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SLC30A10 is highly expressed in the liver and is inducible by manganese. Additionally we are shipping SLC30A10 Kits (8) and SLC30A10 Proteins (4) and many more products for this protein.
Showing 10 out of 22 products:
Human Polyclonal SLC30A10 Primary Antibody for IHC, IHC (p) - ABIN4354225
Lechpammer, Clegg, Muzar, Huebner, Jin, Gospe: Pathology of inherited manganese transporter deficiency. in Annals of neurology 2014
SLC30A10 has a protective role in 1-methyl-4-phenylpyridinium-induced toxicity via PERK (show EIF2AK3 Antibodies)-ATF4 (show ATF4 Antibodies) pathway.
xpressing either wild-type or mutant forms of SLC30A10 was sufficient to inhibit the effect of ATP2C1 (show ATP2C1 Antibodies) in response to Mn challenge in both zebrafish embryos and HeLa cells. These findings suggest that either activating ATP2C1 (show ATP2C1 Antibodies) or restoring the Mn-induced trafficking of ATP2C1 (show ATP2C1 Antibodies) can reduce Mn accumulation, providing a possible target for treating HMDPC.
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 (show SLC30A1 Antibodies) proteins.
allele was also associated with increased sway velocity (15%, P = .033; adjusted for age and sex) and reduced SLC30A10 expression
We describe early disease manifestations (including videos) in 5 previously unreported Indian children, carrying novel homozygous SLC30A10 mutation
SLC30A10 is a cell surface-localized manganese efflux transporter that reduces manganese levels and protects against manganese toxicity.
These results suggest that both the up-regulation of ZIP14 (show SLC39A14 Antibodies) and the down-regulation of ZnT10 by IL-6 (show IL6 Antibodies) might have enhanced the accumulation of manganese in SH-SY5Y cells.
a case of inherited manganism caused by SLC30A10 mutation is presented
ZnT10 is significantly decreased in the frontal cortex in Alzheimer's disease.
This review will address Mn transport proteins, the newly discovered SLC30A10 mutations and their implications to Parkinsonism and Mn regulation.
the hypothyroidism phenotype of Slc30a10 single knockouts is induced by elevated thyroid manganese, which blocks thyroxine production. These findings provide new insights into the mechanisms of manganese detoxification and manganese-induced thyroid dysfunction.
discovery highlights the importance of determining the role of thyroid dysfunction in the onset and progression of manganese-induced disease and identifies Slc30a10 knock-out mice as a new model for studying thyroid biology.
This gene is highly expressed in the liver and is inducible by manganese. Its protein product appears to be critical in maintaining manganese levels, and has higher specificity for manganese than zinc. Loss of function mutations appear to result in a pleomorphic phenotype, including dystonia and adult-onset parkinsonism. Alternatively spliced transcript variants have been observed for this gene.
zinc transporter 10
, zinc transporter 8
, solute carrier family 30, member 10
, solute carrier family 30 (zinc transporter), member 10