Transient receptor potential cation channel subfamily V member 5 is a calcium channel protein that in humans is encoded by the TRPV5 gene.
TRPV5 | |||||||||||||||||||||||||||||||||||||||||||||||||||
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Aliases | TRPV5, CAT2, ECAC1, OTRPC3, transient receptor potential cation channel subfamily V member 5 | ||||||||||||||||||||||||||||||||||||||||||||||||||
External IDs | OMIM: 606679 MGI: 2429764 HomoloGene: 10520 GeneCards: TRPV5 | ||||||||||||||||||||||||||||||||||||||||||||||||||
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The TRPV5 gene is a member of the transient receptor family and the TRPV subfamily. The calcium-selective channel, TRPV5, encoded by this gene has 6 transmembrane-spanning domains, multiple potential phosphorylation sites, an N-linked glycosylation site, and 5 ANK repeats. This protein forms homotetramers or heterotetramers and is activated by a low internal calcium level.
Both TRPV5 and TRPV6 are expressed in kidney and intestinal epithelial cells. TRPV5 is mainly expressed in kidney epithelial cells, where it plays an important role in the reabsorption of Ca2+, whereas TRPV6 is mainly expressed in the intestine. The enzyme α-klotho increases kidney calcium reabsorption by stabilizing TPRV5. Klotho is a beta-glucuronidase-like enzyme that activates TRPV5 by removal of sialic acid.
Normally, about 95% to 98% of Ca2+ filtered from the blood by the kidney is reabsorbed by the kidney's renal tubule, mediated by TRPV5. Genetic deletion of TRPV5 in mice leads to Ca2+ loss in the urine, and consequential hyperparathyroidism, and bone loss.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.
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