PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34753157-9 2021 Select patients with underlying malignancy, those with significant and prolonged Vitamin D deficiency, or those who have acquired a SLC30A10 genetic mutation may be at an increased risk of developing manganese toxicity. Manganese 200-209 solute carrier family 30 member 10 Homo sapiens 132-140 33911374-2 2021 These disorders, predominantly described in children and adolescents, involve mutations in three manganese transporter genes, i.e., SLC30A10 and SLC39A14 which lead to manganese overload, and SLC39A8, which leads to manganese deficiency. Manganese 97-106 solute carrier family 30 member 10 Homo sapiens 132-140 34446561-0 2021 Up-regulation of the manganese transporter SLC30A10 by hypoxia-inducible factors defines a homeostatic response to manganese toxicity. Manganese 115-124 solute carrier family 30 member 10 Homo sapiens 43-51 34315874-4 2021 SLC30A10 excretes manganese from the liver to the bile duct, and rare homozygous loss of function causes the syndrome hypermanganesemia with dystonia-1 (HMNDYT1) which involves cirrhosis. Manganese 18-27 solute carrier family 30 member 10 Homo sapiens 0-8 34849276-0 2021 Treatable Hereditary Manganese Transport Disorder: Novel SLC30A10 Mutation and its Characteristic Neuroimaging Appearance in Two Siblings. Manganese 21-30 solute carrier family 30 member 10 Homo sapiens 57-65 33925013-4 2021 Significant progress was achieved in understanding the role of Mn transporters, such as SLC39A14, SLC39A8, and SLC30A10, in the regulation of systemic and brain manganese handling. Manganese 161-170 solute carrier family 30 member 10 Homo sapiens 111-119 33911374-2 2021 These disorders, predominantly described in children and adolescents, involve mutations in three manganese transporter genes, i.e., SLC30A10 and SLC39A14 which lead to manganese overload, and SLC39A8, which leads to manganese deficiency. Manganese 168-177 solute carrier family 30 member 10 Homo sapiens 132-140 31288771-0 2019 A case of dystonia with polycythemia and hypermanganesemia caused by SLC30A10 mutation: a treatable inborn error of manganese metabolism. Manganese 46-55 solute carrier family 30 member 10 Homo sapiens 69-77 32392784-0 2020 The Functions of ZIP8, ZIP14, and ZnT10 in the Regulation of Systemic Manganese Homeostasis. Manganese 70-79 solute carrier family 30 member 10 Homo sapiens 34-39 32392784-4 2020 In the past eight years, mutations of genes encoding metal transporters ZIP8 (SLC39A8), ZIP14 (SLC39A14), and ZnT10 (SLC30A10) have been identified to cause dysregulated manganese homeostasis in humans, highlighting the critical roles of these genes in manganese metabolism. Manganese 170-179 solute carrier family 30 member 10 Homo sapiens 110-115 32392784-4 2020 In the past eight years, mutations of genes encoding metal transporters ZIP8 (SLC39A8), ZIP14 (SLC39A14), and ZnT10 (SLC30A10) have been identified to cause dysregulated manganese homeostasis in humans, highlighting the critical roles of these genes in manganese metabolism. Manganese 170-179 solute carrier family 30 member 10 Homo sapiens 117-125 32392784-4 2020 In the past eight years, mutations of genes encoding metal transporters ZIP8 (SLC39A8), ZIP14 (SLC39A14), and ZnT10 (SLC30A10) have been identified to cause dysregulated manganese homeostasis in humans, highlighting the critical roles of these genes in manganese metabolism. Manganese 253-262 solute carrier family 30 member 10 Homo sapiens 110-115 32392784-4 2020 In the past eight years, mutations of genes encoding metal transporters ZIP8 (SLC39A8), ZIP14 (SLC39A14), and ZnT10 (SLC30A10) have been identified to cause dysregulated manganese homeostasis in humans, highlighting the critical roles of these genes in manganese metabolism. Manganese 