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血小板中受体脱落的机制。

Mechanisms of receptor shedding in platelets.

机构信息

Australian Cancer Research Foundation (ACRF) Department of Cancer Biology and Therapeutics, The John Curtin School of Medical Research, The Australian National University, Canberra, ACT, Australia; and.

Australian Centre for Blood Diseases, Monash University, Melbourne, VIC, Australia.

出版信息

Blood. 2018 Dec 13;132(24):2535-2545. doi: 10.1182/blood-2018-03-742668. Epub 2018 Oct 22.

Abstract

The ability to upregulate and downregulate surface-exposed proteins and receptors is a powerful process that allows a cell to instantly respond to its microenvironment. In particular, mobile cells in the bloodstream must rapidly react to conditions where infection or inflammation are detected, and become proadhesive, phagocytic, and/or procoagulant. Platelets are one such blood cell that must rapidly acquire and manage proadhesive and procoagulant properties in order to execute their primary function in hemostasis. The regulation of platelet membrane properties is achieved via several mechanisms, one of which involves the controlled metalloproteolytic release of adhesion receptors and other proteins from the platelet surface. Proteolysis effectively lowers receptor density and reduces the reactivity of platelets, and is a mechanism to control robust platelet activation. Recent research has also established clear links between levels of platelet receptors and platelet lifespan. In this review, we will discuss the current knowledge of metalloproteolytic receptor regulation in the vasculature with emphasis on the platelet receptor system to highlight how receptor density can influence both platelet function and platelet survival.

摘要

上调和下调表面暴露蛋白和受体的能力是一种强大的过程,使细胞能够立即对其微环境做出反应。特别是在血流中移动的细胞必须迅速应对检测到感染或炎症的情况,并变得具有亲附性、吞噬性和/或促凝性。血小板是这样一种血细胞,它必须迅速获得和管理亲附性和促凝性特性,以执行其在止血中的主要功能。血小板膜特性的调节是通过几种机制实现的,其中一种机制涉及粘附受体和其他蛋白质从血小板表面的受控金属蛋白酶释放。蛋白水解有效地降低了受体密度并降低了血小板的反应性,是控制血小板强烈激活的一种机制。最近的研究还在血小板受体系统方面建立了血小板受体水平与血小板寿命之间的明确联系,以强调受体密度如何影响血小板功能和血小板存活。

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