{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["6"],"submitter":["Saveljeva S"],"pubmed_abstract":["Endoplasmic reticulum (ER) stress-induced cellular dysfunction and death is associated with several human diseases. It has been widely reported that ER stress kills through activation of the intrinsic mitochondrial apoptotic pathway. Here we demonstrate that ER stress can also induce necroptosis, an receptor-interacting protein kinase 1 (RIPK1)/RIPK3/mixed lineage kinase domain-like protein (MLKL)-dependent form of necrosis. Remarkably, we observed that necroptosis induced by various ER stressors in L929 cells is dependent on tumor necrosis factor receptor 1 (TNFR1), but occurs independently of autocrine TNF or lymphotoxin α production. Moreover, we found that repression of either TNFR1, RIPK1 or MLKL did not protect the cells from death but instead allowed a switch to ER stress-induced ap"],"journal":["Cell death & disease"],"pagination":["e1587"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4669746"],"repository":["biostudies-literature"],"pubmed_title":["Endoplasmic reticulum stress induces ligand-independent TNFR1-mediated necroptosis in L929 cells."],"pmcid":["PMC4669746"],"pubmed_authors":["Mc Laughlin SL","Vandenabeele P","Samali A","Bertrand MJ","Saveljeva S"],"additional_accession":[]},"is_claimable":false,"name":"Endoplasmic reticulum stress induces ligand-independent TNFR1-mediated necroptosis in L929 cells.","description":"Endoplasmic reticulum (ER) stress-induced cellular dysfunction and death is associated with several human diseases. It has been widely reported that ER stress kills through activation of the intrinsic mitochondrial apoptotic pathway. Here we demonstrate that ER stress can also induce necroptosis, an receptor-interacting protein kinase 1 (RIPK1)/RIPK3/mixed lineage kinase domain-like protein (MLKL)-dependent form of necrosis. Remarkably, we observed that necroptosis induced by various ER stressors in L929 cells is dependent on tumor necrosis factor receptor 1 (TNFR1), but occurs independently of autocrine TNF or lymphotoxin α production. Moreover, we found that repression of either TNFR1, RIPK1 or MLKL did not protect the cells from death but instead allowed a switch to ER stress-induced ap","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Jan","modification":"2025-04-22T07:26:24.326Z","creation":"2019-03-27T02:04:36Z"},"accession":"S-EPMC4669746","cross_references":{"pubmed":["25569104"],"doi":["10.1038/cddis.2014.548"]}}