{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSLC30A10 is a member of the solute carrier family 30 (ZnT) transporters that, in contrast to its zinc‐transporting relatives, plays a pivotal role in mediating manganese (Mn) efflux. Highly expressed in the liver and brain—including regions such as the basal ganglia—SLC30A10 is normally up‐regulated by increased Mn levels and other cellular stresses to protect cells from Mn toxicity. Genetic studies in consanguineous families have demonstrated that loss‐of‐function mutations (including frameshift and missense alleles) in SLC30A10 lead to a rare, yet treatable, autosomal recessive syndrome characterized by hypermanganesemia accompanied by early‐onset dystonia, parkinsonism, polycythemia, and liver cirrhosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistic investigations using yeast models, cultured cell systems, and animal models have provided deep insights into SLC30A10’s function. Wild‐type SLC30A10 localizes primarily to the plasma membrane where it efficiently exports Mn, whereas disease‐causing mutations cause mis‐trafficking and intracellular retention—often leading to Mn accumulation in subcellular compartments such as the Golgi apparatus. Structural and mutagenesis studies have identified critical residues in both transmembrane and cytoplasmic domains that together ensure optimal Mn transport. Moreover, regulatory studies reveal that inflammatory signals (for example, interleukin‐6) and endoplasmic reticulum stress can modulate SLC30A10 expression and its cellular distribution, further influencing Mn excretion."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "21"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond these molecular and cellular insights, genetic and clinical investigations have begun to delineate how both rare mutations and common genetic variants in SLC30A10 contribute to human disease. While rare, biallelic mutations lead to overt hypermanganesemia with neurodegeneration and hepatic pathology, genome‐wide association studies and analyses of mRNA expression in patient tissues have linked SLC30A10 polymorphisms with subtle alterations in blood Mn concentrations, liver enzyme levels, and even risk for certain cancers. In cell‐based systems—including CRISPR/Cas9‐modified hepatoma lines—restoration of SLC30A10 function rescues abnormal Mn accumulation, highlighting the transporter’s therapeutic relevance. Collectively, these findings underscore the central role of SLC30A10 in Mn detoxification and provide a framework for targeting Mn dysregulation in diverse clinical settings."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "22", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Michel Seve, Fabrice Chimienti, Séverine Devergnas, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "Mutations in SLC30A10 cause parkinsonism and dystonia with hypermanganesemia, polycythemia, and chronic liver disease."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Am J Hum Genet (2012)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.ajhg.2012.01.017"}], "href": "https://doi.org/10.1016/j.ajhg.2012.01.017"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "22341971"}], "href": "https://pubmed.ncbi.nlm.nih.gov/22341971"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Karin Tuschl, Peter T Clayton, Sidney M Gospe, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Syndrome of hepatic cirrhosis, dystonia, polycythemia, and hypermanganesemia caused by mutations in SLC30A10, a manganese transporter in man."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Am J Hum Genet (2012)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.ajhg.2012.01.018"}], "href": "https://doi.org/10.1016/j.ajhg.2012.01.018"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "22341972"}], "href": "https://pubmed.ncbi.nlm.nih.gov/22341972"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Dinorah Leyva-Illades, Pan Chen, Charles E Zogzas, et al. "}, {"type": "b", "children": [{"type": "t", "text": "SLC30A10 is a cell surface-localized manganese efflux transporter, and parkinsonism-causing mutations block its intracellular trafficking and efflux activity."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Neurosci (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1523/JNEUROSCI.2329-14.2014"}], "href": "https://doi.org/10.1523/JNEUROSCI.2329-14.2014"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "25319704"}], "href": "https://pubmed.ncbi.nlm.nih.gov/25319704"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "Charles E Zogzas, Michael Aschner, Somshuvra Mukhopadhyay "}, {"type": "b", "children": [{"type": "t", "text": "Structural Elements in the Transmembrane and Cytoplasmic Domains of the Metal Transporter SLC30A10 Are Required for Its Manganese Efflux Activity."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Biol Chem (2016)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1074/jbc.M116.726935"}], "href": "https://doi.org/10.1074/jbc.M116.726935"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "27307044"}], "href": "https://pubmed.ncbi.nlm.nih.gov/27307044"}]}, {"type": "r", "ref": 6, "children": [{"type": "t", "text": "Somshuvra Mukhopadhyay "}, {"type": "b", "children": [{"type": "t", "text": "Familial manganese-induced neurotoxicity due to mutations in SLC30A10 or SLC39A14."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Neurotoxicology (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.neuro.2017.07.030"}], "href": "https://doi.org/10.1016/j.neuro.2017.07.030"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "28789954"}], "href": "https://pubmed.ncbi.nlm.nih.gov/28789954"}]}, {"type": "r", "ref": 7, "children": [{"type": "t", "text": "Azita Tavasoli, Khadije Arjmandi Rafsanjani, Saba Hemmati, et al. 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