SLC39A10 — Solute Carrier Family 39 Member 10

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SLC39A10 — Solute Carrier Family 39 Member 10

<table class="infobox infobox-gene">
<tr>
<th class="infobox-header" colspan="2">SLC39A10 — Solute Carrier Family 39 Member 10</th>
</tr>
<tr>
<td class="label">Symbol</td>
<td>SLC39A10</td>
</tr>
<tr>
<td class="label">Full Name</td>
<td>Solute Carrier Family 39 Member 10</td>
</tr>
<tr>
<td class="label">Chromosome</td>
<td>5q31</td>
</tr>
<tr>
<td class="label">NCBI Gene ID</td>
<td>[401024](https://www.ncbi.nlm.nih.gov/gene/401024)</td>
</tr>
<tr>
<td class="label">OMIM</td>
<td>[607342](https://www.omim.org/entry/607342)</td>
</tr>
<tr>
<td class="label">Ensembl ID</td>
<td>ENSG00000155886</td>
</tr>
<tr>
<td class="label">UniProt ID</td>
<td>[Q9UPY5](https://www.uniprot.org/uniprot/Q9UPY5)</td>
</tr>
<tr>
<td class="label">Protein Name</td>
<td>Zinc transporter ZIP10</td>
</tr>
<tr>
<td class="label">Family</td>
<td>ZIP (Zrt-, Irt-like Protein) transporter family</td>
</tr>
<tr>
<td class="label">Associated Diseases</td>
<td>Alzheimer's Disease, Parkinson's Disease, ALS, Breast Cancer, Immune Disorders</td>
</tr>
</table>

{.infobox .infobox-gene}

Overview

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SLC39A10 — Solute Carrier Family 39 Member 10

{.infobox .infobox-gene}

Overview

SLC39A10 (also known as ZIP10) is a member of the solute carrier family 39 (SLC39) encoding zinc transporter proteins. The ZIP family facilitates zinc uptake into the cytoplasm from extracellular spaces or intracellular organelles, playing essential roles in cellular zinc homeostasis[@zhang2015][@liuzzi2004]. Zinc is a critical trace element required for normal brain function, synaptic signaling, and neuronal survival. Dysregulation of zinc homeostasis has been implicated in multiple neurodegenerative diseases, making SLC39A10 an important gene of interest in neuroscience research[@bush2014][@mattson2020].

Gene Structure and Protein

The SLC39A10 gene is located on chromosome 5q31 and encodes a multi-pass transmembrane protein belonging to the ZIP transporter family. Like other ZIP transporters, SLC39A10 contains eight predicted transmembrane domains and facilitates Zn²⁺ import into the cytosol[@zhang2015][@liuzzi2004]. The protein is expressed in various tissues, with particularly high expression in the brain, immune cells, and developing embryos.

Biological Function

Zinc Homeostasis

Zinc is the second most abundant trace metal in the brain after iron, serving as a cofactor for over 300 enzymes and transcription factors. Cellular zinc homeostasis is tightly regulated by two major transporter families[@liuzzi2004]:

ZIP (SLC39) family: Imports zinc into the cytoplasm from extracellular space or intracellular compartments
ZnT (SLC30) family: Exports zinc out of the cytoplasm or into intracellular organelles

SLC39A10 specifically functions as a zinc importer, contributing to the maintenance of intracellular zinc levels necessary for normal cellular function[@zhang2015][@liuzzi2004].

Role in Neuronal Function

In neurons, zinc plays several critical roles:

Synaptic transmission: Synaptic vesicles contain zinc that can be released during neuronal activity, modulating postsynaptic receptor function[@bush2014]

Gene regulation: Zinc finger transcription factors require zinc for DNA binding

Antioxidant defense: Zinc is a cofactor for superoxide dismutase (SOD), a key antioxidant enzyme

Apoptosis regulation: Zinc can inhibit caspase activity and protect against apoptotic cell death[@mattson2020]

Immune System Function

SLC39A10 is highly expressed in immune cells, including T cells, B cells, and macrophages. Studies have shown that ZIP10 is essential for immune cell development and function[@zhang2015]. This connection is relevant to neurodegeneration, as neuroinflammation mediated by immune cells is a key pathological feature of Alzheimer's and Parkinson's diseases.

Disease Associations

Alzheimer's Disease

Zinc dyshomeostasis is a well-documented feature of Alzheimer's disease (AD)[@bush2014][@mattson2020]. Several mechanisms link zinc metabolism to AD pathology:

Amyloid-β aggregation: Zinc binds to amyloid-β peptides, promoting their aggregation into plaques[@bush2014]
Tau phosphorylation: Zinc can activate kinases involved in tau hyperphosphorylation
Synaptic zinc signaling: Disruption of synaptic zinc homeostasis affects learning and memory
Oxidative stress: Zinc deficiency impairs antioxidant defenses, increasing oxidative damage

SLC39A10 expression is altered in AD brain tissue, suggesting a potential role in disease pathogenesis[@mattson2020].

