HIGHLIGHTS
SUMMARY
In MANF-deficient mice, UPR pathways are chronically activated in pancreatic b_cells, neurons, anterior pituitary, and liver, demonstrating that MANF is a crucial regulator of UPR in_vivo. IRE1a non-binding mutant of MANF is unable to regulate IRE1a activity, lacks prosurvival effect in_vitro in SCG and DA neurons, and is inactive in_vivo in an animal model of PD. The authors hypothesized that BiP can prevent the interaction between MANF and IRE1a LD if MANF and BiP have the overlapping binding_site on IRE1a LD. Since the MANF binding_site in IRE1a LD overlaps that of BiP . . .
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