scholarly journals Monoclonal antibodies to the guanine-nucleotide binding proteins of adenylate cyclase

1986 ◽  
Vol 236 (1) ◽  
pp. 267-271 ◽  
Author(s):  
R B Lingham ◽  
P J Brown ◽  
V Holcombe ◽  
C L Schreiber
Keyword(s):  
Monoclonal Antibodies ◽  
Adenylate Cyclase ◽  
Regulatory Proteins ◽  
Beta Subunits ◽  
Guanine Nucleotide ◽  
Activated State ◽  
Guanine Nucleotide Regulatory Proteins ◽  
Guanine Nucleotide Binding ◽  
Nucleotide Binding Proteins ◽  
Guanine Nucleotide Binding Proteins

Monoclonal antibodies (Mabs) to the stimulatory (Ns) and inhibitory (Ni) guanine nucleotide regulatory proteins associated with adenylate cyclase have been developed. Two Mabs (2A3 and 5G12), which are of the IgG2b subclass, recognize the beta-subunits (beta) of Ns, Ni and transducin. Iodinated beta can be immunoprecipitated by either Mab coupled to Affi-Gel 10 and this can be decreased by prior incubation of the Mabs with excess unlabelled beta. The Mabs stabilize the activated state of Ns while decreasing the rate of deactivation of activated Ns in the presence of beta.

Effects of exercise on myocardial adenylate cyclase and Gi alpha expression in senescence

1993 ◽  
Vol 264 (3) ◽  
pp. H805-H814 ◽  
Author(s):  
M. Bohm ◽  
H. Dorner ◽  
P. Htun ◽  
H. Lensche ◽  
D. Platt ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Physical Training ◽  
Binding Proteins ◽  
Guanine Nucleotide ◽  
Aged Rats ◽  
Guanine Nucleotide Binding ◽  
Nucleotide Binding Proteins ◽  
Guanine Nucleotide Binding Proteins ◽  
Gs Alpha ◽  
Camp Formation

The present study investigated the influence of physical training on alterations leading to reduced adenosine 3–,5–-cyclic monophosphate (cAMP) formation in aged myocardium. Senescent (28-mo-old) rats underwent a moderate treadmill exercise program and were compared with sedentary controls. In myocardial membranes from aged rats, isoprenaline-stimulated adenylate cyclase activity (AC) was reduced compared with that in young animals and was accompanied by an increase of pertussis toxin substrates (17.5%) and an increased amount of immunodetectable inhibitory guanine nucleotide-binding proteins (Gi alpha; 72%). Physical training reduced the amount of Gi alpha proteins (30–35%) in young and old animals and enhanced only isoprenaline-stimulated AC in the aged rats, and basal and 5'-guanylylimidodiphosphate [Gpp(NH)p]- as well as isoprenaline-stimulated AC in young rats. Physical training or aging had no effect on the number of beta-adrenoceptors or m-cholinoceptors or on forskolin-stimulated AC in either group. The amount of immunodetectable stimulatory guanine nucleotide-binding proteins (Gs alpha) using an antiserum raised against the COOH-terminal peptide of Gs alpha (RMHLRQYELL) was unchanged in either condition. It is concluded that enhanced Gi alpha expression might be one mechanism leading to depressed cAMP formation in aged myocardium. Depressed AC and increased Gi alpha can be partially reversed by physical training, especially in young myocardium. Gi alpha might serve as a regulator of cardiac AC in a variety of physiological and pathophysiological situations in the absence of beta-adrenoceptor changes.

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