| Autor: |
Jackson, S. F., Schoenwaelder, S. M. |
| Předmět: |
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| Zdroj: |
Cellular & Molecular Life Sciences; May2006, Vol. 63 Issue 10, p1085-1090, 6p, 1 Diagram, 1 Chart |
| Abstrakt: |
Arterial thrombosis is the single most common cause of death and disability in industrialized societies and is the primary pathogenic mechanism underlying acute myocardial infarction and ischemic stroke. Platelets play a central role in this process, and as a consequence, a great deal of effort has gone into identifying the mechanisms regulating the adhesive function of platelets. Platelet adhesion is controlled by intracellular signaling pathways, with growing evidence for a major role for phosphoinositide 3-kinases (PI3Ks) in this process. Platelets express all type I PI3K isoforms, including p110α, p110β, p110δ and p110γ, with recent evidence suggesting important roles for p110γ and p110β in regulating distinct phases of the platelet activation process. Deficiency of p110 γ or inhibition of p110β produces a marked defect in arterial thrombosis without a corresponding increase in bleeding time, raising the possibility that inhibition of one or more PI3K isoforms may represent an effective antithrombotic approach. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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