Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.4.21.5 (
thrombin
)
33,306
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Thrombin-stimulated platelet secretion is accompanied by a 30% reduction in the steady state level of cytosolic ATP, a breakdown that proceeds through ADP, AMP, IMP, and inosine to hypoxanthine. The ATP to hypoxanthine conversion could be blocked at the stage of AMP deamination by incubation of platelet-rich plasma for 6 h with 200 microM coformycin, a transition-state analog inhibitor of
AMP deaminase
. Abolition of
AMP deaminase
activity had no effect on
thrombin
-induced secretion from the dense granules, alpha-granules, or acid hydrolases measured in gel-filtered platelets. Coformycin treatment had no effect on
thrombin
-stimulated lactate production, even when oxidative phosphorylation was blocked by antimycin A, nor on the rate of
thrombin
-stimulated glycogenolysis. In addition, although it was clear that the adenylate energy charge was maintained by activation of
AMP deaminase
following
thrombin
treatment, the adenylate energy charge was also maintained in coformycin-treated platelets, albeit after a short lag, by stimulated ATP production and equilibration through the adenylate kinase reaction. Hydrogen peroxide brings about similar adenylate degradation which could also be inhibited by coformycin. The results indicate that AMP deamination and secretion, although temporally related, are not coupled. The role of
AMP deaminase
appears to be to maintain the adenylate energy charge in the absence of stimulation of ATP production or to buffer the adenylate charge before ATP production is stimulated.
...
PMID:Coformycin inhibition of platelet AMP deaminase has no effect on thrombin-induced platelet secretion nor on glycolysis or glycogenolysis. 684 4
