Slc39a4 in the small intestine predicts zinc absorption and utilization: a comprehensive analysis of zinc transporter expression in response to diets of varied zinc content in young mice.
While Zip4 was not found to be essential for proper glucose homeostasis and insulin secretion in vivo in mice this study found that Zip4 mediates increases in cytoplasmic and granular zinc pools and stimulates glucose dependent insulin secretion in-vitro
These studies strongly suggest that wasting and lethality in acrodermatitis enteropathica patients reflects the loss-of-function of the intestine zinc transporter ZIP4 which leads to abnormal Paneth cell gene expression
Cell migration assays revealed that RNAi knockdown of Zip4 in Hepa cells depressed in vitro migration whereas forced over-expression in Hepa cells and MCF-7 cells enhanced in vitro migration
ZIP4 physically interacts with tPA correlating with an increased intracellular zinc influx and lysosomal sequestration after excitotoxin stimulation. Changes in prosurvival signals support the idea that this sequestration results in neuroprotection.
We'd like to inform you that we have updated our Privacy Notice to comply with Europe’s new General Data Protection Regulation (GDPR) that applies since 25 May 2018.