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Do common genetic variants in endotoxin signaling pathway contribute to predisposition to alcoholic liver cirrhosis?
J. Petrášek, J.A. Hubáček, F. Stickel, J. Šperl, T. Berg, E. Ruf, H.E. Wichmann, A. Pfeufer, T. Meitinger, P. Trunečka, J. Špičák, M. Jirsa
Jazyk angličtina Země Německo
- MeSH
- alkoholická cirhóza jater genetika metabolismus MeSH
- endotoxiny genetika metabolismus MeSH
- financování organizované MeSH
- genetická predispozice k nemoci genetika MeSH
- genetická variace genetika MeSH
- genotyp MeSH
- lidé MeSH
- signální transdukce MeSH
- studie případů a kontrol MeSH
- zdraví MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta), produced by endotoxin-activated Kupffer cells, play a key role in the pathogenesis of alcoholic liver cirrhosis (ALC). Alleles TNFA -238A, IL1B -31T and variant IL1RN*2 of repeat polymorphism in the gene encoding the IL-1 receptor antagonist increase production of TNF-alpha and IL-1beta, respectively. Alleles CD14 -159T, TLR4 c.896G and TLR4 c.1196T modify activation of Kupffer cells by endotoxin. We confirmed the published associations between these common variants and genetic predisposition to ALC by means of a large case-control association study conducted on two Central European populations.
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- $a BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta), produced by endotoxin-activated Kupffer cells, play a key role in the pathogenesis of alcoholic liver cirrhosis (ALC). Alleles TNFA -238A, IL1B -31T and variant IL1RN*2 of repeat polymorphism in the gene encoding the IL-1 receptor antagonist increase production of TNF-alpha and IL-1beta, respectively. Alleles CD14 -159T, TLR4 c.896G and TLR4 c.1196T modify activation of Kupffer cells by endotoxin. We confirmed the published associations between these common variants and genetic predisposition to ALC by means of a large case-control association study conducted on two Central European populations.
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