ArticleThe Journal of biological chemistry2013
The epithelial calcium channel TRPV5 is regulated differentially by klotho and sialidase.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 50 citations in OpenAlex.
- The role of transient receptor potential channels in chronic kidney disease-mineral and bone disorder.Frontiers in pharmacology · 2025Review
- TRP channels in mammalian hearing loss.Frontiers in molecular neuroscience · 2025Review
- Calmodulin regulates TRPV5 intracellular trafficking and plasma membrane abundance.The Journal of physiology · 2024Article
- Decreased calcium permeability caused by biallelic TRPV5 mutation leads to autosomal recessive renal calcium-wasting hypercalciuria.European journal of human genetics : EJHG · 2024Article
- The ion channel TRPV5 regulates B-cell signaling and activation.Frontiers in immunology · 2024Article
- ARL15 modulates magnesium homeostasis through N-glycosylation of CNNMs.Cellular and molecular life sciences : CMLS · 2021Article
- Ameliorating Effect of Klotho Protein on Rat Heart during I/R Injury.Oxidative medicine and cellular longevity · 2020Article
- Role of αKlotho and FGF23 in regulation of type II Na-dependent phosphate co-transporters.Pflugers Archiv : European journal of physiology · 2019Review
- N-linked glycans are required on epithelial NaAmerican journal of physiology. Renal physiology · 2018Article
- The Biological Role of Klotho Protein in the Development of Cardiovascular Diseases.BioMed research international · 2018Review
- Review
- Cooperative roles of glucose and asparagine-linked glycosylation in T-type calcium channel expression.Pflugers Archiv : European journal of physiology · 2016Article
- Mucin-1 Increases Renal TRPV5 Activity In Vitro, and Urinary Level Associates with Calcium Nephrolithiasis in Patients.Journal of the American Society of Nephrology : JASN · 2016Article
- Soluble Serum αKlotho Is a Potential Predictive Marker of Disease Progression in Clear Cell Renal Cell Carcinoma.Medicine · 2015Observational
- The role of protein N-glycosylation in neural transmission.Glycobiology · 2014Review
- Glycosylation of TRPM4 and TRPM5 channels: molecular determinants and functional aspects.Frontiers in cellular neuroscience · 2014Article
- N-glycosylation in regulation of the nervous system.Advances in neurobiologyArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transient receptor potential vanilloid type 5 (TRPV5) Ca(2+) channel facilitates transcellular Ca(2+) transport in the distal convoluted tubule (DCT) of the kidney. The channel is glycosylated with a complex type N-glycan and it has been postulated that hydrolysis of the terminal sialic acid(s) stimulate TRPV5 activity. The present study delineates the role of the N-glycan in TRPV5 activity using biochemical assays in Human Embryonic Kidney 293 cells expressing TRPV5, isoelectric focusing and total internal reflection fluorescent microscopy. The anti-aging hormone klotho and other glycosidases stimulate TRPV5-dependent Ca(2+) uptake. Klotho was found to increase the plasma membrane stability of TRPV5, via the TRPV5 N-glycan. Sialidase mimicked this stimulatory action. However, this effect was independent of the N-glycosylation state of TRPV5, since the N-glycosylation mutant (TRPV5(N358Q)) was activated to the same extent. We showed that the increased TRPV5 activity after sialidase treatment is caused by inhibition of lipid raft-mediated internalization. In addition, sialidase modified the N-glycan of transferrin, a model glycoprotein, differently from klotho. Previous studies showed that after klotho treatment, galectin-1 binds the TRPV5 N-glycan and thereby increases TRPV5 activity. However, galectin-3, but not galectin-1, was expressed in the DCT. Furthermore, an increase in TRPV5-mediated Ca(2+) uptake was detected after galectin-3 treatment. In conclusion, two distinct TRPV5 stimulatory mechanisms were demonstrated; a klotho-mediated effect that is dependent on the N-glycan of TRPV5 and a sialidase-mediated stimulation that is lipid raft-dependent and independent of the N-glycan of TRPV5.
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