Adenosine triphosphate inhibitors

Molybdate is also known as an inhibitor of the important enzyme ATP sulfurylase where ATP is adenosine triphosphate, which activates sulfate for participation in biosynthetic pathways (56). The tetrahedral molybdate dianion, MoO , substitutes for the tetrahedral sulfate dianion, SO , and leads to futile cycling of the enzyme and total inhibition of sulfate activation. Molybdate is also a co-effector in the receptor for steroids (qv) in mammalian systems, a biochemical finding that may also have physiological implications (57). 

The susceptibilities of some of these fluorinated purine nucleosides to the action of enzymes are now described. In contrast to the inertness of the 2 -deoxy-2 -fluoro- and 3 -deoxy-3 -fluorocytidine analogs 739, 744, and 821 towards cytidine deaminase, the adenosine compounds 867, 883, and 906 are readily deaminated - by the adenosine deaminase in erythrocytes and calf intestine, but the resulting (deaminated) inosine compounds (from 867 and 883), as well as 888, are highly resistant - to cleavage by purine nucleoside phosphorylase (to give hypoxanthine base for the first two). The reason was discussed. Both 867 and 883 can form the 5 -triphosphates, without deamination, in human erythrocytes or murine sarcoma cells in the presence of 2 -deoxycoformycin, an adenosine deaminase inhibitor, but... 

Omeprazole is classified as a proton pump inhibitor, as it acts by blocking the hydrogen-potassium adenosine triphosphate enzyme system of the gastric parietal cells. Omeprazole therefore inhibits gastric acid release. Common side-effects associated with omeprazole include diarrhoea, headache, nausea and vomiting. Concurrent administration of omeprazole and phenytoin results in enhanced effects of phenytoin, which may lead to phenytoin toxicity. 

The first step of this sequence, which is not unique to de novo purine nucleotide biosynthesis, is the synthesis of 5-phosphoribosylpyrophosphate (PRPP) from ribose-5-phosphate and adenosine triphosphate. Phosphoribosyl-pyrophosphate synthetase, the enzyme that catalyses this reaction [278], is under feedback control by adenosine triphosphate [279]. Cordycepin interferes with thede novo pathway [229, 280, 281), and cordycepin triphosphate inhibits the synthesis of PRPP in extracts from Ehrlich ascites tumour cells [282]. Formycin [283], probably as the triphosphate, 9-0-D-xylofuranosyladenine [157] triphosphate, and decoyinine (LXXlll) [284-286] (p. 89) also inhibit the synthesis of PRPP in tumour cells, and this is held to be the blockade most important to their cytotoxic action. It has been suggested but not established that tubercidin (triphosphate) may also be an inhibitor of this reaction [193]. 

Mechanism of Action Aproton pump inhibitor that is converted to active metabolites that irreversibly bind to and inhibit hydrogen-potassium adenosine triphosphates, an enzyme on the surface of gastricparietal cells. Inhibits hydrogen ion transport into gastric lumen. Therapeutic Effect Increases gastricpH, reducing gastric acid production. 

The selection of transformed chloroplasts usually involves the use of an antibiotic resistance marker. Spectinomycin is used most routinely because of the high specificity it displays as a prokaryotic translational inhibitor as well as the relatively low side effects it exerts on plants. The bacterial aminoglycoside 3 -adenyltransferase gene (ciadA) confers resistance to both streptomycin and spectinomycin. The aadA protein catalyzes the covalent transfer of an adenosine monophosphate (AMP) residue from adenosine triphosphate (ATP) to spectinomycin, thereby converting the antibiotic into an inactive form that no longer inhibits protein synthesis for prokaryotic 70S ribosomes that are present in the chloroplast. 

Platelet aggregation different pathways of activation. Abbreviations ADR adenosine diphosphate ATP, adenosine triphosphate COX, cyclooxygenase PAI, plasminogen activator inhibitor PDGF, platelet derived growth factor. 

Several classes of serine/threonine kinases are known and these enzymes consist of a catalytic domain which transfers phosphate groups from adenosine triphosphate (ATP) to the targets, and a regulatory domain which modulates the activity of the catalytic domain through interaction with second messengers such as cyclic nucleotides, calcium ion, and DAGs. The family of kinases, their activators, and typical synthetic inhibitors are shown in Table 4.5. 

Diuretic drug preparations have promoted urine formation. They are derivatives of mercury propanol RCH2CH(OH)CH2HgX, where R is a polar hydrophilic group. The mercury diuretic preparations act as ferment inhibitors (latter containing-. They also inhibit adenosine triphosphate (ATP). These properties led to the use of mercury drug compounds in the treatment of bacterial infections. In these cases, they interacted with -SH groups of the bacteria proteins. 

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