253-262 solute carrier family 30 member 10 Homo sapiens 117-125 31288771-3 2019 Manganese intoxication can be acquired, but an inherited form due to autosomal-recessive mutations in the SLC30A10 gene encoding a Mn transporter protein has also been reported recently. Manganese 0-9 solute carrier family 30 member 10 Homo sapiens 106-114 31089831-3 2019 While the manganese efflux transporter SLC30A10 and the uptake transporter SLC39A14 work synergistically to reduce the manganese load, SLC39A8 has an opposing function facilitating manganese uptake into the organism. Manganese 10-19 solute carrier family 30 member 10 Homo sapiens 39-47 31089831-3 2019 While the manganese efflux transporter SLC30A10 and the uptake transporter SLC39A14 work synergistically to reduce the manganese load, SLC39A8 has an opposing function facilitating manganese uptake into the organism. Manganese 119-128 solute carrier family 30 member 10 Homo sapiens 39-47 30755481-1 2019 Manganese (Mn2+) is extruded from the cell by the zinc transporter 10 (ZnT10). Manganese 0-9 solute carrier family 30 member 10 Homo sapiens 50-69 30755481-1 2019 Manganese (Mn2+) is extruded from the cell by the zinc transporter 10 (ZnT10). Manganese 0-9 solute carrier family 30 member 10 Homo sapiens 71-76 27107558-7 2016 SLC30A10 is critical for zinc and manganese homeostasis and mutations in this gene, resulting in impaired ZnT10 function or expression, cause manganese intoxication, with Parkinson-like symptoms. Manganese 34-43 solute carrier family 30 member 10 Homo sapiens 0-8 30272946-0 2019 SLC30A10 Mutation Involved in Parkinsonism Results in Manganese Accumulation within Nanovesicles of the Golgi Apparatus. Manganese 54-63 solute carrier family 30 member 10 Homo sapiens 0-8 30619481-0 2018 Polymorphisms in Manganese Transporters SLC30A10 and SLC39A8 Are Associated With Children"s Neurodevelopment by Influencing Manganese Homeostasis. Manganese 17-26 solute carrier family 30 member 10 Homo sapiens 40-48 29382362-1 2018 BACKGROUND: The SLC39A14, SLC30A10 and SLC39A8 are considered to be key genes involved in manganese (Mn) homeostasis in humans. Manganese 90-99 solute carrier family 30 member 10 Homo sapiens 26-34 29429640-10 2018 New evidence indicates that the transporter genes SLC30A10 and SLC39A8 influence both manganese homeostasis and toxicity. Manganese 86-95 solute carrier family 30 member 10 Homo sapiens 50-58 29989630-2 2018 SLC30A10 mediates manganese efflux, while other SLC30 members transport zinc. Manganese 18-27 solute carrier family 30 member 10 Homo sapiens 0-8 29989630-5 2018 This critical histidine-to-asparagine substitution, at residue 43, was proposed to underlie manganese transport specificity of SLC30A10. Manganese 92-101 solute carrier family 30 member 10 Homo sapiens 127-135 29989630-12 2018 These results imply that the mechanisms of ion coordination within the transmembrane domain of SLC30A10 substantially differ from previously-studied CDFs, suggest that factors beyond Site A residues may confer metal specificity to CDFs, and improve understanding of the pathobiology of manganese toxicity due to mutations in SLC30A10. Manganese 286-295 solute carrier family 30 member 10 Homo sapiens 95-103 28789954-0 2018 Familial manganese-induced neurotoxicity due to mutations in SLC30A10 or SLC39A14. Manganese 9-18 solute carrier family 30 member 10 Homo sapiens 61-69 28860195-4 2017 Liver manganese is increased in patients lacking SLC30A10 but not SLC39A14. Manganese 6-15 solute carrier family 30 member 10 Homo sapiens 49-57 28860195-8 2017 Compared with wild-type controls, Slc39a14 single and Slc30a10/Slc39a14 double knockouts had higher manganese levels in the blood and brain but not in the liver. Manganese 100-109 solute carrier family 30 member 10 Homo