{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["24(11)"],"submitter":["Stope MB"],"pubmed_abstract":["Receptor tyrosine kinase regulation of phospholipase C-epsilon (PLC-epsilon), which is under the control of Ras-like and Rho GTPases, was studied with HEK-293 cells endogenously expressing PLC-coupled epidermal growth factor (EGF) receptors. PLC and Ca(2+) signaling by the EGF receptor, which activated both PLC-gamma1 and PLC-epsilon, was specifically suppressed by inactivation of Ras-related GTPases with clostridial toxins and expression of dominant-negative Rap2B. EGF induced rapid and sustained GTP loading of Rap2B, binding of Rap2B to PLC-epsilon, and Rap2B-dependent translocation of PLC-epsilon to the plasma membrane. GTP loading of Rap2B by EGF was inhibited by chelation of intracellular Ca(2+) and expression of lipase-inactive PLC-gamma1 but not of PLC-epsilon. Expression of RasGRP3"],"journal":["Molecular and cellular biology"],"pagination":["4664-76"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC416426"],"repository":["biostudies-literature"],"pubmed_title":["Rap2B-dependent stimulation of phospholipase C-epsilon by epidermal growth factor receptor mediated by c-Src phosphorylation of RasGRP3."],"pmcid":["PMC416426"],"pubmed_authors":["Oude Weernink PA","Vom Dorp F","Schmidt M","Stope MB","Rosskopf D","Szatkowski D","Jakobs KH","Evellin S","Nolte J","Bohm A","Keiper M"],"additional_accession":[]},"is_claimable":false,"name":"Rap2B-dependent stimulation of phospholipase C-epsilon by epidermal growth factor receptor mediated by c-Src phosphorylation of RasGRP3.","description":"Receptor tyrosine kinase regulation of phospholipase C-epsilon (PLC-epsilon), which is under the control of Ras-like and Rho GTPases, was studied with HEK-293 cells endogenously expressing PLC-coupled epidermal growth factor (EGF) receptors. PLC and Ca(2+) signaling by the EGF receptor, which activated both PLC-gamma1 and PLC-epsilon, was specifically suppressed by inactivation of Ras-related GTPases with clostridial toxins and expression of dominant-negative Rap2B. EGF induced rapid and sustained GTP loading of Rap2B, binding of Rap2B to PLC-epsilon, and Rap2B-dependent translocation of PLC-epsilon to the plasma membrane. GTP loading of Rap2B by EGF was inhibited by chelation of intracellular Ca(2+) and expression of lipase-inactive PLC-gamma1 but not of PLC-epsilon. Expression of RasGRP3","dates":{"release":"2004-01-01T00:00:00Z","publication":"2004 Jun","modification":"2025-04-20T00:33:56.927Z","creation":"2019-03-27T00:50:28Z"},"accession":"S-EPMC416426","cross_references":{"pubmed":["15143162"],"doi":["10.1128/mcb.24.11.4664-4676.2004","10.1128/MCB.24.11.4664-4676.2004"]}}