<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Crook M</submitter><funding>NIGMS NIH HHS</funding><pagination>3533-3540</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5100852</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>6(11)</volume><pubmed_abstract>Identification of pro-cell survival signaling pathways has implications for cancer, cardiovascular, and neurodegenerative disease. We show that the &lt;i>Caenorhabditis elegans&lt;/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 &lt;i>C. elegans&lt;/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 &lt;i>C. elegans&lt;/i> and find that the LET-60 Ras/MAPK pathway, but not the IP&lt;sub>3&lt;/sub> re</pubmed_abstract><journal>G3 (Bethesda, Md.)</journal><pubmed_title>Epidermal Growth Factor Receptor Cell Survival Signaling Requires Phosphatidylcholine Biosynthesis.</pubmed_title><pmcid>PMC5100852</pmcid><funding_grant_id>R01 GM086786</funding_grant_id><pubmed_authors>Crook M</pubmed_authors><pubmed_authors>Hanna-Rose W</pubmed_authors><pubmed_authors>Upadhyay A</pubmed_authors><pubmed_authors>Ido LJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Epidermal Growth Factor Receptor Cell Survival Signaling Requires Phosphatidylcholine Biosynthesis.</name><description>Identification of pro-cell survival signaling pathways has implications for cancer, cardiovascular, and neurodegenerative disease. We show that the &lt;i>Caenorhabditis elegans&lt;/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 &lt;i>C. elegans&lt;/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 &lt;i>C. elegans&lt;/i> and find that the LET-60 Ras/MAPK pathway, but not the IP&lt;sub>3&lt;/sub> re</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Nov</publication><modification>2025-04-22T08:57:31.801Z</modification><creation>2019-03-27T02:28:34Z</creation></dates><accession>S-EPMC5100852</accession><cross_references><pubmed>27605519</pubmed><doi>10.1534/g3.116.034850</doi></cross_references></HashMap>