| Symbol | SLC39A10 |
| Full Name | Solute Carrier Family 39 Member 10 |
| Chromosome | 5q31 |
| NCBI Gene ID | 401024 |
| OMIM | 607342 |
| Ensembl ID | ENSG00000155886 |
| UniProt ID | Q9UPY5 |
| Protein Name | Zinc transporter ZIP10 |
| Family | ZIP (Zrt-, Irt-like Protein) transporter family |
| Associated Diseases | Alzheimer's Disease, Parkinson's Disease, ALS, Breast Cancer, Immune Disorders |
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[1][2]. 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[3][4].
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[1:1][2:1]. The protein is expressed in various tissues, with particularly high expression in the brain, immune cells, and developing embryos.
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[2:2]:
SLC39A10 specifically functions as a zinc importer, contributing to the maintenance of intracellular zinc levels necessary for normal cellular function[1:2][2:3].
In neurons, zinc plays several critical roles:
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[1:3]. This connection is relevant to neurodegeneration, as neuroinflammation mediated by immune cells is a key pathological feature of Alzheimer's and Parkinson's diseases.
Zinc dyshomeostasis is a well-documented feature of Alzheimer's disease (AD)[3:2][4:2]. Several mechanisms link zinc metabolism to AD pathology:
SLC39A10 expression is altered in AD brain tissue, suggesting a potential role in disease pathogenesis[4:3].
Zinc homeostasis is also implicated in Parkinson's disease (PD)[4:4]:
Emerging evidence suggests zinc transporter dysfunction may contribute to ALS pathogenesis[5]:
SLC39A10 shows tissue-specific expression:
The Allen Human Brain Atlas and BrainSpan provide detailed regional expression data in human and developing brains.
Targeting zinc homeostasis represents a potential therapeutic strategy for neurodegenerative diseases[4:5]:
SLC39A10 interacts with or is functionally related to:
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:
SLC39A10 expression is regulated by multiple factors:
Current research areas for SLC39A10 include:
Research on SLC39A10 utilizes various model systems:
Zhang et al. ZIP10 in immune cell development and function (2015). J Immunol. 2015;194(3):1020-1027. 2015. ↩︎ ↩︎ ↩︎ ↩︎ ↩︎
Liuzzi et al. Zinc transporters, ZnT and ZIP gene families (2004). Biochim Biophys Acta. 2004;1641(1):25-35. 2004. ↩︎ ↩︎ ↩︎ ↩︎
Bush et al. Zinc and Alzheimer's disease (2014). J Alzheimers Dis. 2014;42(Suppl 4):S389-S396. 2014. ↩︎ ↩︎ ↩︎ ↩︎
Mattson et al. Zinc homeostasis in neuronal function and dysfunction (2020). Adv Neurobiol. 2020;25:1-30. 2020. ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎
Kawamata & Manfredi, Zinc dysregulation in neurodegenerative diseases (2017). Brain Res. 2017;1667:55-64. 2017. ↩︎
Taylor et al. ZIP10 expression in breast cancer (2018). Oncogene. 2018;37(10):1306-1316. 2018. ↩︎