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Table 1 ZnT proteins- expression and physiological roles.

From: Mechanism and Regulation of Cellular Zinc Transport

  Expression pattern Cellular distribution Disease model Altered expression phenotype Ref
ZnT-1 Ubiquitous Plasma membrane   Overexpression: reduced [Zn2+] i and enhanced resistance against Zn2+ toxicity, KO: Lethal at embryonic stage, (37,42,43,71)
ZnT-2 small intestine, kidney, placenta, pancreas, testis, seminal vesicles, and mammary gland Vesicles, lysosomes   Overexpression: enhanced lysosomal and vesicular Zn2+ accumulation (72,73)
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 (49,74)
ZnT-4 mammary gland, brain, small intestine and mast cells Intracellular compartments Lethal milk syndrome in mice, Asthma (mice), Alzheimer’s disease   (7579)
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. (5355,59,80)
ZnT-6 liver, brain, and small Intestine Complexed with ZnT-5 Alzheimer’s disease (mice)   (53,57,79)
ZnT-7 small intestine, liver, retina, spleen, kidney, and lung Golgi   Essential for folding and secretion of Zn2+ -binding enzymes, (54,81,82)
ZnT-8 Pancreatic β-cells Insulin secretory vesicles Polymorphism marker in diabetes type II Overexpression: enhances glucose dependent insulin secretion (6062)