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thrombophilia/proline
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3 results
Hypercoagulability causes atrial fibrosis and promotes atrial fibrillation.
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Atrial fibrillation (AF) produces a hypercoagulable state. Stimulation of protease-activated receptors by coagulation factors provokes pro-fibrotic, pro-hypertrophic, and pro-inflammatory responses in a variety of tissues. We studied the effects of thrombin on atrial fibroblasts and tested the
PAR4 activation involves extracellular loop-3 and transmembrane residue Thr153
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Protease activated receptor 4 (PAR4) mediates sustained thrombin signaling in platelets and is required for a stable thrombus. PAR4 is activated by proteolysis of the N-terminus to expose a tethered ligand. The structural basis for PAR4 activation and the location of its ligand binding site (LBS)
Heerlen polymorphism associated with type III protein S deficiency and factor V Leiden mutation in a Polish patient with deep vein thrombosis.
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Protein S is one of the major natural anticoagulants. A missense serine 501 to proline (S501P) Heerlen polymorphism is associated with reduced levels of free protein S. Heerlen polymorphism, especially when combined with other thrombophilia risk factors, can lead to thromboembolic complications. To
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