http://purl.uniprot.org/citations/29844315 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/29844315 | http://www.w3.org/2000/01/rdf-schema#comment | "Endoplasmic reticulum (ER) stress contributes to the development and progression of many chronic inflammatory diseases, including type 2 diabetes, obesity, atherosclerosis, neurodegenerative diseases, and cancer. ER stress has been reported to induce inflammasome activation and release of mature IL-1β, which contributes to many inflammatory diseases. The molecular mechanisms that activate the inflammasome during ER stress are still poorly understood. Here we report that the kinase receptor-interacting protein 1 (RIP1) plays an important role in ER stress-induced activation of inflammasome. Inhibition of RIP1 kinase activity by Necrostatin-1 or siRNA-mediated RIP1 knockdown significantly reduced ER stress-induced caspase-1 cleavage and IL-1β secretion in both bone marrow-derived macrophages (BMDMs) and J774A.1 macrophages. We speculate that the mitochondria fission factor dynamin-related protein 1 (DRP1) and reactive oxygen species (ROS) might function as the effectors downstream of RIP1 to mediate inflammasome activation. Our study reveals a critical role for RIP1 in regulating ER stress-induced inflammation responses, and proposes RIP1 as a potential pharmaceutical target to treat diseases resulting from unresolved ER stress-related inflammation."xsd:string |
http://purl.uniprot.org/citations/29844315 | http://purl.org/dc/terms/identifier | "doi:10.1038/s41419-018-0694-7"xsd:string |
http://purl.uniprot.org/citations/29844315 | http://purl.uniprot.org/core/author | "Gao Y."xsd:string |
http://purl.uniprot.org/citations/29844315 | http://purl.uniprot.org/core/author | "Lin H."xsd:string |
http://purl.uniprot.org/citations/29844315 | http://purl.uniprot.org/core/author | "Sun Q."xsd:string |
http://purl.uniprot.org/citations/29844315 | http://purl.uniprot.org/core/author | "Tao L."xsd:string |
http://purl.uniprot.org/citations/29844315 | http://purl.uniprot.org/core/author | "Wang J."xsd:string |
http://purl.uniprot.org/citations/29844315 | http://purl.uniprot.org/core/author | "Zhang J."xsd:string |
http://purl.uniprot.org/citations/29844315 | http://purl.uniprot.org/core/author | "Xu X."xsd:string |
http://purl.uniprot.org/citations/29844315 | http://purl.uniprot.org/core/author | "Wen J."xsd:string |
http://purl.uniprot.org/citations/29844315 | http://purl.uniprot.org/core/author | "Weng D."xsd:string |
http://purl.uniprot.org/citations/29844315 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
http://purl.uniprot.org/citations/29844315 | http://purl.uniprot.org/core/name | "Cell Death Dis"xsd:string |
http://purl.uniprot.org/citations/29844315 | http://purl.uniprot.org/core/pages | "641"xsd:string |
http://purl.uniprot.org/citations/29844315 | http://purl.uniprot.org/core/title | "The kinase receptor-interacting protein 1 is required for inflammasome activation induced by endoplasmic reticulum stress."xsd:string |
http://purl.uniprot.org/citations/29844315 | http://purl.uniprot.org/core/volume | "9"xsd:string |
http://purl.uniprot.org/citations/29844315 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/29844315 |
http://purl.uniprot.org/citations/29844315 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/29844315 |
http://purl.uniprot.org/uniprot/#_Q13546-mappedCitation-29844315 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29844315 |
http://purl.uniprot.org/uniprot/#_Q60855-mappedCitation-29844315 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29844315 |
http://purl.uniprot.org/uniprot/Q13546 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/29844315 |
http://purl.uniprot.org/uniprot/Q60855 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/29844315 |