Abstract
Introduction: Glucose entry in pancreatic β-cells triggers insulin secretion and the biosynthesis of insulin secretory granules (SGs). Previously we showed that glucose and cAMP independently promote the binding of PTBP1 to mRNAs for proteins, thus enhancing their stability and translation. PTBP1 is also key for IRES-mediated translation of picornaviruses, including coxsackieviruses B (CVB). It has been suggested that CVB infection may trigger or precipitate type 1 diabetes. Since PTBP1 is required for translation of both picornaviruses and most T1D autoantigens we asked if and how CVB infection of insulin-expressing cells affects the expression of SG proteins.
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