adenosine diphosphate

PlateletMapping percentage inhibition using adenosine diphosphate (ADP).

Type of platelet Diagnoses Protein or functional function defect deficiency Cytoskeletal assembly Wiskott-Aldrich Wiskott-Aldrich syndrome syndrome protein Granule storage or Storage pool Granule platelet release deficiencies content Platelet adhesion Von Willebrand VWF disease Bernard-Soulier GPIb syndrome Platelet aggregation Glanzmann's GPIIb/IIIa thrombasthenia Congenital Fibrinogen hypofibrinogenemia Platelet-agonist Agonist receptor ADP or thromboxane interactions deficiencies A2 Platelet coagulant- Scott syndrome Platelet membrane protein interactions phospholipid signaling ADP, adenosine diphosphate; GP, glycoprotein; VWF, Von Willebrand factor.

Effron et al., "Clusterrandomized clinical trial examining the impact of platelet function testing on practice: The Treatment with Adenosine Diphosphate Receptor Inhibitors: Longitudinal assessment of treatment patterns and events after acute coronary syndrome prospective open label antiplatelet therapy study," Circulation: Cardiovascular Interventions, vol.

(1974) Studies on poly(adenosine diphosphate ribose) antibody.

Antiplatelet tests showed decreases in aggregation in response to arachidonic acid (P = 0.034) and adenosine diphosphate (P<0.0001) for patients treated with aspirin and clopidogrel, respectively.

A comprehensive comparative review of adenosine diphosphate receptor antagonists.

Most drugs designed to act on AMPK do so by increasing levels of adenosine monophosphate (AMP) and adenosine diphosphate (ADP).

Pomolic acid (PA), triterpenoid isolated from Licania pittieri, has previously shown a potent ability to inhibit adenosine diphosphate (ADP)-and epinephrine-induced human platelet aggregation.

During anaerobic muscle contraction ATP is rapidly hydrolyzed to adenosine diphosphate (ADP) and phosphate anion.

Platelet aggregation induced by low concentrations of adenosine diphosphate (ADP) and epinephrine, and serum thromboxane B2 decreased by 45% both in humans and animals after GLA supplementation.

When supplied with an excess of adenosine diphosphate (ADP), AK acts as a catalyst converting ADP into ATP.

According to the company, ticagrelor is the first reversibly binding oral adenosine diphosphate receptor antagonist.

(1) The enzyme catalyses the conversion of phosphoenolpyruvate (PEP) to pyruvate, producing adenosine triphosphate (ATP) from adenosine diphosphate (ADP) in the process.