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Novel mechanism links mTORC2 and actin filaments to insulin secretion, highlighting GLP-1's role.
The current studies uncover a novel mechanism linking mTORC2 signaling to glucose-stimulated insulin secretion by modulation of the actin filaments. This work also underscores the important role of GLP-1 in rescuing defects in insulin secretion by modulating actin polymerization and suggests that this effect is independent of mTORC2 signaling.
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Blandino-Rosano et al. (2022) studied this question.
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