Inappropriate movement of Rac1 contributes to glucotoxicity of the islet β-cell

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• Glucotoxicity promotes aberrant activation and mislocalization of Ras-related C3 botulinum toxin substrate 1 [Rac1] and metabolic dysfunction in pancreatic islet β-cells: Reversal of such metabolic defects by metformin
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• Tiam1/Vav2-Rac1 axis: A tug-of-war between islet function and dysfunction
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