A role for PAK1 mediated phosphorylation of β-catenin Ser552 in the regulation of insulin secretion

The presence of adherens junctions and the associated protein β-catenin are requirements for development glucose-stimulated insulin secretion (GSIS) in β-cells. Evidence indicates that modulation function response to changes glucose levels can modulate from β-cells but role phosphorylation this process has not been established. We find a Ser552Ala version attenuates indicating functional Ser552 secretion. This is with alterations F/G actin ratio transcriptional activity β-catenin. Both GLP-1 stimulated serine 552 residue on investigated possibility an EPAC-PAK1 pathway might be involved event. reduction PAK1 using siRNA both effects these β-cell models. Furthermore, EPAC inhibitor ESI-09 IPA3 do same models mouse islets. Together identifies at as part cell signalling mechanism linking nutrient hormonal regulation secretory capacity event regulated downstream