{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pontier SM"],"funding":["Medical Research Council"],"pagination":["2698-709"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC1500845"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["25(12)"],"pubmed_abstract":["The obligatory heterodimerization of the GABAB receptor (GBR) raises fundamental questions about molecular mechanisms controlling its signaling efficacy. Here, we show that NEM sensitive fusion (NSF) protein interacts directly with the GBR heterodimer both in rat brain synaptosomes and in CHO cells, forming a ternary complex that can be regulated by agonist stimulation. Inhibition of NSF binding with a peptide derived from GBR2 (TAT-Pep-27) did not affect basal signaling activity but almost completely abolished agonist-promoted GBR desensitization in both CHO cells and hippocampal slices. Taken with the role of PKC in the desensitization process, our observation that TAT-Pep-27 prevented both agonist-promoted recruitment of PKC and receptor phosphorylation suggests that NSF is a priming fa"],"journal":["The EMBO journal"],"pubmed_title":["Coordinated action of NSF and PKC regulates GABAB receptor signaling efficacy."],"pmcid":["PMC1500845"],"funding_grant_id":["MC_U138162357"],"pubmed_authors":["McIlhinney J","Ginham R","Bouvier M","Flynn H","White JH","Bonin H","Bell DJ","Trudeau LE","Pontier SM","Lahaie N","St-Gelais F"],"additional_accession":[]},"is_claimable":false,"name":"Coordinated action of NSF and PKC regulates GABAB receptor signaling efficacy.","description":"The obligatory heterodimerization of the GABAB receptor (GBR) raises fundamental questions about molecular mechanisms controlling its signaling efficacy. Here, we show that NEM sensitive fusion (NSF) protein interacts directly with the GBR heterodimer both in rat brain synaptosomes and in CHO cells, forming a ternary complex that can be regulated by agonist stimulation. Inhibition of NSF binding with a peptide derived from GBR2 (TAT-Pep-27) did not affect basal signaling activity but almost completely abolished agonist-promoted GBR desensitization in both CHO cells and hippocampal slices. Taken with the role of PKC in the desensitization process, our observation that TAT-Pep-27 prevented both agonist-promoted recruitment of PKC and receptor phosphorylation suggests that NSF is a priming fa","dates":{"release":"2006-01-01T00:00:00Z","publication":"2006 Jun","modification":"2026-03-16T16:20:42.502Z","creation":"2019-03-27T01:45:35Z"},"accession":"S-EPMC1500845","cross_references":{"pubmed":["16724110"],"doi":["10.1038/sj.emboj.7601157"]}}