sapiens 54-62 28860195-9 2017 In contrast, Slc30a10 single knockouts had elevated manganese levels in the liver as well as in the blood and brain. Manganese 52-61 solute carrier family 30 member 10 Homo sapiens 13-21 28860195-11 2017 Thus, transport activities of both SLC39A14 and SLC30A10 are required for hepatic manganese excretion. Manganese 82-91 solute carrier family 30 member 10 Homo sapiens 48-56 28860195-12 2017 Compared with Slc30a10 single knockouts, Slc39a14 single and Slc30a10/Slc39a14 double knockouts had lower thyroid manganese levels and normal thyroid function. Manganese 114-123 solute carrier family 30 member 10 Homo sapiens 61-69 27107558-7 2016 SLC30A10 is critical for zinc and manganese homeostasis and mutations in this gene, resulting in impaired ZnT10 function or expression, cause manganese intoxication, with Parkinson-like symptoms. Manganese 142-151 solute carrier family 30 member 10 Homo sapiens 0-8 27107558-7 2016 SLC30A10 is critical for zinc and manganese homeostasis and mutations in this gene, resulting in impaired ZnT10 function or expression, cause manganese intoxication, with Parkinson-like symptoms. Manganese 142-151 solute carrier family 30 member 10 Homo sapiens 106-111 27107558-13 2016 Because SLC30A10 is highly expressed in the small intestine, it is possible that the control of zinc and manganese systemic levels is regulated by vitamin D3 in the intestine. Manganese 105-114 solute carrier family 30 member 10 Homo sapiens 8-16 27307044-12 2016 Overall, our results indicate that residues in the transmembrane and C-terminal domains together confer optimal manganese transport capability to SLC30A10 and suggest that the mechanism of ion coordination in the transmembrane domain of SLC30A10 may be substantially different from that in YiiP/other SLC30 proteins. Manganese 112-121 solute carrier family 30 member 10 Homo sapiens 237-245 27307044-0 2016 Structural Elements in the Transmembrane and Cytoplasmic Domains of the Metal Transporter SLC30A10 Are Required for Its Manganese Efflux Activity. Manganese 120-129 solute carrier family 30 member 10 Homo sapiens 90-98 27307044-1 2016 Homozygous mutations in SLC30A10 lead to the development of familial manganese-induced parkinsonism. Manganese 69-78 solute carrier family 30 member 10 Homo sapiens 24-32 27307044-4 2016 Determining the mechanisms that allow SLC30A10 to transport manganese, which are unclear, is essential to understand its role in parkinsonism. Manganese 60-69 solute carrier family 30 member 10 Homo sapiens 38-46 27307044-12 2016 Overall, our results indicate that residues in the transmembrane and C-terminal domains together confer optimal manganese transport capability to SLC30A10 and suggest that the mechanism of ion coordination in the transmembrane domain of SLC30A10 may be substantially different from that in YiiP/other SLC30 proteins. Manganese 112-121 solute carrier family 30 member 10 Homo sapiens 146-154 24576911-3 2014 Recent studies have shown that another zinc transporter ZnT10 may be involved in manganese excretion. Manganese 81-90 solute carrier family 30 member 10 Homo sapiens 56-61 26628504-0 2016 Common Polymorphisms in the Solute Carrier SLC30A10 are Associated With Blood Manganese and Neurological Function. Manganese 78-87 solute carrier family 30 member 10 Homo sapiens 43-51 25778823-0 2015 Manganese transport disorder: novel SLC30A10 mutations and early phenotypes. Manganese 0-9 solute carrier family 30 member 10 Homo sapiens 36-44 27226609-3 2016 Here, we compared six proteins, which were reported to be involved in manganese detoxification/efflux, by evaluating their ability to reduce manganese toxicity in chicken DT40 cells, finding that human ZnT10 (hZnT10) was the most significant contributor. Manganese 70-79 solute carrier