| http://purl.uniprot.org/citations/22456092 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22456092 | http://www.w3.org/2000/01/rdf-schema#comment | "Autosomal dominant polycystic kidney disease is caused by loss-of-function mutations in the PKD1 or PKD2 genes encoding respectively polycystin-1 and polycystin-2. Polycystin-2 stimulates the inositol trisphosphate (IP(3)) receptor (IP(3)R), a Ca(2+)-release channel in the endoplasmic reticulum (ER). The effect of ER-located polycystin-1 is less clear. Polycystin-1 has been reported both to stimulate and to inhibit the IP(3)R. We now studied the effect of polycystin-1 and of polycystin-2 on the IP(3)R activity under conditions where the cytosolic Ca(2+) concentration was kept constant and the reuptake of released Ca(2+) was prevented. We also studied the interdependence of the interaction of polycystin-1 and polycystin-2 with the IP(3)R. The experiments were done in conditionally immortalized human proximal-tubule epithelial cells in which one or both polycystins were knocked down using lentiviral vectors containing miRNA-based short hairpins. The Ca(2+) release was induced in plasma membrane-permeabilized cells by various IP(3) concentrations at a fixed Ca(2+) concentration under unidirectional (45)Ca(2+)-efflux conditions. We now report that knock down of polycystin-1 or of polycystin-2 inhibited the IP(3)-induced Ca(2+) release. The simultaneous presence of the two polycystins was required to fully amplify the IP(3)-induced Ca(2+) release, since the presence of polycystin-1 alone or of polycystin-2 alone did not result in an increased Ca(2+) release. These novel findings indicate that ER-located polycystin-1 and polycystin-2 operate as a functional complex. They are compatible with the view that loss-of-function mutations in PKD1 and in PKD2 both cause autosomal dominant polycystic kidney disease."xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.ceca.2012.03.002"xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://purl.uniprot.org/core/author | "van den Heuvel L.P."xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://purl.uniprot.org/core/author | "Gijsbers R."xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://purl.uniprot.org/core/author | "Missiaen L."xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://purl.uniprot.org/core/author | "Bultynck G."xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://purl.uniprot.org/core/author | "De Smedt H."xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://purl.uniprot.org/core/author | "Luyten T."xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://purl.uniprot.org/core/author | "Parys J.B."xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://purl.uniprot.org/core/author | "Levtchenko E.N."xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://purl.uniprot.org/core/author | "Sammels E."xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://purl.uniprot.org/core/author | "Mekahli D."xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://purl.uniprot.org/core/author | "Welkenhuyzen K."xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/22456092 | http://purl.uniprot.org/core/name | "Cell Calcium"xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://purl.uniprot.org/core/pages | "452-458"xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://purl.uniprot.org/core/title | "Polycystin-1 and polycystin-2 are both required to amplify inositol-trisphosphate-induced Ca2+ release."xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://purl.uniprot.org/core/volume | "51"xsd:string |
| http://purl.uniprot.org/citations/22456092 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/22456092 |
| http://purl.uniprot.org/citations/22456092 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/22456092 |
| http://purl.uniprot.org/uniprot/#_A0A097HUC6-mappedCitation-22456092 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/22456092 |
| http://purl.uniprot.org/uniprot/#_A0A0C5G176-mappedCitation-22456092 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/22456092 |
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| http://purl.uniprot.org/uniprot/#_B4DFN3-mappedCitation-22456092 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/22456092 |