{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Suhail A"],"funding":["Regional Centre for Biotechnology","DBT/Wellcome Trust India Alliance","Wellcome Trust/DBT","Wellcome Trust"],"pagination":["3522-3538.e7"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7617169"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["29(11)"],"pubmed_abstract":["Inflammatory bowel disease (IBD) is a complex autoimmune disorder recently shown to be associated with SUMOylation, a post-translational modification mechanism. Here, we have identified a link between epithelial deSUMOylases and inflammation in IBD. DeSUMOylase SENP7 was seen to be upregulated specifically in intestinal epithelial cells in both human IBD and a mouse model. In steady state, but not IBD, SENP7 expression was negatively regulated by a direct interaction and ubiquitination by SIAH2. Upregulated SENP7 in inflamed tissue displayed a distinct interactome. These changes led to an expansion of localized proinflammatory γδ T cells. Furthermore, in vivo knockdown of SENP7 or depletion of γδ T cells abrogated dextran sulfate sodium (DSS)-induced gut inflammation. Strong statistical co"],"journal":["Cell reports"],"pubmed_title":["DeSUMOylase SENP7-Mediated Epithelial Signaling Triggers Intestinal Inflammation via Expansion of Gamma-Delta T Cells."],"pmcid":["PMC7617169"],"funding_grant_id":["IA/I/11/2500284"],"pubmed_authors":["Gaur P","Mujagond P","Ahuja V","Suhail A","Singh M","Awasthi A","Srikanth CV","Rizvi ZA","Ali SA"],"additional_accession":[]},"is_claimable":false,"name":"DeSUMOylase SENP7-Mediated Epithelial Signaling Triggers Intestinal Inflammation via Expansion of Gamma-Delta T Cells.","description":"Inflammatory bowel disease (IBD) is a complex autoimmune disorder recently shown to be associated with SUMOylation, a post-translational modification mechanism. Here, we have identified a link between epithelial deSUMOylases and inflammation in IBD. DeSUMOylase SENP7 was seen to be upregulated specifically in intestinal epithelial cells in both human IBD and a mouse model. In steady state, but not IBD, SENP7 expression was negatively regulated by a direct interaction and ubiquitination by SIAH2. Upregulated SENP7 in inflamed tissue displayed a distinct interactome. These changes led to an expansion of localized proinflammatory γδ T cells. Furthermore, in vivo knockdown of SENP7 or depletion of γδ T cells abrogated dextran sulfate sodium (DSS)-induced gut inflammation. Strong statistical co","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Dec","modification":"2026-06-01T16:14:40.275Z","creation":"2025-04-03T23:32:42.897Z"},"accession":"S-EPMC7617169","cross_references":{"pubmed":["31825833"],"doi":["10.1016/j.celrep.2019.11.028"]}}