{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wright JD"],"funding":["NIDDK NIH HHS","National Institute of Diabetes and Digestive and Kidney Diseases","National Institutes of Health","Welch Foundation"],"pagination":["3574-3586"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5503716"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["31(8)"],"pubmed_abstract":["Soluble Klotho (sKlotho) is the shed ectodomain of antiaging membrane Klotho that contains 2 extracellular domains KL1 and KL2, each of which shares sequence homology to glycosyl hydrolases. sKlotho elicits pleiotropic cellular responses with a poorly understood mechanism of action. Notably, in injury settings, sKlotho confers cardiac and renal protection by down-regulating calcium-permeable transient receptor potential canonical type isoform 6 (TRPC6) channels in cardiomyocytes and glomerular podocytes. Inhibition of PI3K-dependent exocytosis of TRPC6 is thought to be the underlying mechanism, and recent studies showed that sKlotho interacts with α2-3-sialyllactose-containing gangliosides enriched in lipid rafts to inhibit raft-dependent PI3K signaling. However, the structural basis for b"],"journal":["FASEB journal : official publication of the Federation of American Societies for Experimental Biology"],"pubmed_title":["Modeled structural basis for the recognition of α2-3-sialyllactose by soluble Klotho."],"pmcid":["PMC5503716"],"funding_grant_id":["I‐1686","R01 DK109887","DK100605","DK109887","R01 DK100605"],"pubmed_authors":["Yoon J","Nischan N","An SW","Wright JD","Lim C","Xie J","Oliver N","Kohler JJ","Huang CL"],"additional_accession":[]},"is_claimable":false,"name":"Modeled structural basis for the recognition of α2-3-sialyllactose by soluble Klotho.","description":"Soluble Klotho (sKlotho) is the shed ectodomain of antiaging membrane Klotho that contains 2 extracellular domains KL1 and KL2, each of which shares sequence homology to glycosyl hydrolases. sKlotho elicits pleiotropic cellular responses with a poorly understood mechanism of action. Notably, in injury settings, sKlotho confers cardiac and renal protection by down-regulating calcium-permeable transient receptor potential canonical type isoform 6 (TRPC6) channels in cardiomyocytes and glomerular podocytes. Inhibition of PI3K-dependent exocytosis of TRPC6 is thought to be the underlying mechanism, and recent studies showed that sKlotho interacts with α2-3-sialyllactose-containing gangliosides enriched in lipid rafts to inhibit raft-dependent PI3K signaling. However, the structural basis for b","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Aug","modification":"2026-05-05T19:43:32.81Z","creation":"2026-04-07T21:53:07.557Z"},"accession":"S-EPMC5503716","cross_references":{"pubmed":["28442546"],"doi":["10.1096/fj.201700043R","10.1096/fj.201700043r"]}}