Disease relevance of Pact1

• Platelet activation at sites of vascular injury is essential for the arrest of bleeding; however, excessive platelet accumulation at regions of atherosclerotic plaque rupture can result in the development of arterial thrombi, precipitating diseases such as acute myocardial infarction and ischemic stroke [1].
• Platelet activation In mice and human Helicobacter pylori infection [2].
• Platelet activation is a hallmark of severe preeclampsia, and platelet PGH synthase 1-derived (PGHS1-derived) thromboxane A(2) (TxA(2)) has been implicated in its pathogenesis [3].
• Platelet activation plays a central role in hemostasis and thrombosis [4].
• Platelet activation by a relapsing fever spirochaete results in enhanced bacterium-platelet interaction via integrin alphaIIbbeta3 activation [5].

High impact information on Pact1

• Platelet activation at sites of vascular injury is essential for primary hemostasis, but also underlies arterial thrombosis leading to myocardial infarction or stroke [6].
• Platelet activation with thrombin ex vivo revealed higher and lower sensitivity for surface P-selectin expression in platelets of apoE-/-IP-/- and apoE-/-TP-/- mice, respectively, than in those of apoE-/- mice [7].
• Platelet activation by KKO required heparin and was abrogated by blockade of FcgammaRIIA [8].
• Platelet activation is tightly regulated by products of the endothelium and platelets including nitric oxide (NO) [9].
• Platelet activation and the formation of platelet microaggregates in coronary vessels play pivotal roles in myocardial ischemia and reperfusion injury [10].

Biological context of Pact1

• Platelet activation at 60 min was partially inhibited by dexamethasone, rhodostomin synthetic peptide 45-59, or platelet activation factor antagonist (WEB 2086) [11].

Anatomical context of Pact1

• Platelet activation by cultured mouse peritoneal macrophages [12].

Associations of Pact1 with chemical compounds

• Platelet activation causes conformational changes of integrin GPIIb/IIIa (alpha(IIb)beta3), resulting in the exposure of its ligand-binding pocket [13].
• Platelet activation and "Crossover Appeal": rab and rho families United by common links to serotonin [14].
• Platelet activation in vivo led to an immediate and continuous rise of dhS1P in plasma, while S1P remained stable [15].
• Platelet activation causes loss of dhS1P and breakdown of ceramide, implying ceramidase activation [15].

Regulatory relationships of Pact1

• Platelet activation and aggregation were studied in HP-infected patients and controls by measuring the platelet-aggregate ratio and platelet P-selectin expression [2].

Other interactions of Pact1

• OBJECTIVE: Platelet activation occurs in response to adhesion receptors for von Willebrand factor (GPIb-V-IX) and collagen (GPVI and alpha2beta1 integrin) acting upstream of phospholipase C (PLC) gamma2 [16].

References