GP6

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GP6

A gene on chromosome 19q13.4 that encodes a 58-kD platelet membrane glycoprotein, which plays a central role in the collagen-induced platelet activation and aggregation. Injury to the vessel wall and damage to the endothelial lining exposes the subendothelial matrix to blood flow, resulting in deposition of platelets. Collagen, especially types I, III and VI, are the most thrombogenic macromolecules of the extracellular matrix. The adhesion of platelets to collagen results in activation, leading to platelet secretion, recruitment of additional platelets and aggregation resulting in a platelet plug, which limits blood loss. However, collagen exposure after rupture of atherosclerotic plaques results in thrombus formation and may lead to myocardial infarction or stroke.
References in periodicals archive ?
Rat monoclonal antibodies (mAbs) against human GPVI were developed and generated as described (15).
Plasma concentrations of sGPVI were determined by use of a bead-based sandwich immunoassay and mAb 8E9 reactive with human GPVI as capture antibody.
To test whether sGPVI is influenced by confounders, comparison of the decadic logarithm of GPVI between ACS and SAP was adjusted by possible confounders such as age, sex, cardiovascular risk factors, and medical treatment.
Therefore, the relevance and frequency of innate issues of GPVI remain low.
Platelet-collagen interaction: is GPVI the central receptor?
In damaged areas of the blood vessel wall, where there is an abundance of collagens, this stage is frequently mediated by the interaction of collagen receptors, such as the integrin [[alpha].sub.2][[beta].sub.1] and the platelet-specific receptor GPVI. Integrin [[alpha].sub.2][[beta].sub.1] primarily supports platelet attachment to collagen, whereas GPVI and to a lesser extent [[alpha].sub.2][[beta].sub.1] work in concert to transduce signals through the membrane.
STAGE 2: STABLE ADHESION TO COLLAGENS MEDIATED BY INTEGRIN [[alpha].sub.2][[beta].sub.1] AND GPVI
They are the integrin [[alpha].sub.2][[beta].sub.1], which is expressed on a variety of cells including platelets, and an immunoglobulin superfamily collagen receptor GPVI. (35,36) Upon interaction with the platelet receptors, collagens will induce platelet shape change, secretion, and aggregation, accompanied by phosphoinositide hydrolysis, TX[A.sub.2] synthesis, phosphorylation of specific protein substrates, and an increase in cytoplasmic [Ca.sup.2+].
Glycoprotein VI is a major platelet glycoprotein (60-65 kd) that has been considered a putative receptor for collagen since the identification of a patient with a mild bleeding disorder whose platelets lacked GPVI and exhibited defective collagen-induced responses.
Furthermore, as BmooPAi did not inhibit ADP- or collagen-induced platelet aggregation, we can rule out the possibility of activity toward [[alpha].sub.2][[beta].sub.1], GPVI, P2Y1, and P2Y12 receptors.
Stegner et al., "Differentially regulated GPVI ectodomain shedding by multiple platelet-expressed proteinases," Blood, vol.
Watson, "Platelet-collagen interaction: is GPVI the central receptor?" Blood, vol.