family 30 member 10 Homo sapiens 202-207 27226609-3 2016 Here, we compared six proteins, which were reported to be involved in manganese detoxification/efflux, by evaluating their ability to reduce manganese toxicity in chicken DT40 cells, finding that human ZnT10 (hZnT10) was the most significant contributor. Manganese 70-79 solute carrier family 30 member 10 Homo sapiens 209-215 27226609-3 2016 Here, we compared six proteins, which were reported to be involved in manganese detoxification/efflux, by evaluating their ability to reduce manganese toxicity in chicken DT40 cells, finding that human ZnT10 (hZnT10) was the most significant contributor. Manganese 141-150 solute carrier family 30 member 10 Homo sapiens 202-207 27226609-3 2016 Here, we compared six proteins, which were reported to be involved in manganese detoxification/efflux, by evaluating their ability to reduce manganese toxicity in chicken DT40 cells, finding that human ZnT10 (hZnT10) was the most significant contributor. Manganese 141-150 solute carrier family 30 member 10 Homo sapiens 209-215 27226609-4 2016 A domain swapping and substitution analysis between hZnT10 and the zinc-specific transporter hZnT1 showed that residue Asn(43), which corresponds to the His residue constituting the potential intramembranous zinc coordination site in other ZnT transporters, is necessary to impart hZnT10"s unique manganese mobilization activity; residues Cys(52) and Leu(242) in transmembrane domains II and V play a subtler role in controlling the metal specificity of hZnT10. Manganese 297-306 solute carrier family 30 member 10 Homo sapiens 52-58 24576911-4 2014 Here we examined the roles of ZIP8, ZIP14, and ZnT10 in the transport of manganese in human SH-SY5Y neuroblastoma cells. Manganese 73-82 solute carrier family 30 member 10 Homo sapiens 47-52 24576911-8 2014 The treatment of SH-SH5Y cells with IL-6 clearly decreased both the mRNA and protein levels of ZnT10 with a concomitant decrease in the manganese excretion efficiency. Manganese 136-145 solute carrier family 30 member 10 Homo sapiens 95-100 24576911-9 2014 These results suggest that both the up-regulation of ZIP14 and the down-regulation of ZnT10 by IL-6 might have enhanced the accumulation of manganese in SH-SY5Y cells. Manganese 140-149 solute carrier family 30 member 10 Homo sapiens 86-91 22341971-9 2012 We also show that the expression of SLC30A10 and the levels of the encoded protein are markedly induced by manganese in vitro. Manganese 107-116 solute carrier family 30 member 10 Homo sapiens 36-44 23357421-0 2013 Manganese efflux in Parkinsonism: insights from newly characterized SLC30A10 mutations. Manganese 0-9 solute carrier family 30 member 10 Homo sapiens 68-76 22926781-0 2012 Dystonia with brain manganese accumulation resulting from SLC30A10 mutations: a new treatable disorder. Manganese 20-29 solute carrier family 30 member 10 Homo sapiens 58-66 22341971-13 2012 In conclusion, we show that SLC30A10 mutations cause a treatable recessive disease with pleomorphic phenotype, and provide compelling evidence that SLC30A10 plays a pivotal role in manganese transport. Manganese 181-190 solute carrier family 30 member 10 Homo sapiens 28-36 22341971-13 2012 In conclusion, we show that SLC30A10 mutations cause a treatable recessive disease with pleomorphic phenotype, and provide compelling evidence that SLC30A10 plays a pivotal role in manganese transport. Manganese 181-190 solute carrier family 30 member 10 Homo sapiens 148-156 34877518-3 2021 Elevated blood levels of Manganese secondary to SLC30A10 gene mutation presents distinctly with dystonia, polycythemia, chronic liver disease and a characteristic high T1 signal in basal ganglia on brain MRI. Manganese 25-34 solute carrier family 30 member 10 Homo sapiens 48-56