Results 41 to 50 of about 9,380 (213)

GRK6 regulates the hemostatic response to injury through its rate-limiting effects on GPCR signaling in platelets. [PDF]

open access: yes, 2020
G protein-coupled receptors (GPCRs) mediate the majority of platelet activation in response to agonists. However, questions remain regarding the mechanisms that provide negative feedback toward activated GPCRs to limit platelet activation and thrombus ...
Benovic, Jeffrey   +13 more
core   +1 more source

G protein-coupled receptor kinase 2 (GRK2) is localized to centrosomes and mediates epidermal growth factor-promoted centrosomal separation. [PDF]

open access: yes, 2013
G protein-coupled receptor kinases (GRKs) play a central role in regulating receptor signaling, but recent studies suggest a broader role in modulating normal cellular functions.
Benovic, Jeffrey L   +4 more
core   +2 more sources

Regulation of GPR54 Signaling by GRK2 and β-Arrestin [PDF]

open access: yesMolecular Endocrinology, 2009
AbstractKisspeptin and its receptor, GPR54, are major regulators of the hypothalamic-pituitary-gonadal axis as well as regulators of human placentation and tumor metastases. GPR54 is a Gq/11-coupled G protein-coupled receptor (GPCR), and activation by kisspeptin stimulates phosphatidy linositol 4, 5-biphosphate hydrolysis, Ca2+ mobilization ...
Macarena, Pampillo   +8 more
openaire   +2 more sources

GRK2: putting the brakes on the circadian clock

open access: yesReceptors & Clinical Investigation, 2016
G protein-coupled receptor kinases (GRKs) are a family of serine/threonine protein kinases that terminate G protein-coupled receptor (GPCR) signaling by phosphorylating the receptor and inducing its internalization. In addition to their canonical function, some GRKs can phosphorylate non-GPCR substrates and regulate GPCR signaling in a kinase ...
Lucia, Mendoza-Viveros   +2 more
openaire   +2 more sources

Structural and Functional Analysis of a β2-Adrenergic Receptor Complex with GRK5. [PDF]

open access: yes, 2017
The phosphorylation of agonist-occupied G-protein-coupled receptors (GPCRs) by GPCR kinases (GRKs) functions to turn off G-protein signaling and turn on arrestin-mediated signaling.
Adams, Christopher M.   +12 more
core   +2 more sources

Interaction between the Conserved Region in the C-terminal Domain of GRK2 and Rhodopsin Is Necessary for GRK2 to Catalyze Receptor Phosphorylation [PDF]

open access: yesJournal of Biological Chemistry, 2000
The C-terminal domain of G protein-coupled receptor kinases (GRKs) consists of a conserved region and a variable region, and the variable region has been shown to direct the membrane translocation of cytosolic enzymes. The present work has revealed that the C-terminal domain may also be involved in kinase-receptor interaction that is primarily mediated
X Q, Gan   +6 more
openaire   +2 more sources

Degradation of GRK2 and AKT is an early and detrimental event in myocardial ischemia/reperfusionResearch in context

open access: yesEBioMedicine, 2019
Background: Identification of signaling pathways altered at early stages after cardiac ischemia/reperfusion (I/R) is crucial to develop timely therapies aimed at reducing I/R injury.
Petronila Penela   +5 more
doaj   +1 more source

Mdm2-Mediated Downmodulation of GRK2 Restricts Centrosome Separation for Proper Chromosome Congression

open access: yesCells, 2021
The timing of centrosome separation and the distance moved apart influence the formation of the bipolar spindle, affecting chromosome stability. Epidermal growth factor receptor (EGFR) signaling induces early centrosome separation through downstream G ...
Clara Reglero   +4 more
doaj   +1 more source

Role of G protein-coupled receptor kinases in cell migration [PDF]

open access: yes, 2014
G protein-coupled receptor kinases (GRKs) are emerging as important integrative nodes in cell migration processes. Recent evidence links GRKs (particularly the GRK2 isoform) to the complex modulation of diverse aspects of cell motility.
Mayor, Federico   +2 more
core   +2 more sources

Myocardial pathology induced by aldosterone is dependent on non-canonical activities of G protein-coupled receptor kinases [PDF]

open access: yes, 2016
Hyper-aldosteronism is associated with myocardial dysfunction including induction of cardiac fibrosis and maladaptive hypertrophy. Mechanisms of these cardiotoxicities are not fully understood. Here we show that mineralocorticoid receptor (MR) activation
CANNAVO, ALESSANDRO   +10 more
core   +1 more source

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