1.A.4.2.10
TRPV5 epithelial Ca²⁺ channel (ECaC1) (forms homo- and heterotetrameric channels with TRPV6; requires the S100A10-annexin 2 complex for routing to the plasma membrane) (Hoenderop et al., 2003; van de Graaf et al., 2003).  The kidney maintains whole body calcium homoeostasis due to the reabsorption of Ca²⁺ filtered by the kidney glomerulus. TRPV5 regulates urinary Ca²⁺ excretion by mediating active Ca²⁺ reabsorption in the distal convoluted tubule of the kidney. The histidine kinase, nucleoside diphosphate kinase B (NDPK-B), activates TRPV5 channel activity and Ca²⁺ flux, and this activation requires histidine 711 in the carboxy terminal tail of TRPV5. In addition, the histidine phosphatase, protein histidine phosphatase 1 (PHPT1), inhibits NDPK-B activated TRPV5 (Cai et al. 2014).  TRPV5 also transports cadmium (Cd²⁺). The L530R mutation is associated with recurrent kidney stones (Wang et al. 2017).  May be stabilized by Mucin-1 (Muc1; P15941) (Al-Bataineh et al. 2017). TRPV5 inhibitors have been identified (Hughes et al. 2019). A modular and reusable model of epithelial transport in the proximal convoluted tubule of the kidney has appeared (Noroozbabaee et al. 2022). Only TrpV5 and TrpV6 are calcium selective, while others are general for inorganic cations, and an explanatory mechanism has been proposed (Ives et al. 2023). The structural basis for the activation of TRPV5 channels by long-chain acyl-Coenzyme-Ahas been elucidated (Lee et al. 2023).