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  • Toward understanding the role of G-protein signaling
    Every GPCR activates a unique set of downstream signals, depending on their signaling partners To understand the roles of individual GPCRs, it is important to elucidate how GPCRs activate divergent signaling pathways
  • Structure, Function, Pharmacology, and Therapeutic Potential . . .
    Pharmacological agents to inhibit downstream signaling intermediated of Gαq Once GPCR is activated by its agonist, Gαq signaling activates phospholipase C β (PLCβ), which leads to the hydrolysis of phosphatidylinositol 4,5-biphosphate (PIP 2) and diacylglycerol (DAG)
  • 12 Neurotransmitter Action: G-Protein-Coupled Receptors
    These receptors activate G-proteins upon neurotransmitter binding, leading to the initiation of diverse intracellular signaling cascades that regulate ion channels, protein activity, and gene transcription
  • Side-by-side comparison of the effects of Gq- and Gi-DREADD . . .
    Here, we show that agonism of Gq-DREADDs, but not Gi-DREADDs, induced consistent increases in spontaneous astrocytic Ca 2+ events Moreover, we demonstrate that both Gq-DREADD as well as Gi-DREADD-mediated activation of CA1 astrocytes induces long-lasting synaptic potentiation in the hippocampal CA1 Schaffer collateral pathway in the absence of
  • A molecular mechanism to diversify Ca2+ signaling downstream . . .
    We show, using CRISPR Cas9 genome-editing and pharmacological perturbations, that Gs-GPCRs—via Gs-derived Gβγ—partake in inositol-lipid signaling by providing the key mediator—Ca 2+ —for
  • Biochemistry : G Protein Pathway - Varsity Tutors
    Upon binding of a ligand to a GPCR, a conformational change in the receptor is transmitted to a G protein bound to the cell membrane within the cell This subsequently causes the alpha-subunit of the G protein to lose its bound GDP, and in exchange it receives GTP





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