ArticleAmerican journal of physiology. Cell physiology2012
Suppression of intestinal calcium entry channel TRPV6 by OCRL, a lipid phosphatase associated with Lowe syndrome and Dent disease.
Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 35 citations in OpenAlex.
- Open-channel block of human TRPV6 by polyamine spermine.Nature communications · 2026Article
- The locking mechanism of human TRPV6 inhibition by intracellular magnesium.Nature communications · 2025Article
- Phenotype and genotype analyses of 21 Chinese patients with Dent disease.Journal of biomedical research · 2025Article
- Structure-function analyses of human TRPV6 ancestral and derived haplotypes.Structure (London, England : 1993) · 2025Article
- Advances in the Study for Modulators of Transient Receptor Potential Vanilloid (TRPV) Channel Family.Current topics in medicinal chemistry · 2025Review
- Atypical phenotypes and novel OCRL variations in southern Chinese patients with Lowe syndrome.Pediatric nephrology (Berlin, Germany) · 2024Article
- Bidirectional Allosteric Coupling between PIPInternational journal of molecular sciences · 2024Article
- Molecular pharmacology of the onco-TRP channel TRPV6.Channels (Austin, Tex.) · 2023Review
- Molecular pathway and structural mechanism of human oncochannel TRPV6 inhibition by the phytocannabinoid tetrahydrocannabivarin.Nature communications · 2023Article
- Structural mechanism of human oncochannel TRPV6 inhibition by the natural phytoestrogen genistein.Nature communications · 2023Article
- Dent-2 disease with a Bartter-like phenotype caused by the Asp631Glu mutation in the OCRL gene.BMC nephrology · 2022Article
- Calcium selective channel TRPV6: Structure, function, and implications in health and disease.Gene · 2022Review
- Structural mechanisms of TRPV6 inhibition by ruthenium red and econazole.Nature communications · 2021Article
- Structure and function of the calcium-selective TRP channel TRPV6.The Journal of physiology · 2021Review
- Genetics and phenotypic heterogeneity of Dent disease: the dark side of the moon.Human genetics · 2021Review
- Comparison of clinical and genetic characteristics between Dent disease 1 and Dent disease 2.Pediatric nephrology (Berlin, Germany) · 2020Article
- Intestinal CaWorld journal of gastroenterology · 2020Review
- Complete oculocerebrorenal phenotype of Lowe syndrome in a female patient with half reduction of inositol polyphosphate 5-phosphatase.CEN case reports · 2020Article
- Post-mortem histology in transient receptor potential cation channel subfamily V member 6 (TRPV6) under-mineralising skeletal dysplasia suggests postnatal skeletal recovery: a case report.BMC medical genetics · 2020Article
- The oculocerebrorenal syndrome of Lowe: an update.Pediatric nephrology (Berlin, Germany) · 2016Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Oculocerebrorenal syndrome of Lowe (OCRL) gene product is a phosphatidyl inositol 4,5-bisphosphate [PI(4,5)P(2)] 5-phosphatase, and mutations of OCRL cause Lowe syndrome and Dent disease, both of which are frequently associated with hypercalciuria. Transient receptor potential, vanilloid subfamily, subtype 6 (TRPV6) is an intestinal epithelial Ca(2+) channel mediating active Ca(2+) absorption. Hyperabsorption of Ca(2+) was found in patients of Dent disease with increased Ca(2+) excretion. In this study, we tested whether TRPV6 is regulated by OCRL and, if so, to what extent it is altered by Dent-causing OCRL mutations using Xenopus laevis oocyte expression system. Exogenous OCRL decreased TRPV6-mediated Ca(2+) uptake by regulating the function and trafficking of TRPV6 through different domains of OCRL. The PI(4,5)P(2) 5-phosphatase domain suppressed the TRPV6-mediated Ca(2+) transport likely through regulating the PI(4,5)P(2) level needed for TRPV6 function without affecting TRPV6 protein abundance of TRPV6 at the cell surface. The forward trafficking of TRPV6 was decreased by OCRL. The Rab binding domain in OCRL was involved in regulating the trafficking of TRPV6. Knocking down endogenous X. laevis OCRL by antisense approach increased TRPV6-mediated Ca(2+) transport and TRPV6 forward trafficking. All seven Dent-causing OCRL mutations examined exhibited alleviation of the inhibitory effect on TRPV6-mediated Ca(2+) transport together with decreased overall PI(4,5)P(2) 5-phosphatase activity. In conclusion, OCRL suppresses TRPV6 via two separate mechanisms. The disruption of PI(4,5)P(2) 5-phosphatase activity by Dent-causing mutations of OCRL may lead to increased intestinal Ca(2+) absorption and, in turn, hypercalciuria.
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