Identification of a Short Sequence Highly Divergent Between beta-Adrenergic-Receptor Kinases 1 and 2 that Determines the Affinity of Binding to betagamma Subunits of Heterotrimeric Guanine-Nucleotide-Binding Regulatory Proteins

1997 ◽  
Vol 245 (3) ◽  
pp. 533-540 ◽  
Author(s):  
Tsu Tshen Chuang ◽  
Elena Pompili ◽  
Lina Paolucci ◽  
Michele Sallese ◽  
Luca Gioia ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Nucleotide Binding ◽  
Regulatory Proteins ◽  
Guanine Nucleotide ◽  
Short Sequence ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic ◽  
Receptor Kinases ◽  
Betagamma Subunits ◽  
Guanine Nucleotide Binding

Hepatocyte beta-adrenergic responsiveness and guanine nucleotide-binding regulatory proteins

1989 ◽  
Vol 256 (2) ◽  
pp. C384-C389 ◽  
Author(s):  
J. A. Garcia-Sainz ◽  
M. E. Huerta-Bahena ◽  
C. C. Malbon
Keyword(s):  
Binding Protein ◽  
Nucleotide Binding ◽  
Regulatory Proteins ◽  
Guanine Nucleotide ◽  
Guanine Nucleotide Binding Protein ◽  
Beta Adrenergic ◽  
Adp Ribosylation ◽  
Liver Membranes ◽  
Guanine Nucleotide Binding ◽  
Nucleotide Binding Protein

Hepatocytes isolated from hypothyroid, adrenalectomized, or partially hepatectomized rats display an enhanced beta-adrenergic responsiveness as compared with cells from control animals. The enhanced beta-adrenergic responsiveness is evidenced by both increased ureagenesis and adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in response to isoproterenol. The role of stimulatory guanine nucleotide-binding protein (Gs) and inhibitory guanine nucleotide-binding protein (Gi) in the enhanced responsiveness was studied. It was observed, contrary to what would have been anticipated, that the level of Gs [as reflected by cholera toxin-catalyzed ADP ribosylation, 5'-guanosine gamma-thiotriphosphate (GTP gamma S)-stimulated adenylate cyclase activity, and a functional reconstitution assay] was decreased in liver membranes from adrenalectomized and partially hepatectomized rats as compared with the controls. Furthermore, the level of Gi was increased in these conditions as reflected by pertussis toxin-catalyzed ADP ribosylation. The data suggest that changes in beta-adrenergic receptor levels rather than the levels of guanine nucleotide-binding (G) regulatory proteins predominate in regulation of hepatic beta-adrenergic responses by hypothyroidism, adrenalectomy, or partial hepatectomy.

Effect of exercise duration on density and coupling of beta-adrenergic receptors on human mononuclear cells

1989 ◽  
Vol 66 (3) ◽  
pp. 1494-1500 ◽  
Author(s):  
M. J. Frey ◽  
D. Mancini ◽  
D. Fischberg ◽  
J. R. Wilson ◽  
P. B. Molinoff
Keyword(s):  
Heart Rate ◽  
Adrenergic Receptors ◽  
Regulatory Protein ◽  
Nucleotide Binding ◽  
Plasma Norepinephrine ◽  
Base Line ◽  
Guanine Nucleotide ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Guanine Nucleotide Binding

The effect of maximal exercise on lymphocyte beta-adrenergic receptors was examined in 26 normal subjects. Exercise increased O2 consumption (Vo2) from 5 +/- 1 to 50 +/- 4 ml.min-1.kg-1, plasma norepinephrine level from 188 +/- 28 to 2,682 +/- 160 pg/ml, and plasma epinephrine level from 94 +/- 72 to 857 +/- 180 pg/ml. The density of beta-adrenergic receptors on lymphocytes obtained at rest was 31 +/- 3.7 fmol/mg protein; exercise increased the density of receptors by 86 +/- 33% (range 0–257%) to 58.3 +/- 1.5 fmol/mg protein but did not alter the affinity of the receptor for [125I]iodopindolol or the coupling of the receptor to the guanine nucleotide-binding regulatory protein. The density of beta-adrenergic receptors increased progressively throughout exercise and paralleled the increase in heart rate. The magnitude of the change in the density of beta-adrenergic receptors did not correlate with the magnitude of the increase in heart rate, Vo2, or plasma levels of catecholamines. The density of receptors was still elevated 15 min after completion of exercise but fell below base line 1 h after peak exercise to 18.2 +/- 6.7 fmol/mg protein (P less than 0.05 vs. base-line levels). These results demonstrate that exhaustive exercise results in a progressive increase in the number of beta-adrenergic receptors on lymphocyte membranes, followed by a reduction in the density of receptors during the recovery phase of exercise. Despite a significant increase in the level of plasma catecholamines, the receptor remains coupled to the guanine nucleotide-binding regulatory protein.

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