{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Crook M"],"funding":["NIGMS NIH HHS"],"pagination":["3533-3540"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5100852"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["6(11)"],"pubmed_abstract":["Identification of pro-cell survival signaling pathways has implications for cancer, cardiovascular, and neurodegenerative disease. We show that the <i>Caenorhabditis elegans</i> epidermal growth factor receptor LET-23 (LET-23 EGFR) has a prosurvival function in counteracting excitotoxicity, and we identify novel molecular players required for this prosurvival signaling. uv1 sensory cells in the <i>C. elegans</i> uterus undergo excitotoxic death in response to activation of the OSM-9/OCR-4 TRPV channel by the endogenous agonist nicotinamide. Activation of LET-23 EGFR can effectively prevent this excitotoxic death. We investigate the roles of signaling pathways known to act downstream of LET-23 EGFR in <i>C. elegans</i> and find that the LET-60 Ras/MAPK pathway, but not the IP<sub>3</sub> re"],"journal":["G3 (Bethesda, Md.)"],"pubmed_title":["Epidermal Growth Factor Receptor Cell Survival Signaling Requires Phosphatidylcholine Biosynthesis."],"pmcid":["PMC5100852"],"funding_grant_id":["R01 GM086786"],"pubmed_authors":["Crook M","Hanna-Rose W","Upadhyay A","Ido LJ"],"additional_accession":[]},"is_claimable":false,"name":"Epidermal Growth Factor Receptor Cell Survival Signaling Requires Phosphatidylcholine Biosynthesis.","description":"Identification of pro-cell survival signaling pathways has implications for cancer, cardiovascular, and neurodegenerative disease. We show that the <i>Caenorhabditis elegans</i> epidermal growth factor receptor LET-23 (LET-23 EGFR) has a prosurvival function in counteracting excitotoxicity, and we identify novel molecular players required for this prosurvival signaling. uv1 sensory cells in the <i>C. elegans</i> uterus undergo excitotoxic death in response to activation of the OSM-9/OCR-4 TRPV channel by the endogenous agonist nicotinamide. Activation of LET-23 EGFR can effectively prevent this excitotoxic death. We investigate the roles of signaling pathways known to act downstream of LET-23 EGFR in <i>C. elegans</i> and find that the LET-60 Ras/MAPK pathway, but not the IP<sub>3</sub> re","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Nov","modification":"2025-04-22T08:57:31.801Z","creation":"2019-03-27T02:28:34Z"},"accession":"S-EPMC5100852","cross_references":{"pubmed":["27605519"],"doi":["10.1534/g3.116.034850"]}}