作者: Alan T Nurden
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摘要: The haemostatic response of platelets any one individual will be influenced by the genetic profile total population receptors expressed on platelet surface. Among parameters to consider (i) density each receptor, (ii) rate at which genes are transcribed and produced (iii) presence or not structural polymorphisms. Already, consideration known polymorphisms GP IIb IIIa raises most interesting questions structure/function relationship for this receptor. For example, there is often no obvious pattern as influence function risk giving rise a diallelic alloantigen system. Thus, mutation Arg 214 results in loss ability complex support aggregation, whereas 143 has resulted production an immune (see above). As I have pointed out earlier, examples from inherited disorders show that even single mutated allele can receptor function. Others shown plasma proteins 52) membrane glycoproteins such E-selectin endothelial cells 53) give factors thrombosis and/or atherosclerosis. It would know whether glycoprotein (and those shared with other vascular cells) also represent cardiovascular disease.