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It is thus tempting to suggest that in addition to modulating GLP-1R desensitization and thus the GLP-1R/Gs/cAMP axis, GRK2 may regulate GLP-1R-dependent insulin release by sequestering -arrestin1 away from EPAC2 (see scheme in Fig

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Notably, AzaA8 achieved these benefits without the need for fatty acid derivatization or other extensive modifications beyond the aza-substitution

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