Titlebook: G Protein-Coupled Receptor Kinases; Vsevolod V. Gurevich,Eugenia V. Gurevich,John J.G. Book 2016 Springer Science+Business Media New York

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100 Jahre Dermatologische Klinik Zürich control GPCRs activation of effectors that depend on the G protein βγ subunits (Gβγ), independent of their catalytic activity. GPCR-coupled potassium channels (GIRK) are found in excitable tissues such as neurons, heart, and endocrine organs, where they are known to decrease cells’ excitability fol

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https://doi.org/10.1007/978-3-0348-6714-6eptor desensitization, a procedure initiated by a group of kinases, including GPCR kinases (GRKs). GRK2 upregulation and GRK5 deficiency were reported to occur in Alzheimer’s disease. GRK2 accumulation was proposed to participate in cerebral vascular pathology, whereas GRK5 deficiency is believed to

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100 Jahre Schiffbautechnische Gesellschaftin-coupled receptors (GPCRs). Agonist-activated GPCRs are selectively phosphorylated by GRKs, whereupon arrestin proteins bind active phosphoreceptors, blocking further G protein activation, facilitating GPCR internalization via coated pits, and initiating G protein-independent round of signaling. G

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100 Keywords Wirtschaftsprüfungroteins that transduce cell signals via heterotrimeric G proteins from neurohormones, ions, and sensory stimuli to regulate virtually every aspect of mammalian physiology. In the normal and diseased heart, it is apparent that major players include the β-adrenergic receptors (βARs) and the angiotensi

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https://doi.org/10.1007/978-3-642-17267-0gnaling. Proteins of the arrestin family then bind to the phosphorylated receptor, blocking both receptor and G-protein reactivation. Thus, GRKs are critical regulators of GPCR signaling that function to protect cells against receptor overstimulation, maintain sensitivity to changing environmental s

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