Abstract
The reason for preferential autoimmunity towards insulin, ICA512/IA-2 and other cargoes of beta cell secretory granules in type 1 diabetes (T1D) remains unknown. We have shown that glucose stimulation of beta cells rapidly and selectively up-regulates the Polypyrimidine tract binding protein 1 (PTBP1) -dependent cap-independent translation of granule precursor cargoes, including proinsulin, proICA512/IA-2, prochromogranin A and hormone convertases proPC1/3 and proPC2 [Knoch, K.-P. et al. 2014]. PTBP1-dependent cap-independent translation is also required for replication of Enteroviruses (Evs) in beta cells potentially triggering or accelerating T1D onset, such as Coxsackieviruses B or Echoviruses.
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