G protein-coupled receptor kinase 4γ interacts with inactive Gαs and Gα13

Keever, Lindsay B.; Jones, John E.; Andresen, Bradley T.

doi:10.1016/j.bbrc.2007.12.181

Cited by 8 publications

(5 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, GRK4 has constitutive activity under basal conditions, which may, in part, be due to its ability to bind to inactive Gα S and Gα 13 subunits. 31 It is the only GRK subtype that is capable of phosphorylating unstimulated GPCRs. 32 GRK4 is expressed in a limited number of tissues, e.g., artery, bone, cerebellum, heart, kidney, myometrium, small intestines, and testes, unlike GRK2, GRK3, GRK5, and GRK6, which are ubiquitously expressed.…”

Section: Role Of Grk4 In Hypertensionmentioning

confidence: 99%

G Protein-Coupled Receptor Kinase 4

et al. 2015

Self Cite

View full text Add to dashboard Cite

Section: Role Of Grk4 In Hypertensionmentioning

confidence: 99%

G Protein-Coupled Receptor Kinase 4

et al. 2015

Self Cite

View full text Add to dashboard Cite

“…GRK4 is constitutively active which may be due to its ability to bind to inactive G α S and Gβ subunits (319). Unlike the other GRKs, GRK4 has several splice variants; four ( α , β, γ, and δ ) have been reported in humans, five (A, B, C, D, E) in rats, and one in mice (493,494,527,537,637).…”

Section: Regulation Of Dopamine Receptor Functionmentioning

confidence: 99%

Dopamine and Renal Function and Blood Pressure Regulation

Armando

Villar

José

2011

Comprehensive Physiology

104

215

View full text Add to dashboard Cite

Dopamine is an important regulator of systemic blood pressure via multiple mechanisms. It affects fluid and electrolyte balance by its actions on renal hemodynamics and epithelial ion and water transport and by regulation of hormones and humoral agents. The kidney synthesizes dopamine from circulating or filtered L-DOPA independently from innervation. The major determinants of the renal tubular synthesis/release of dopamine are probably sodium intake and intracellular sodium. Dopamine exerts its actions via two families of cell surface receptors, D1-like receptors comprising D1R and D5R, and D2-like receptors comprising D2R, D3R, and D4R, and by interactions with other G protein-coupled receptors. D1-like receptors are linked to vasodilation, while the effect of D2-like receptors on the vasculature is variable and probably dependent upon the state of nerve activity. Dopamine secreted into the tubular lumen acts mainly via D1-like receptors in an autocrine/paracrine manner to regulate ion transport in the proximal and distal nephron. These effects are mediated mainly by tubular mechanisms and augmented by hemodynamic mechanisms. The natriuretic effect of D1-like receptors is caused by inhibition of ion transport in the apical and basolateral membranes. D2-like receptors participate in the inhibition of ion transport during conditions of euvolemia and moderate volume expansion. Dopamine also controls ion transport and blood pressure by regulating the production of reactive oxygen species and the inflammatory response. Essential hypertension is associated with abnormalities in dopamine production, receptor number, and/or posttranslational modification.

show abstract

“…This may be due to its ability to bind to inactive Gα S and Gβ subunits [125]. Unlike the other GRKs, GRK4 has several splice variants.…”

Section: 4 Grk4 Isoforms and Renal Dopamine Receptorsmentioning

confidence: 99%

Dopamine and G protein-coupled receptor kinase 4 in the kidney: Role in blood pressure regulation

José

Soares-da-Silva

Eisner

et al. 2010

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

138

View full text Add to dashboard Cite

Complex interactions between genes and environment result in a sodium-induced elevation in blood pressure (salt sensitivity) and/or hypertension that lead to significant morbidity and mortality affecting up to 25% of the middle-aged adult population worldwide. Determining the etiology of genetic and/or environmentally-induced high blood pressure has been difficult because of the many interacting systems involved. Two main pathways have been implicated as principal determinants of blood pressure since they are located in the kidney (the key organ responsible for blood pressure regulation), and have profound effects on sodium balance: the dopaminergic and renin-angiotensin systems. These systems counteract or modulate each other, in concert with a host of intracellular second messenger pathways to regulate sodium and water balance. In particular, the G protein-coupled receptor kinase type 4 (GRK4) appears to play a key role in regulating dopaminergic-mediated natriuresis. Constitutively activated GRK4 gene variants (R65L, A142V, and A486V), by themselves or by their interaction with other genes involved in blood pressure regulation, are associated with essential hypertension and/or salt-sensitive hypertension in several ethnic groups. GRK4γ 142V transgenic mice are hypertensive on normal salt intake while GRK4γ 486V transgenic mice develop hypertension only with an increase in salt intake. GRK4 gene variants have been shown to hyperphosphorylate, desensitize, and internalize two members of the dopamine receptor family, the D1 (D1R) and D3 (D3R) dopamine receptors, but also increase the expression of a key receptor of the renin-angiotensin system, the angiotensin type 1 receptor (AT1R). Knowledge of the numerous blood pressure regulatory pathways involving angiotensin and dopamine may provide new therapeutic approaches to the pharmacological regulation of sodium excretion and ultimately blood pressure control.

show abstract

G protein-coupled receptor kinase 4γ interacts with inactive Gαs and Gα13

Cited by 8 publications

References 18 publications

G Protein-Coupled Receptor Kinase 4

G Protein-Coupled Receptor Kinase 4

Dopamine and Renal Function and Blood Pressure Regulation

Dopamine and G protein-coupled receptor kinase 4 in the kidney: Role in blood pressure regulation

Contact Info

Product

Resources

About