肽LSARLAF通过直接激活整合素αIIbβ3引起血小板分泌和聚集。
The peptide LSARLAF causes platelet secretion and aggregation by directly activating the integrin alphaIIbbeta3.
作者信息
Derrick J M, Taylor D B, Loudon R G, Gartner T K
机构信息
Microbiology and Molecular Cell Sciences, University of Memphis, Campus Box 526041, Memphis, TN 38152, USA.
出版信息
Biochem J. 1997 Jul 15;325 ( Pt 2)(Pt 2):309-13. doi: 10.1042/bj3250309.
Abstract
A novel peptide (designed to bind to alphaIIbbeta3) caused platelet aggregation and aggregation-independent secretion of the contents of alpha-granules in an alphaIIbbeta3-dependent fashion. The agonist peptide induced secretion in the presence of prostaglandin E1. In cell-free assays, alphaIIbbeta3 bound specifically to immobilized agonist peptide and the peptide enhanced the binding of fibrinogen to immobilized alphaIIbbeta3. The agonist peptide apparently activates alphaIIbbeta3 by directly inducing a conformational change in the receptor. This change activates the platelets and causes secretion in a manner independent of fibrinogen binding.
摘要
一种新型肽（设计用于与αIIbβ3结合）以αIIbβ3依赖性方式引起血小板聚集和α颗粒内容物的聚集非依赖性分泌。激动剂肽在前列腺素E1存在下诱导分泌。在无细胞试验中，αIIbβ3特异性结合固定化的激动剂肽，且该肽增强纤维蛋白原与固定化αIIbβ3的结合。激动剂肽显然通过直接诱导受体构象变化来激活αIIbβ3。这种变化激活血小板并以与纤维蛋白原结合无关的方式引起分泌。
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