| pubmed-article:17725654 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17725654 | lifeskim:mentions | umls-concept:C0040300 | lld:lifeskim |
| pubmed-article:17725654 | lifeskim:mentions | umls-concept:C0030281 | lld:lifeskim |
| pubmed-article:17725654 | lifeskim:mentions | umls-concept:C1514559 | lld:lifeskim |
| pubmed-article:17725654 | lifeskim:mentions | umls-concept:C0004359 | lld:lifeskim |
| pubmed-article:17725654 | lifeskim:mentions | umls-concept:C1261381 | lld:lifeskim |
| pubmed-article:17725654 | lifeskim:mentions | umls-concept:C1442792 | lld:lifeskim |
| pubmed-article:17725654 | lifeskim:mentions | umls-concept:C1419119 | lld:lifeskim |
| pubmed-article:17725654 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:17725654 | pubmed:dateCreated | 2007-9-12 | lld:pubmed |
| pubmed-article:17725654 | pubmed:abstractText | IA-2 is a major autoantigen in type 1 diabetes and autoantibodies to it have become important diagnostic and predictive markers. IA-2 also is an intrinsic transmembrane component of dense core secretory vesicles and knock-out studies showed that IA-2 is a regulator of insulin secretion. Here we show that overexpression of IA-2 puts mouse insulinoma MIN-6 beta cells into a pre-apoptotic state and that exposure to high glucose results in G2/M arrest and apoptosis. Molecular study revealed a decrease in phosphoinositide-dependent kinase (PDK)-1 and Akt/protein kinase B (PKB) phosphorylation. Treatment of IA-2-transfected cells with IA-2 siRNA prevented both G2/M arrest and apoptosis and increased Akt/PKB phosphorylation. A search for IA-2 interacting proteins revealed that IA-2 interacts with sorting nexin (SNX)19 and that SNX19, but not IA-2, inhibits the conversion of PtdIns(4,5)P2 to PtdIns(3,4,5)P3 and thereby suppresses the phosphorylation of proteins in the Akt signalling pathway resulting in apoptosis. We conclude that IA-2 acts through SNX19 to initiate the pre-apoptotic state. Our findings point to the possibility that in autoimmune diseases, tissue destruction may be autoantigen-induced, but not necessarily immunologically mediated. | lld:pubmed |
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| pubmed-article:17725654 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17725654 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17725654 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17725654 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17725654 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:17725654 | pubmed:issn | 0009-9104 | lld:pubmed |
| pubmed-article:17725654 | pubmed:author | pubmed-author:NishimuraTT | lld:pubmed |
| pubmed-article:17725654 | pubmed:author | pubmed-author:NotkinsA LAL | lld:pubmed |
| pubmed-article:17725654 | pubmed:author | pubmed-author:ORRS HSH | lld:pubmed |
| pubmed-article:17725654 | pubmed:author | pubmed-author:HarashimaCC | lld:pubmed |
| pubmed-article:17725654 | pubmed:author | pubmed-author:HarashimaS-IS... | lld:pubmed |
| pubmed-article:17725654 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17725654 | pubmed:volume | 150 | lld:pubmed |
| pubmed-article:17725654 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17725654 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17725654 | pubmed:pagination | 49-60 | lld:pubmed |
| pubmed-article:17725654 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:17725654 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17725654 | pubmed:articleTitle | Overexpression of the autoantigen IA-2 puts beta cells into a pre-apoptotic state: autoantigen-induced, but non-autoimmune-mediated, tissue destruction. | lld:pubmed |
| pubmed-article:17725654 | pubmed:affiliation | Experimental Medicine Section, Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institute of Health, Bethesda, Maryland 20892, USA. | lld:pubmed |
| pubmed-article:17725654 | pubmed:publicationType | Journal Article | lld:pubmed |
