ArticleThe Journal of biological chemistry2009
A pathogenic C terminus-truncated polycystin-2 mutant enhances receptor-activated Ca2+ entry via association with TRPC3 and TRPC7.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 43 citations in OpenAlex.
- Physiological functions and pharmacological targeting of transient receptor potential channels.Pharmacological reviews · 2025Review
- Review
- Molecular mechanism of hyperactivation conferred by a truncation of TRPA1.Nature communications · 2023Article
- TRPC Channels in the Physiology and Pathophysiology of the Renal Tubular System: What Do We Know?International journal of molecular sciences · 2022Review
- Distribution and Assembly of TRP Ion Channels.Advances in experimental medicine and biology · 2021Article
- Modulation of polycystic kidney disease by G-protein coupled receptors and cyclic AMP signaling.Cellular signalling · 2020Review
- Intravascular flow stimulates PKD2 (polycystin-2) channels in endothelial cells to reduce blood pressure.eLife · 2020Article
- Fundamental insights into autosomal dominant polycystic kidney disease from human-based cell models.Pediatric nephrology (Berlin, Germany) · 2019Article
- Mitochondrial TRPC3 promotes cell proliferation by regulating the mitochondrial calcium and metabolism in renal polycystin-2 knockdown cells.International urology and nephrology · 2019Article
- MicroRNA501-5p induces p53 proteasome degradation through the activation of the mTOR/MDM2 pathway in ADPKD cells.Journal of cellular physiology · 2018Article
- The functions of TRPP2 in the vascular system.Acta pharmacologica Sinica · 2016Review
- Vasopressin and disruption of calcium signalling in polycystic kidney disease.Nature reviews. Nephrology · 2015Review
- Polycystins and partners: proposed role in mechanosensitivity.The Journal of physiology · 2014Review
- Transient receptor potential canonical 7: a diacylglycerol-activated non-selective cation channel.Handbook of experimental pharmacology · 2014Review
- Ion channels in renal disease.Chemical reviews · 2012Review
- Atomic force microscopy reveals the alternating subunit arrangement of the TRPP2-TRPV4 heterotetramer.Biophysical journal · 2010Article
- Transient receptor potential channelopathies.Pflugers Archiv : European journal of physiology · 2010Review
- Polycystin-2 activation by inositol 1,4,5-trisphosphate-induced Ca2+ release requires its direct association with the inositol 1,4,5-trisphosphate receptor in a signaling microdomain.The Journal of biological chemistry · 2010Article
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in PKD2 gene result in autosomal dominant polycystic kidney disease (ADPKD). PKD2 encodes polycystin-2 (TRPP2), which is a homologue of transient receptor potential (TRP) cation channel proteins. Here we identify a novel PKD2 mutation that generates a C-terminal tail-truncated TRPP2 mutant 697fsX with a frameshift resulting in an aberrant 17-amino acid addition after glutamic acid residue 697 from a family showing mild ADPKD symptoms. When recombinantly expressed in HEK293 cells, wild-type (WT) TRPP2 localized at the endoplasmic reticulum (ER) membrane significantly enhanced Ca(2+) release from the ER upon muscarinic acetylcholine receptor (mAChR) stimulation. In contrast, 697fsX, which showed a predominant plasma membrane localization characteristic of TRPP2 mutants with C terminus deletion, prominently increased mAChR-activated Ca(2+) influx in cells expressing TRPC3 or TRPC7. Coimmunoprecipitation, pulldown assay, and cross-linking experiments revealed a physical association between 697fsX and TRPC3 or TRPC7. 697fsX but not WT TRPP2 elicited a depolarizing shift of reversal potentials and an enhancement of single-channel conductance indicative of altered ion-permeating pore properties of mAChR-activated currents. Importantly, in kidney epithelial LLC-PK1 cells the recombinant 679fsX construct was codistributed with native TRPC3 proteins at the apical membrane area, but the WT construct was distributed in the basolateral membrane and adjacent intracellular areas. Our results suggest that heteromeric cation channels comprised of the TRPP2 mutant and the TRPC3 or TRPC7 protein induce enhanced receptor-activated Ca(2+) influx that may lead to dysregulated cell growth in ADPKD.
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