| http://purl.uniprot.org/citations/25642769 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/25642769 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/25642769 | http://www.w3.org/2000/01/rdf-schema#comment | "The intracellular protein HMGB1 is released from cells and acts as a damage-associated molecular pattern molecule during many diseases, including inflammatory bowel disease (IBD); however, the intracellular function of HMGB1 during inflammation is poorly understood. Here, we demonstrated that cytosolic HMGB1 regulates apoptosis by protecting the autophagy proteins beclin 1 and ATG5 from calpain-mediated cleavage during inflammation. Colitis in mice with an intestinal epithelial cell-specific Hmgb1 deletion and patients with IBD were both characterized by increased calpain activation, beclin 1 and ATG5 cleavage, and intestinal epithelial cell (IEC) death compared with controls. In vitro cleavage assays and studies of enteroids verified that HMGB1 protects beclin 1 and ATG5 from calpain-mediated cleavage events that generate proapoptotic protein fragments. Together, our results indicate that HMGB1 is essential for mitigating the extent and severity of inflammation-associated cellular injury by controlling the switch between the proautophagic and proapoptotic functions of beclin 1 and ATG5 during inflammation. Moreover, these studies demonstrate that HMGB1 is pivotal for reducing tissue injury in IBD and other complex inflammatory disorders."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.org/dc/terms/identifier | "doi:10.1172/jci76344"xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.org/dc/terms/identifier | "doi:10.1172/jci76344"xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Chang J."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Chang J."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Lin F."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Lin F."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Wang Y."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Wang Y."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Zhu X."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Zhu X."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Boone D.L."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Boone D.L."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Messer J.S."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Messer J.S."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Lotze M.T."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Lotze M.T."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Billiar T.R."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Billiar T.R."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Chang E.B."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Chang E.B."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Cham C.M."xsd:string |
| http://purl.uniprot.org/citations/25642769 | http://purl.uniprot.org/core/author | "Cham C.M."xsd:string |