Parkinson's Disease

Zinc homeostasis is also implicated in Parkinson's disease (PD)[@mattson2020]:

Dopaminergic neuron vulnerability: Zinc can modulate dopamine metabolism and oxidative stress
α-Synuclein aggregation: Zinc binding may influence α-synuclein aggregation kinetics
Mitochondrial function: Zinc is important for mitochondrial enzyme function
Neuroinflammation: Zinc modulates microglial activation and inflammatory responses

Amyotrophic Lateral Sclerosis (ALS)

Emerging evidence suggests zinc transporter dysfunction may contribute to ALS pathogenesis[@kawamata2017]:

Motor neurons are particularly sensitive to zinc dysregulation
ZnT proteins are expressed in motor neurons
Altered zinc homeostasis may contribute to excitotoxicity

Other Conditions

Breast cancer: SLC39A10 overexpression has been reported in certain breast cancers[@taylor2018]
Immune deficiency: ZIP10 deficiency affects lymphocyte development[@zhang2015]

Expression Patterns

SLC39A10 shows tissue-specific expression:

Brain: High expression in cortex, hippocampus, and cerebellum
Immune system: Abundant in spleen, thymus, and peripheral blood cells
Liver: Moderate expression
Kidney: Moderate expression

The Allen Human Brain Atlas and BrainSpan provide detailed regional expression data in human and developing brains.

Therapeutic Implications

Targeting zinc homeostasis represents a potential therapeutic strategy for neurodegenerative diseases[@mattson2020]:

Zinc supplementation: May benefit patients with zinc deficiency

Zinc chelation: May reduce zinc-mediated amyloid aggregation

Modulator drugs: Compounds targeting ZIP/ZnT transporters

Gene therapy: Potential for restoring proper zinc transport

Interacting Proteins

SLC39A10 interacts with or is functionally related to:

Other ZIP family members (SLC39A1-14)
ZnT family exporters (SLC30A1-10)
Metallothioneins (MT1, MT2) - zinc buffering proteins
ZIP1, ZIP3 - other zinc importers

External Links

[NCBI Gene: 401024](https://www.ncbi.nlm.nih.gov/gene/401024)
[Ensembl: ENSG00000155886](https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000155886)
[UniProt: Q9UPY5](https://www.uniprot.org/uniprot/Q9UPY5)
[OMIM: 607342](https://www.omim.org/entry/607342)

Brain Atlas Resources

[Allen Human Brain Atlas - SLC39A10](https://human.brain-map.org/microarray/search/show?search_term=SLC39A10)
[BrainSpan Atlas of the Developing Human Brain](https://www.brainspan.org/search?gene=SLC39A10)
[Allen Mouse Brain Atlas](https://mouse.brain-map.org/search?query=SLC39A10)
[Allen Cell Type Atlas](https://celltypes.brain-map.org/)

Genetic Variation and Polymorphisms

Genetic variants in SLC39A10 have been studied in the context of neurodegenerative diseases. While specific disease-causing mutations are less well-characterized compared to other zinc transporter genes, polymorphisms in SLC39A10 may influence:

Zinc uptake efficiency: Variants affecting transporter function
Brain expression levels: Regulatory variants affecting gene expression
Disease susceptibility: Association studies in AD and PD cohorts

Regulation of Expression

SLC39A10 expression is regulated by multiple factors:

Zinc status: Zinc availability affects ZIP transporter expression
Hormonal regulation: Thyroid hormones and corticosteroids
Cytokines: Inflammatory cytokines can modulate expression
Cellular stress: Oxidative stress and ER stress responses

Research Directions

Current research areas for SLC39A10 include:

Understanding ZIP transporter structure-function relationships

Developing selective modulators of zinc transport

Elucidating ZIP10-specific roles in neuronal vs. non-neuronal cells

Investigating ZIP10 as a therapeutic target

Determining how ZIP10 dysfunction contributes to specific disease features

Model Systems

Research on SLC39A10 utilizes various model systems:

Cell culture: HEK293, neuronal cell lines, primary neurons
Knockout mice: ZIP10 null mice show immune defects
Zebrafish: Model for developmental studies
In vitro assays: Zinc uptake measurements, transport kinetics

References

[Zhang et al., ZIP10 in immune cell development and function (2015) (2015)](https://pubmed.ncbi.nlm.nih.gov/25632028/)

[Liuzzi et al., Zinc transporters, ZnT and ZIP gene families (2004) (2004)](https://pubmed.ncbi.nlm.nih.gov/15090553/)

[Bush et al., Zinc and Alzheimer's disease (2014) (2014)](https://pubmed.ncbi.nlm.nih.gov/24613826/)

[Mattson et al., Zinc homeostasis in neuronal function and dysfunction (2020) (2020)](https://pubmed.ncbi.nlm.nih.gov/32848260/)

[Unknown, Kawamata & Manfredi, Zinc dysregulation in neurodegenerative diseases (2017) (2017)](https://pubmed.ncbi.nlm.nih.gov/28453035/)

[Taylor et al., ZIP10 expression in breast cancer (2018) (2018)](https://pubmed.ncbi.nlm.nih.gov/29628875/)

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SLC39A10 — Solute Carrier Family 39 Member 10

SLC39A10 — Solute Carrier Family 39 Member 10

Overview

SLC39A10 — Solute Carrier Family 39 Member 10

Overview

Gene Structure and Protein

Biological Function

Zinc Homeostasis

Role in Neuronal Function

Immune System Function

Disease Associations

Alzheimer's Disease

Parkinson's Disease

Amyotrophic Lateral Sclerosis (ALS)

Other Conditions

Expression Patterns

Therapeutic Implications

Interacting Proteins

See Also

External Links

Brain Atlas Resources

Genetic Variation and Polymorphisms

Regulation of Expression

Research Directions

Model Systems

References