| pubmed-article:18281285 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18281285 | lifeskim:mentions | umls-concept:C0014239 | lld:lifeskim |
| pubmed-article:18281285 | lifeskim:mentions | umls-concept:C0149784 | lld:lifeskim |
| pubmed-article:18281285 | lifeskim:mentions | umls-concept:C1418407 | lld:lifeskim |
| pubmed-article:18281285 | lifeskim:mentions | umls-concept:C1424881 | lld:lifeskim |
| pubmed-article:18281285 | lifeskim:mentions | umls-concept:C1825938 | lld:lifeskim |
| pubmed-article:18281285 | lifeskim:mentions | umls-concept:C1511545 | lld:lifeskim |
| pubmed-article:18281285 | pubmed:issue | 18 | lld:pubmed |
| pubmed-article:18281285 | pubmed:dateCreated | 2008-4-28 | lld:pubmed |
| pubmed-article:18281285 | pubmed:abstractText | We have previously shown that ASK1-interacting protein 1 (AIP1) transduces tumor necrosis factor-induced ASK1-JNK signaling. Because endoplasmic reticulum (ER) stress activates ASK1-JNK signaling cascade, we investigated the role of AIP1 in ER stress-induced signaling. We created AIP1-deficient mice (AIP1-KO) from which mouse embryonic fibroblasts and vascular endothelial cells were isolated. AIP1-KO cells show dramatic reductions in ER stress-induced, but not oxidative stress-induced, ASK1-JNK activation and cell apoptosis. The ER stress-induced IRE1-JNK/XBP-1 axis, but not the PERK-CHOP1 axis, is blunted in AIP1-KO cells. ER stress induced formation of an AIP1-IRE1 complex, and the PH domain of AIP1 is critical for the IRE1 interaction. Furthermore, reconstitution of AIP1-KO cells with AIP1 wild type, not an AIP1 mutant with a deletion of the PH domain (AIP1-DeltaPH), restores ER stress-induced IRE1-JNK/XBP-1 signaling. AIP1-IRE1 association facilitates IRE1 dimerization, a critical step for activation of IRE1 signaling. More importantly, AIP1-KO mice show impaired ER stress-induced IRE1-dependent signaling in vivo. We conclude that AIP1 is essential for transducing the IRE1-mediated ER stress response. | lld:pubmed |
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| pubmed-article:18281285 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18281285 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18281285 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18281285 | pubmed:month | May | lld:pubmed |
| pubmed-article:18281285 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:18281285 | pubmed:author | pubmed-author:WebbS LSL | lld:pubmed |
| pubmed-article:18281285 | pubmed:author | pubmed-author:ChenHongH | lld:pubmed |
| pubmed-article:18281285 | pubmed:author | pubmed-author:UranoFumihiko... | lld:pubmed |
| pubmed-article:18281285 | pubmed:author | pubmed-author:TangShiboS | lld:pubmed |
| pubmed-article:18281285 | pubmed:author | pubmed-author:XuZheZ | lld:pubmed |
| pubmed-article:18281285 | pubmed:author | pubmed-author:HeYunY | lld:pubmed |
| pubmed-article:18281285 | pubmed:author | pubmed-author:ZhangHaifengH | lld:pubmed |
| pubmed-article:18281285 | pubmed:author | pubmed-author:LuoDianhongD | lld:pubmed |
| pubmed-article:18281285 | pubmed:author | pubmed-author:YuLuyangL | lld:pubmed |
| pubmed-article:18281285 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18281285 | pubmed:day | 2 | lld:pubmed |
| pubmed-article:18281285 | pubmed:volume | 283 | lld:pubmed |
| pubmed-article:18281285 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18281285 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18281285 | pubmed:pagination | 11905-12 | lld:pubmed |
| pubmed-article:18281285 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:18281285 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18281285 | pubmed:articleTitle | AIP1 is critical in transducing IRE1-mediated endoplasmic reticulum stress response. | lld:pubmed |
| pubmed-article:18281285 | pubmed:affiliation | Interdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. | lld:pubmed |
| pubmed-article:18281285 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18281285 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
