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ASB3 expression aggravates inflammatory bowel disease by targeting TRAF6 protein stability and affecting the intestinal microbiota
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ASB3 expression aggravates inflammatory bowel disease by targeting TRAF6 protein stability and affecting the intestinal microbiota
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ASB3 expression aggravates inflammatory bowel disease by targeting TRAF6 protein stability and affecting the intestinal microbiota
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Journal Article
ASB3 expression aggravates inflammatory bowel disease by targeting TRAF6 protein stability and affecting the intestinal microbiota
2024
Overview
Ubiquitination is a key process that controls protein stability. We determined the ubiquitination of TRAF6 by ASB3 in intestinal epithelial cells during colonic inflammation. Inflammatory bowel disease patients exhibit upregulated ASB3 expression at focal sites, supporting the involvement of degradation of TRAF6, which promotes TLR-Myd88/TRIF-independent NF-κB aberrant activation and intestinal microbiota imbalance. Sustained inflammatory signaling in intestinal epithelial cells and dysregulated protective probiotic immune responses mediated by ASB3 collectively contribute to the exacerbation of inflammatory bowel disease. These findings provide insights into the pathogenesis of inflammatory bowel disease and suggest a novel mechanism by which ASB3 increases the risk of colitis. Our results suggest that future inhibition of ASB3 in intestinal epithelial cells may be a novel clinical strategy.
Publisher
American Society for Microbiology
Subject
/ Ankyrins
/ Anus
/ ASB3
/ Colitis
/ Colitis - chemically induced
/ Colon
/ Dextran
/ Humans
/ Inflammatory Bowel Diseases - genetics
/ Inflammatory Bowel Diseases - immunology
/ Inflammatory Bowel Diseases - metabolism
/ Inflammatory Bowel Diseases - microbiology
/ Intestinal Mucosa - immunology
/ Intestinal Mucosa - metabolism
/ Intestinal Mucosa - microbiology
/ Intracellular Signaling Peptides and Proteins
/ Mice
/ Pathogenesis and Host Response
/ Patients
/ Plasmids
/ Proteins
/ Suppressor of Cytokine Signaling Proteins - genetics
/ Suppressor of Cytokine Signaling Proteins - metabolism
/ TNF Receptor-Associated Factor 6 - genetics
/ TNF Receptor-Associated Factor 6 - metabolism
/ TRAF6
