| http://purl.uniprot.org/citations/31540954 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/31540954 | http://www.w3.org/2000/01/rdf-schema#comment | "The transient receptor potential (TRP; C-classical, TRPC) channel TRPC3 allows a cation (Na+/Ca2+) influx that is favored by the stimulation of Gq protein-coupled receptors (GPCRs). An enhanced TRPC3 activity is related to adverse effects, including pathological hypertrophy in chronic cardiac disease states. In the present study, we identified FK506-binding protein 52 (FKBP52, also known as FKBP4) as a novel interaction partner of TRPC3 in the heart. FKBP52 was recovered from a cardiac cDNA library by a C-terminal TRPC3 fragment (amino acids 742-848) in a yeast two-hybrid screen. Downregulation of FKBP52 promoted a TRPC3-dependent hypertrophic response in neonatal rat cardiomyocytes (NRCs). A similar effect was achieved by overexpressing peptidyl-prolyl isomerase (PPIase)-deficient FKBP52 mutants. Mechanistically, expression of the FKBP52 truncation mutants elevated TRPC3-mediated currents and Ca2+ fluxes, and the activation of calcineurin and the nuclear factor of activated T-cells in NRCs. Our data demonstrate that FKBP52 associates with TRPC3 via an as-yet-undescribed binding site in the C-terminus of TRPC3 and modulates TRPC3-dependent Ca2+ signals in a PPIase-dependent manner. This functional interaction might be crucial for limiting TRPC3-dependent signaling during chronic hypertrophic stimulation."xsd:string |
| http://purl.uniprot.org/citations/31540954 | http://purl.org/dc/terms/identifier | "doi:10.1242/jcs.231506"xsd:string |
| http://purl.uniprot.org/citations/31540954 | http://purl.uniprot.org/core/author | "Miranda-Laferte E."xsd:string |
| http://purl.uniprot.org/citations/31540954 | http://purl.uniprot.org/core/author | "Cellini A."xsd:string |
| http://purl.uniprot.org/citations/31540954 | http://purl.uniprot.org/core/author | "Tiapko O."xsd:string |
| http://purl.uniprot.org/citations/31540954 | http://purl.uniprot.org/core/author | "Eder-Negrin P."xsd:string |
| http://purl.uniprot.org/citations/31540954 | http://purl.uniprot.org/core/author | "Bandleon S."xsd:string |
| http://purl.uniprot.org/citations/31540954 | http://purl.uniprot.org/core/author | "Pickel S."xsd:string |
| http://purl.uniprot.org/citations/31540954 | http://purl.uniprot.org/core/author | "Strunz P.P."xsd:string |
| http://purl.uniprot.org/citations/31540954 | http://purl.uniprot.org/core/date | "2019"xsd:gYear |
| http://purl.uniprot.org/citations/31540954 | http://purl.uniprot.org/core/name | "J Cell Sci"xsd:string |
| http://purl.uniprot.org/citations/31540954 | http://purl.uniprot.org/core/pages | "jcs231506"xsd:string |
| http://purl.uniprot.org/citations/31540954 | http://purl.uniprot.org/core/title | "FKBP52 regulates TRPC3-dependent Ca2+ signals and the hypertrophic growth of cardiomyocyte cultures."xsd:string |
| http://purl.uniprot.org/citations/31540954 | http://purl.uniprot.org/core/volume | "132"xsd:string |
| http://purl.uniprot.org/citations/31540954 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/31540954 |
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