146 | lifeskim:mentions | umls-concept:C0664613 | lld:lifeskim |
| pubmed-article:16954146 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:16954146 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
| pubmed-article:16954146 | lifeskim:mentions | umls-concept:C0911469 | lld:lifeskim |
| pubmed-article:16954146 | lifeskim:mentions | umls-concept:C1332098 | lld:lifeskim |
| pubmed-article:16954146 | lifeskim:mentions | umls-concept:C2610698 | lld:lifeskim |
| pubmed-article:16954146 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:16954146 | lifeskim:mentions | umls-concept:C1709305 | lld:lifeskim |
| pubmed-article:16954146 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:16954146 | pubmed:issue | Pt 19 | lld:pubmed |
| pubmed-article:16954146 | pubmed:dateCreated | 2006-9-21 | lld:pubmed |
| pubmed-article:16954146 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16954146 | pubmed:abstractText | Accumulation of unfolded proteins induces endoplasmic reticulum (ER) stress. Excessive and prolonged stresses lead cells to apoptosis. However, the precise molecular mechanisms of ER stress-induced apoptosis have not been fully elucidated. We investigated the involvement of the apoptosome in ER stress-induced cell death pathway using mouse embryonic fibroblasts (MEFs) and mice deficient for Apaf-1. Apaf-1-deficient MEFs showed more resistance to ER stress-inducing reagents as compared with wild type cells. Despite comparable induction of ER stress in both wild type and Apaf-1-deficient cells, activation of caspase-3 was only observed in wild type, but not Apaf-1-deficient, MEFs. Under ER stress conditions, BAX translocated to mitochondria and cytochrome c was released from mitochondria. We also demonstrated that caspase-12 was processed downstream of Apaf-1 and caspase-3, and neither overexpression nor knockdown of caspase-12 affected susceptibility of the cells to ER stress-induced cell death. Furthermore, in the kidneys of Apaf-1-deficient mice, apoptosis induced by in vivo administration of tunicamycin was remarkably suppressed as compared with wild type mice. These data collectively demonstrated that Apaf-1 and the mitochondrial pathway of apoptosis play significant roles in ER stress-induced apoptosis. | lld:pubmed |
| pubmed-article:16954146 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16954146 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16954146 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16954146 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16954146 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16954146 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:16954146 | pubmed:issn | 0021-9533 | lld:pubmed |
| pubmed-article:16954146 | pubmed:author | pubmed-author:YoshidaHiroki... | lld:pubmed |
| pubmed-article:16954146 | pubmed:author | pubmed-author:YoshimuraAkih... | lld:pubmed |
| pubmed-article:16954146 | pubmed:author | pubmed-author:OkamotoHideak... | lld:pubmed |
| pubmed-article:16954146 | pubmed:author | pubmed-author:ShiraishiHiro... | lld:pubmed |
| pubmed-article:16954146 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16954146 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:16954146 | pubmed:volume | 119 | lld:pubmed |
| pubmed-article:16954146 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16954146 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16954146 | pubmed:pagination | 3958-66 | lld:pubmed |
| pubmed-article:16954146 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:16954146 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16954146 | pubmed:articleTitle | ER stress-induced apoptosis and caspase-12 activation occurs downstream of mitochondrial apoptosis involving Apaf-1. | lld:pubmed |
| pubmed-article:16954146 | pubmed:affiliation | Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Japan. | lld:pubmed |
| pubmed-article:16954146 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16954146 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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