{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hanna AD"],"funding":["National Institutes of Health Cancer Center","NIDDK NIH HHS","The Mouse Metabolism and Phenotyping Core","NHGRI NIH HHS","NCI NIH HHS","National Institutes of Health","NIAMS NIH HHS","NIH HHS"],"pagination":["e202413583"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11633665"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["157(1)"],"pubmed_abstract":["Dilated cardiomyopathy (DCM) is a highly prevalent and genetically heterogeneous condition that results in decreased contractility and impaired cardiac function. The FK506-binding protein FKBP12 has been implicated in regulating the ryanodine receptor in skeletal muscle, but its role in cardiac muscle remains unclear. To define the effect of FKBP12 in cardiac function, we generated conditional mouse models of FKBP12 deficiency. We used Cre recombinase driven by either the α-myosin heavy chain, (αMHC) or muscle creatine kinase (MCK) promoter, which are expressed at embryonic day 9 (E9) and E13, respectively. Both conditional models showed an almost total loss of FKBP12 in adult hearts compared with control animals. However, only the early embryonic deletion of FKBP12 (αMHC-Cre) resulted in "],"journal":["The Journal of general physiology"],"pubmed_title":["Mechanisms underlying dilated cardiomyopathy associated with FKBP12 deficiency."],"pmcid":["PMC11633665"],"funding_grant_id":["R21 AR082613","R01 DK114356","R01 AR082209","UM1HG006348","P30 CA125123","UM1 HG006348","R01DK114356","2R01AR082209","R01 AR072475","1R21AR082613-01","R01AR072475","S10 OD032380","S10OD032380"],"pubmed_authors":["Ho KS","Lee CS","Chang T","Agha N","Dickinson ME","Ward CS","Hsu CW","Yee RSZ","Samee MAH","Jung SY","Walker WC","Hanna AD","Hamilton SL","Rodney GG"],"additional_accession":[]},"is_claimable":false,"name":"Mechanisms underlying dilated cardiomyopathy associated with FKBP12 deficiency.","description":"Dilated cardiomyopathy (DCM) is a highly prevalent and genetically heterogeneous condition that results in decreased contractility and impaired cardiac function. The FK506-binding protein FKBP12 has been implicated in regulating the ryanodine receptor in skeletal muscle, but its role in cardiac muscle remains unclear. To define the effect of FKBP12 in cardiac function, we generated conditional mouse models of FKBP12 deficiency. We used Cre recombinase driven by either the α-myosin heavy chain, (αMHC) or muscle creatine kinase (MCK) promoter, which are expressed at embryonic day 9 (E9) and E13, respectively. Both conditional models showed an almost total loss of FKBP12 in adult hearts compared with control animals. However, only the early embryonic deletion of FKBP12 (αMHC-Cre) resulted in ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jan","modification":"2026-06-01T16:03:45.926Z","creation":"2026-04-08T14:01:38.658Z"},"accession":"S-EPMC11633665","cross_references":{"pubmed":["39661086"],"doi":["10.1085/jgp.202413583"]}}