Zinc uptake transporter, ZIP8, belongs to the SLC39 transporter family. ZIP transporters are responsible for zinc transport into the cytoplasm across cellular membranes, either influx from the extracellular space or efflux from intracellular organelles. Regulation and maintenance of proper concentration and distribution of cellular zinc nutrient by ZIP transporters are essential to the function, metabolism, growth, proliferation and survival of cells^1,2.

ZIP structure contains eight predicted transmembrane (TM) domains while the N- and C-termini are extracellular. A long loop region is present between TM3 and TM4 domains, harboring a histidine-rich region. TM4 and TM5 domains are amphipathic and are thought to form a cavity through which metals are transported¹.

ZIP8 protein is encoded by the SLC39A8 gene and is highly expressed in T cells. ZIP8 also plays an important role at the onset of inflammation².

Zinc deficiency can cause growth retardation, cognitive impairment, metabolic disorders, infertility, dysfunction of the immune system, abnormalities in T-cells, natural killer cells and monocytes, and reduction in antibody formation^1,2. Studies exploring knockdown of ZIP8 protein show a reduction of cellular zinc content, impaired mitochondrial function in response to TNF-α and increased cell death².