ArticleMetallomics : integrated biometal science2018
Putative metal binding site in the transmembrane domain of the manganese transporter SLC30A10 is different from that of related zinc transporters.
Article in Metallomics : integrated biometal science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 29 citations in OpenAlex.
- Manganese: biology, physiology and role in disease.Cell discovery · 2026Review
- Zinc as a master regulator of intracellular organelle homeostasis.Experimental & molecular medicine · 2026Review
- Molecular mechanisms of SLC30A10-mediated manganese transport.Nature communications · 2025Article
- Gut to brain: essential micronutrient and trace element manganese transport, function and toxicity.Frontiers in physiology · 2025Review
- Elevated thyroid manganese reduces thyroid iodine to induce hypothyroidism in mice, but not rats, lacking SLC30A10 transporter.Metallomics : integrated biometal science · 2024Article
- PHD2 enzyme is an intracellular manganese sensor that initiates the homeostatic response against elevated manganese.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Integrated meta-omics reveals the regulatory landscape involved in lipid metabolism between pig breeds.Microbiome · 2024Article
- Loss of SLC30A10 manganese transporter alters expression of neurotransmission genes and activates hypoxia-inducible factor signaling in mice.Metallomics : integrated biometal science · 2024Article
- Divalent metal content in diet affects severity of manganese toxicity in Drosophila.Biology open · 2024Article
- Hepatic and intestinal manganese excretion are both required to regulate brain manganese during elevated manganese exposure.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- SLC30A10 manganese transporter in the brain protects against deficits in motor function and dopaminergic neurotransmission under physiological conditions.Metallomics : integrated biometal science · 2023Article
- Manganese efflux transporter SLC30A10 missense polymorphism T95I associated with liver injury retains manganese efflux activity.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- Role of excretion in manganese homeostasis and neurotoxicity: a historical perspective.American journal of physiology. Gastrointestinal and liver physiology · 2022Review
- Up-regulation of the manganese transporter SLC30A10 by hypoxia-inducible factors defines a homeostatic response to manganese toxicity.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Characterization of in vitro models of SLC30A10 deficiency.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2021Article
- Transmembrane 163 (TMEM163) Protein: A New Member of the Zinc Efflux Transporter Family.Biomedicines · 2021Review
- Titanium Tackles the Endoplasmic Reticulum: A First Genomic Study on a Titanium Anticancer Metallodrug.iScience · 2020Article
- Maintaining Translational Relevance in Animal Models of Manganese Neurotoxicity.The Journal of nutrition · 2020Article
- Identification of a selective manganese ionophore that enables nonlethal quantification of cellular manganese.The Journal of biological chemistry · 2020Article
- Functional analyses of the UDP-galactose transporter SLC35A2 using the binding of bacterial Shiga toxins as a novel activity assay.Glycobiology · 2019Article
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2 authors at 1 institution in 2 countries.
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Abstract
SLC30 proteins belong to the cation diffusion facilitator (CDF) superfamily of metal transporters. SLC30A10 mediates manganese efflux, while other SLC30 members transport zinc. Metal specificity of CDFs may be conferred by amino acids that form a transmembrane metal binding site (Site A). Site A of zinc-transporting CDFs, such as SLC30A1/ZnT1, have a HXXXD motif, but manganese transporters, such as SLC30A10, harbor a NXXXD motif. This critical histidine-to-asparagine substitution, at residue 43, was proposed to underlie manganese transport specificity of SLC30A10. However, we recently discovered that asparagine-43 was dispensable for manganese efflux in HeLa cells; instead, glutamate-25, aspartate-40, asparagine-127, and aspartate-248 were required. In contrast, another group reported that asparagine-43 was required in a chicken cell line. The goal of this study was to resolve the divergent results about the requirement of the crucial asparagine-43 residue. For this, we compared the manganese efflux activity of four cell types that stably over-expressed SLC30A10wild-type (WT), SLC30A10N43A or SLC30A10E25A: physiologically-relevant hepatic HepG2 and neuronal AF5 cells, HEK cells, and embryonic fibroblasts from Slc30a10-/- mice. In all cell types, manganese efflux activity of SLC30A10N43A was comparable to WT, while SLC30A10E25A lacked activity. Importantly, unlike SLC30A10, the histidine residue of the HXXXD motif of SLC30A1/ZnT1 was required for zinc transport. 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.
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