Indirect interaction between p21 and the adenyl cyclase system

1987 ◽  
Vol 11 (3) ◽  
pp. 234
Author(s):  
L GUTIERREZ ◽  
A MAGEE ◽  
L MAHADEVAN ◽  
I MCKAY ◽  
C MARSHALL ◽  
...  
1975 ◽  
Vol 34 (01) ◽  
pp. 042-049 ◽  
Author(s):  
Shuichi Hashimoto ◽  
Sachiko Shibata ◽  
Bokro Kobayashi

SummaryThe radioactive adenosine 3′,5′-monophosphate (cyclic AMP) level derived from 8-14C adenine in intact rabbit platelets decreased in the presence of mitochondrial inhibitor (potassium cyanide) or uncoupler (sodium azide), and markedly increased by the addition of NaF, monoiodoacetic acid (MIA), or 2-deoxy-D-glucose. The stimulative effect of the glycolytic inhibitors was distinctly enhanced by the simultaneous addition of sodium succinate. MIA did neither directly stimulate the adenyl cyclase activity nor inhibit the phosphodiesterase activity. These results suggest that cyclic AMP synthesis in platelets is closely linked to mitochondrial oxidative phosphorylation.


1971 ◽  
Vol 51 (1) ◽  
pp. 67-78 ◽  
Author(s):  
T. ATKINS ◽  
A. J. MATTY

SUMMARY Radiometric estimations of adenyl cyclase and cyclic AMP (cAMP) phosphodiesterase showed significantly higher enzyme activities in the islet tissue of obese-hyperglycaemic mice than in that of their normal litter mates, but the ratios of the two enzymes in both types of islets were found to be the same, i.e. 1:1. Adenyl cyclase and phosphodiesterase activity increased linearly with incubation time and protein concentration. Sodium fluoride (10 mmol/1) increased cyclase activity in the islets of obese mice by 33·4%; theophylline (10 mmol/1) in the presence of cAMP (1 mmol/1) reduced phosphodiesterase activity by almost 100%. Glucose (2 g/1) reduced, while adrenaline (10−5 mol/1) increased cyclase activity in islets from both normal and obese animals. An evaluation of the effects of α- and β-adrenergic receptor stimulating and blocking agents on islets of both normal and obese mice showed the stimulation of adenyl cyclase to be a β-adrenergic receptor function and the inhibition an α-adrenergic receptor function. The possible role of the adenyl cyclase system in diabetes mellitus and insulin secretion is discussed.


1974 ◽  
Vol 2 (3) ◽  
pp. 249-252 ◽  
Author(s):  
P M O'Flanagan

This paper attempts to establish that affective illnesses are disorders involving the whole body, that mood change is not the primary symptom and that the cause may be a biochemical fault, temporary or permanent, genetically transmitted or acquired. It is the author's belief that this fault lies in the adenyl cyclase system. The belief is based upon observations made during an extended study of the treatment of affective disorders with clomipramine infusion (O'Flanagan 1973).


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