{{.infobox .infobox-gene}}
| Symbol | SLC39A2 |
| Full Name | Solute Carrier Family 39 Member 2 |
| Chromosome | 14q11.2 |
| NCBI Gene ID | 54101 |
| OMIM | 608739 |
| Ensembl ID | ENSG00000141882 |
| UniProt ID | Q9H3Y0 |
| Associated Diseases | Alzheimer's disease, Parkinson's disease, acrodermatitis enteropathica |
SLC39A2 (Solute Carrier Family 39 Member 2), also known as ZIP2, is a zinc transporter protein that belongs to the ZIP (Zrt-, Irt-like Protein) family of metal ion transporters.[1] This protein plays a critical role in cellular zinc homeostasis by facilitating zinc uptake into the cytoplasm from the extracellular space and intracellular compartments.
Zinc is an essential trace metal that serves as a catalytic cofactor for over 300 enzymes and a structural component of numerous proteins. In the brain, zinc is particularly important for neuronal function, synaptic signaling, and antioxidant defense. Dysregulation of zinc homeostasis has been implicated in various neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD).[2]
| Property | Value |
|---|---|
| Gene Symbol | SLC39A2 |
| Protein Name | Zinc transporter ZIP2 |
| Gene Family | SLC39 (ZIP) family |
| Chromosomal Location | 14q11.2 |
| Gene ID (NCBI) | 54101 |
| Protein Length | 310 amino acids |
| UniProt ID | Q9H3Y0 |
| Tissue Specificity | Broad, highest in prostate, kidney, intestine |
ZIP2 is a multi-pass transmembrane protein predicted to contain 8 transmembrane domains. Like other ZIP family members, it features a histidine-rich motif in the extracellular loop that may serve as a zinc-binding site. The protein is localized to the plasma membrane where it functions as a zinc importer.
ZIP2 facilitates zinc transport through a proton-coupled mechanism:
ZIP2 expression is regulated at multiple levels:
Zinc homeostasis is critically disrupted in Alzheimer's disease:[3]
| Approach | Mechanism | Development Status |
|---|---|---|
| Zinc supplementation | Restore cellular zinc levels | Investigational |
| ZIP inhibitors | Block pathological zinc influx | Preclinical |
| Zinc chelation | Reduce excess zinc in specific contexts | Research phase |
Key areas of ongoing research include:
Kim et al. ZIP family zinc transporters (2004). 2004. ↩︎
Grabrucker et al. Zinc homeostasis in the brain (2011). 2011. ↩︎
Bush et al. Zinc and Alzheimer's disease (2003). 2003. ↩︎