{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Mercadante CJ"],"funding":["NIDDK NIH HHS","NIEHS NIH HHS","National Institutes of Health","NIGMS NIH HHS"],"pagination":["5442-5461"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6877324"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["129(12)"],"pubmed_abstract":["Manganese (Mn), an essential metal and nutrient, is toxic in excess. Toxicity classically results from inhalational exposures in individuals who work in industrial settings. The first known disease of inherited Mn excess, identified in 2012, is caused by mutations in the metal exporter SLC30A10 and is characterized by Mn excess, dystonia, cirrhosis, and polycythemia. To investigate the role of SLC30A10 in Mn homeostasis, we first generated whole-body Slc30a10-deficient mice, which developed severe Mn excess and impaired systemic and biliary Mn excretion. Slc30a10 localized to canalicular membranes of hepatocytes, but mice with liver Slc30a10 deficiency developed minimal Mn excess despite impaired biliary Mn excretion. Slc30a10 also localized to the apical membrane of enterocytes, but mice "],"journal":["The Journal of clinical investigation"],"pubmed_title":["Manganese transporter Slc30a10 controls physiological manganese excretion and toxicity."],"pmcid":["PMC6877324"],"funding_grant_id":["T32 GM077995","R01 DK110049","K99 DK084122","P30 GM103410","DK84122,DK110049,DK117524,ES007272,GM077995","T32 ES007272","R00 DK084122","F31 DK117524"],"pubmed_authors":["Salesky MA","Bartnikas TB","Herrera C","Dash ME","Prajapati M","Cintron-Rivera L","Rao DB","Conboy HL","Mercadante CJ","Pettiglio MA"],"additional_accession":[]},"is_claimable":false,"name":"Manganese transporter Slc30a10 controls physiological manganese excretion and toxicity.","description":"Manganese (Mn), an essential metal and nutrient, is toxic in excess. Toxicity classically results from inhalational exposures in individuals who work in industrial settings. The first known disease of inherited Mn excess, identified in 2012, is caused by mutations in the metal exporter SLC30A10 and is characterized by Mn excess, dystonia, cirrhosis, and polycythemia. To investigate the role of SLC30A10 in Mn homeostasis, we first generated whole-body Slc30a10-deficient mice, which developed severe Mn excess and impaired systemic and biliary Mn excretion. Slc30a10 localized to canalicular membranes of hepatocytes, but mice with liver Slc30a10 deficiency developed minimal Mn excess despite impaired biliary Mn excretion. Slc30a10 also localized to the apical membrane of enterocytes, but mice ","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Dec","modification":"2026-06-04T02:18:22.621Z","creation":"2025-04-07T05:51:41.874Z"},"accession":"S-EPMC6877324","cross_references":{"pubmed":["31527311"],"doi":["10.1172/JCI129710","10.1172/jci129710"]}}