| pubmed-article:10385418 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10385418 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:10385418 | lifeskim:mentions | umls-concept:C0021670 | lld:lifeskim |
| pubmed-article:10385418 | lifeskim:mentions | umls-concept:C0030281 | lld:lifeskim |
| pubmed-article:10385418 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
| pubmed-article:10385418 | lifeskim:mentions | umls-concept:C0333516 | lld:lifeskim |
| pubmed-article:10385418 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:10385418 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:10385418 | lifeskim:mentions | umls-concept:C0205225 | lld:lifeskim |
| pubmed-article:10385418 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:10385418 | pubmed:dateCreated | 1999-7-15 | lld:pubmed |
| pubmed-article:10385418 | pubmed:abstractText | Tumor necrosis factor-alpha (TNFalpha) is a potential mediator of beta cell destruction in insulin-dependent diabetes mellitus. We have studied TNF-responsive pathways leading to apoptosis in beta cells. Primary beta cells express low levels of the type I TNF receptor (TNFR1) but do not express the type 2 receptor (TNFR2). Evidence for TNFR1 expression on beta cells came from flow cytometry using monoclonal antibodies specific for TNFR1 and TNFR2 and from RT-PCR of beta cell RNA. NIT-1 insulinoma cells similarly expressed TNFR1 (at higher levels than primary beta cells) as detected by flow cytometry and radio-binding studies. TNF induced NF-kappaB activation in both primary islet cells and NIT-1 cells. Apoptosis in response to TNFalpha was observed in NIT-1 cells whereas apoptosis of primary beta cells required both TNFalpha and interferon-gamma (IFNgamma). Apoptosis could be prevented in NIT-1 cells by expression of dominant negative Fas-associating protein with death domain (dnFADD). Apoptosis in NIT-1 cells was increased by coincubation with IFNgamma, which also increased caspase 1 expression. These data show that TNF-activated pathways capable of inducing apoptotic cell death are present in beta cells. Caspase activation is the dominant pathway of TNF-induced cell death in NIT-1 cells and may be an important mechanism of beta cell damage in insulin-dependent diabetes mellitus. | lld:pubmed |
| pubmed-article:10385418 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10385418 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10385418 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:10385418 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10385418 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10385418 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10385418 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10385418 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10385418 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10385418 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10385418 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:10385418 | pubmed:issn | 0013-7227 | lld:pubmed |
| pubmed-article:10385418 | pubmed:author | pubmed-author:ThomasH EHE | lld:pubmed |
| pubmed-article:10385418 | pubmed:author | pubmed-author:FOXF AFA | lld:pubmed |
| pubmed-article:10385418 | pubmed:author | pubmed-author:MineJJ | lld:pubmed |
| pubmed-article:10385418 | pubmed:author | pubmed-author:GrellMM | lld:pubmed |
| pubmed-article:10385418 | pubmed:author | pubmed-author:StephensL ALA | lld:pubmed |
| pubmed-article:10385418 | pubmed:author | pubmed-author:DarwicheRR | lld:pubmed |
| pubmed-article:10385418 | pubmed:author | pubmed-author:VolodinLL | lld:pubmed |
| pubmed-article:10385418 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10385418 | pubmed:volume | 140 | lld:pubmed |
| pubmed-article:10385418 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10385418 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10385418 | pubmed:pagination | 3219-27 | lld:pubmed |
| pubmed-article:10385418 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:10385418 | pubmed:meshHeading | pubmed-meshheading:10385418... | lld:pubmed |
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| pubmed-article:10385418 | pubmed:meshHeading | pubmed-meshheading:10385418... | lld:pubmed |
| pubmed-article:10385418 | pubmed:meshHeading | pubmed-meshheading:10385418... | lld:pubmed |
| pubmed-article:10385418 | pubmed:meshHeading | pubmed-meshheading:10385418... | lld:pubmed |
| pubmed-article:10385418 | pubmed:meshHeading | pubmed-meshheading:10385418... | lld:pubmed |
| pubmed-article:10385418 | pubmed:meshHeading | pubmed-meshheading:10385418... | lld:pubmed |
| pubmed-article:10385418 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10385418 | pubmed:articleTitle | Tumor necrosis factor-alpha-activated cell death pathways in NIT-1 insulinoma cells and primary pancreatic beta cells. | lld:pubmed |
| pubmed-article:10385418 | pubmed:affiliation | The Walter and Eliza Hall Institute of Medical Research, Post Office Royal Melbourne Hospital, Parkville, Victoria, Australia. | lld:pubmed |
| pubmed-article:10385418 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10385418 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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