Abstract
Glucose entry in the pancreatic beta cell triggers insulin secretion and the rapid biosynthesis of insulin granules (ISGs). We have shown that glucose and cAMP independently promote the nucleocytoplasmic translocation of polypyrimidine tract-binding protein (PTBP1) in beta cells (Knoch et al., 2004 and 2006). Cytosolic PTBP1 binds the mRNAs encoding ISG proteins, thus enhancing their stability and translation. PTBP1 can also foster the IRES-mediated translation of picornaviruses, including enteroviruses. Several prospective studies have suggested that enterovirus infection may trigger type 1 diabetes, Thus, we investigated whether diabetogenic enteroviruses hijack the machinery for ISG biogenesis, and in particular PTBP1, for their effective propagation in beta cells.
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