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- aggregation classification "A1".
- aggregation creator B173831.
- aggregation creator B173832.
- aggregation creator B173833.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation date "2010".
- aggregation format "application/pdf".
- aggregation hasFormat 1017066.bibtex.
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- aggregation hasFormat 1017066.dc.
- aggregation hasFormat 1017066.didl.
- aggregation hasFormat 1017066.doc.
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- aggregation hasFormat 1017066.txt.
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- aggregation hasFormat 1017066.yaml.
- aggregation isPartOf urn:issn:0022-1007.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Biology and Life Sciences".
- aggregation title "Enterocyte-specific A20 deficiency sensitizes to tumor necrosis factor-induced toxicity and experimental colitis".
- aggregation abstract "A20 is a nuclear factor kappa B (NF-kappa B) target gene that encodes a ubiquitin-editing enzyme that is essential for the termination of NF-kappa B activation after tumor necrosis factor (TNF) or microbial product stimulation and for the prevention of TNF-induced apoptosis. Mice lacking A20 succumb to inflammation in several organs, including the intestine, and A20 mutations have been associated with Crohn's disease. However, ablation of NF-kappa B activity, specifically in intestinal epithelial cells (IECs), promotes intestinal inflammation. As A20 deficiency sensitizes cells to TNF-induced apoptosis yet also promotes NF-kappa B activity, it is not clear if A20 deficiency in IECs would exacerbate or ameliorate intestinal inflammation. We generated mice lacking A20 specifically in IECs. These mice did not show spontaneous intestinal inflammation but exhibited increased susceptibility to experimental colitis, and their IECs were hypersensitive to TNF-induced apoptosis. The resulting TNF-driven breakdown of the intestinal barrier permitted commensal bacterial infiltration and led to systemic inflammation. These studies define A20 as a major antiapoptotic protein in the intestinal epithelium and further indicate that defects in A20 might contribute to inflammatory bowel disease in humans.".
- aggregation authorList BK426593.
- aggregation endPage "1523".
- aggregation issue "7".
- aggregation startPage "1513".
- aggregation volume "207".
- aggregation aggregates 2937389.
- aggregation isDescribedBy 1017066.
- aggregation similarTo jem.20092474.
- aggregation similarTo LU-1017066.