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• W2567371399 endingPage "27169" @default.
• W2567371399 startingPage "27160" @default.
• W2567371399 abstract "G protein-coupled receptors (GPCRs) activate PI3K/v-AKT thymoma viral oncoprotein (AKT) to regulate many cellular functions that promote cell survival, proliferation, and growth. However, the mechanism by which GPCRs activate PI3K/AKT remains poorly understood. We used ovarian preantral granulosa cells (GCs) to elucidate the mechanism by which the GPCR agonist FSH via PKA activates the PI3K/AKT cascade. Insulin-like growth factor 1 (IGF1) is secreted in an autocrine/paracrine manner by GCs and activates the IGF1 receptor (IGF1R) but, in the absence of FSH, fails to stimulate YXXM phosphorylation of IRS1 (insulin receptor substrate 1) required for PI3K/AKT activation. We show that PKA directly phosphorylates the protein phosphatase 1 (PP1) regulatory subunit myosin phosphatase targeting subunit 1 (MYPT1) to activate PP1 associated with the IGF1R-IRS1 complex. Activated PP1 is sufficient to dephosphorylate at least four IRS1 Ser residues, Ser318, Ser346, Ser612, and Ser789, and promotes IRS1 YXXM phosphorylation by the IGF1R to activate the PI3K/AKT cascade. Additional experiments indicate that this mechanism also occurs in breast cancer, thyroid, and preovulatory granulosa cells, suggesting that the PKA-dependent dephosphorylation of IRS1 Ser/Thr residues is a conserved mechanism by which GPCRs signal to activate the PI3K/AKT pathway downstream of the IGF1R." @default.
• W2567371399 created "2017-01-06" @default.
• W2567371399 creator A5018150817 @default.
• W2567371399 creator A5054486557 @default.
• W2567371399 creator A5065856781 @default.
• W2567371399 date "2016-12-01" @default.
• W2567371399 modified "2023-10-17" @default.
• W2567371399 title "G protein-coupled receptors (GPCRs) That Signal via Protein Kinase A (PKA) Cross-talk at Insulin Receptor Substrate 1 (IRS1) to Activate the phosphatidylinositol 3-kinase (PI3K)/AKT Pathway" @default.
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• W2567371399 doi "https://doi.org/10.1074/jbc.m116.763235" @default.
• W2567371399 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5207145" @default.
• W2567371399 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27856640" @default.
• W2567371399 hasPublicationYear "2016" @default.
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