pubmed-article:17084712 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17084712 | lifeskim:mentions | umls-concept:C0038435 | lld:lifeskim |
pubmed-article:17084712 | lifeskim:mentions | umls-concept:C0030281 | lld:lifeskim |
pubmed-article:17084712 | lifeskim:mentions | umls-concept:C0014239 | lld:lifeskim |
pubmed-article:17084712 | lifeskim:mentions | umls-concept:C0007613 | lld:lifeskim |
pubmed-article:17084712 | lifeskim:mentions | umls-concept:C0332161 | lld:lifeskim |
pubmed-article:17084712 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
pubmed-article:17084712 | lifeskim:mentions | umls-concept:C0378073 | lld:lifeskim |
pubmed-article:17084712 | lifeskim:mentions | umls-concept:C1514758 | lld:lifeskim |
pubmed-article:17084712 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:17084712 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:17084712 | pubmed:dateCreated | 2006-11-6 | lld:pubmed |
pubmed-article:17084712 | pubmed:abstractText | Perturbation of endoplasmic reticulum (ER) homeostasis impairs insulin biosynthesis, beta cell survival, and glucose homeostasis. We show that a murine model of diabetes is associated with the development of ER stress in beta cells and that treatment with the GLP-1R agonist exendin-4 significantly reduced biochemical markers of islet ER stress in vivo. Exendin-4 attenuated translational downregulation of insulin and improved cell survival in purified rat beta cells and in INS-1 cells following induction of ER stress in vitro. GLP-1R agonists significantly potentiated the induction of ATF-4 by ER stress and accelerated recovery from ER stress-mediated translational repression in INS-1 beta cells in a PKA-dependent manner. The effects of exendin-4 on the induction of ATF-4 were mediated via enhancement of ER stress-stimulated ATF-4 translation. Moreover, exendin-4 reduced ER stress-associated beta cell death in a PKA-dependent manner. These findings demonstrate that GLP-1R signaling directly modulates the ER stress response leading to promotion of beta cell adaptation and survival. | lld:pubmed |
pubmed-article:17084712 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17084712 | pubmed:language | eng | lld:pubmed |
pubmed-article:17084712 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17084712 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:17084712 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:17084712 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17084712 | pubmed:month | Nov | lld:pubmed |
pubmed-article:17084712 | pubmed:issn | 1550-4131 | lld:pubmed |
pubmed-article:17084712 | pubmed:author | pubmed-author:DruckerDaniel... | lld:pubmed |
pubmed-article:17084712 | pubmed:author | pubmed-author:LingZhidongZ | lld:pubmed |
pubmed-article:17084712 | pubmed:author | pubmed-author:LiHongyunH | lld:pubmed |
pubmed-article:17084712 | pubmed:author | pubmed-author:YustaBernardo... | lld:pubmed |
pubmed-article:17084712 | pubmed:author | pubmed-author:BaggioLaurie... | lld:pubmed |
pubmed-article:17084712 | pubmed:author | pubmed-author:EstallJennife... | lld:pubmed |
pubmed-article:17084712 | pubmed:author | pubmed-author:PipeleersDann... | lld:pubmed |
pubmed-article:17084712 | pubmed:author | pubmed-author:KoehlerJackie... | lld:pubmed |
pubmed-article:17084712 | pubmed:author | pubmed-author:HollandDianne... | lld:pubmed |
pubmed-article:17084712 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17084712 | pubmed:volume | 4 | lld:pubmed |
pubmed-article:17084712 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17084712 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17084712 | pubmed:pagination | 391-406 | lld:pubmed |
pubmed-article:17084712 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:17084712 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:17084712 | pubmed:articleTitle | GLP-1 receptor activation improves beta cell function and survival following induction of endoplasmic reticulum stress. | lld:pubmed |
pubmed-article:17084712 | pubmed:affiliation | Department of Medicine, Banting and Best Diabetes Centre, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada. | lld:pubmed |
pubmed-article:17084712 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17084712 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:17084712 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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