Mechanism of differential translation regulation of Ins2 splice variants.

<p>Under basal condition, PABP and HuD bind to long variant preferentially causing translation inhibition by making stable inhibitory complex. Upon glucose stimulation activated/phosphorylated PDI brings disulfide bond rearrangement in PABP thereby interfering with the interaction between HuD and PABP. This results in displacement of HuD from insulin transcript into P-bodies. The bound activator complex upregulates insulin translation and insulin is produced.