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Establishment of a membrane contact site (MCS) between endosomal GLP-1R, ERMCS-localised VAPB and SPHKAP leads to the generation of a highly-localised cAMP/PKA signalling hub that triggers the PKA-dependent phosphorylation of the mitochondrial contact site and cristae organising system (MICOS) complex, mitochondrial remodelling, and improved mitochondrial function, leading to potentiation of insulin secretion and survival to ER stress downstream of GLP-1R action

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JX is the guarantor of this work and had full access to all the data in the study and also takes responsibility for the integrity of the data

Compounded formulas do not