SLC39A7 (ZIP7) is a zinc transporter localized to the endoplasmic reticulum (ER) and Golgi apparatus that mediates zinc release from intracellular stores to the cytosol, serving as a critical regulator of cytosolic zinc homeostasis 12. The protein requires post-translational phosphorylation for activation and subsequently activates downstream pathways promoting cell growth and proliferation 34. SLC39A7 functions as a rate-limiting factor in endoplasmic reticulum-associated protein degradation (ERAD) by enhancing Rpn11-mediated deubiquitination of misfolded proteins, with therapeutic potential in neurodegenerative diseases 5. The protein plays essential roles in B cell development and receptor signaling 6, and maintains mitochondrial zinc homeostasis through formation of NLRX1-SLC39A7 complexes that regulate mitochondrial dynamics and mitophagy 78. SLC39A7 mediates zinc-induced ferroptosis and protects against ER stress 910. Disease relevance includes agammaglobulinemia 9 (autosomal recessive) and contributions to intervertebral disc degeneration, colorectal cancer proliferation (via Akt/mTOR signaling), gastric cancer progression (regulated by miR-139-5p), systemic sclerosis-associated skin fibrosis, and hepatotoxicity under PFOS exposure 11121314. Additionally, METTL9-mediated methylation of SLC39A7 suppresses ferroptosis and regulates mesenchymal stem cell adipogenesis, with implications for osteoporosis 15.
No tissue expression data available for this gene.