| Expression pattern | Cellular distribution | Disease model | Altered expression phenotype | Ref |
---|---|---|---|---|---|
ZnT-1 | Ubiquitous | Plasma membrane | Â | Overexpression: reduced [Zn2+] i and enhanced resistance against Zn2+ toxicity, KO: Lethal at embryonic stage, | |
ZnT-2 | small intestine, kidney, placenta, pancreas, testis, seminal vesicles, and mammary gland | Vesicles, lysosomes | Â | Overexpression: enhanced lysosomal and vesicular Zn2+ accumulation | |
ZnT-3 | brain | Synaptic vesicles (Glutamatergic and GABAergic) |  | KO: synaptic Zn2+ deficiency, enhanced susceptibility to seizure, loss of gender specific Alzheimer’s disease plaque formation in a mouse model, decreased susceptibility to amyloid angiopathy | |
ZnT-4 | mammary gland, brain, small intestine and mast cells | Intracellular compartments | Lethal milk syndrome in mice, Asthma (mice), Alzheimer’s disease |  | |
ZnT-5 | Pancreatic β-cells, intestine, heart brain, liver, kidney | Insulin secretory vesicles, Golgi Spliced isoform: plasma membrane Complexed with ZnT-6 |  | KO: poor growth, osteopenia, male specific fatal arrhythmias. Essential for folding and secretion of Zn2+ -binding enzymes. | |
ZnT-6 | liver, brain, and small Intestine | Complexed with ZnT-5 | Alzheimer’s disease (mice) |  | |
ZnT-7 | small intestine, liver, retina, spleen, kidney, and lung | Golgi | Â | Essential for folding and secretion of Zn2+ -binding enzymes, | |
ZnT-8 | Pancreatic β-cells | Insulin secretory vesicles | Polymorphism marker in diabetes type II | Overexpression: enhances glucose dependent insulin secretion |