{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lazelle RA"],"funding":["NIDDK NIH HHS","NIGMS NIH HHS"],"pagination":["1456-64"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4849833"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["27(5)"],"pubmed_abstract":["Tacrolimus is a widely used immunosuppressive drug that inhibits the phosphatase calcineurin when bound to the 12 kDa FK506-binding protein (FKBP12). When this binding occurs in T cells, it leads to immunosuppression. Tacrolimus also causes side effects, however, such as hypertension and hyperkalemia. Previously, we reported that tacrolimus stimulates the renal thiazide-sensitive sodium chloride cotransporter (NCC), which is necessary for the development of hypertension. However, it was unclear if tacrolimus-induced hypertension resulted from tacrolimus effects in renal epithelial cells directly or in extrarenal tissues, and whether inhibition of calcineurin was required. To address these questions, we developed a mouse model in which FKBP12 could be deleted along the nephron. FKBP12 disru"],"journal":["Journal of the American Society of Nephrology : JASN"],"pubmed_title":["Renal Deletion of 12 kDa FK506-Binding Protein Attenuates Tacrolimus-Induced Hypertension."],"pmcid":["PMC4849833"],"funding_grant_id":["R01 DK095841","T32 DK067864","T32 GM071338","R01 DK051496"],"pubmed_authors":["Terker AS","Blankenstein KI","Himmerkus N","Ellison DH","Lazelle RA","Yang CL","Bleich M","McCully BH","Mutig K","Bachmann S"],"additional_accession":[]},"is_claimable":false,"name":"Renal Deletion of 12 kDa FK506-Binding Protein Attenuates Tacrolimus-Induced Hypertension.","description":"Tacrolimus is a widely used immunosuppressive drug that inhibits the phosphatase calcineurin when bound to the 12 kDa FK506-binding protein (FKBP12). When this binding occurs in T cells, it leads to immunosuppression. Tacrolimus also causes side effects, however, such as hypertension and hyperkalemia. Previously, we reported that tacrolimus stimulates the renal thiazide-sensitive sodium chloride cotransporter (NCC), which is necessary for the development of hypertension. However, it was unclear if tacrolimus-induced hypertension resulted from tacrolimus effects in renal epithelial cells directly or in extrarenal tissues, and whether inhibition of calcineurin was required. To address these questions, we developed a mouse model in which FKBP12 could be deleted along the nephron. FKBP12 disru","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 May","modification":"2025-04-04T07:30:39.012Z","creation":"2019-03-27T02:12:40Z"},"accession":"S-EPMC4849833","cross_references":{"pubmed":["26432904"],"doi":["10.1681/ASN.2015040466","10.1681/asn.2015040466"]}}