Redox regulation of platelet adhesion receptors

血小板粘附受体的氧化还原调节

• 批准号: nhmrc : 606501
• 负责人: A/Pr Robert Andrews
• 金额: $ 39.52万
• 依托单位: Monash University
• 依托单位国家: 澳大利亚
• 项目类别: NHMRC Project Grants
• 财政年份: 2010
• 资助国家: 澳大利亚
• 起止时间: 2010-01-01 至 2012-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/redox-regulation-platelet-adhesion-receptors/82837
• 关键词: Redox; regulation; platelet; adhesion; receptors

Formation of clots to prevent blood loss is initiated by the platelet receptors, glycoprotein (GP)Ib-IX-V and GPVI. Unfortunately, there is a gap in our knowledge regarding the events immediately following activation of these receptors and the known downstream signalling. We have identified a novel binding partner for these platelet receptors, which we believe links reactive oxygen species to platelet signalling events. This opens new avenues for therapies to prevent aberrant clotting.

血栓的形成是由血小板受体、糖蛋白（GP）Ib-IX-V和GPVI发起的，以防止失血。不幸的是，我们对这些受体激活后立即发生的事件和已知的下游信号传导的了解还存在空白。我们已经确定了这些血小板受体的一种新的结合伙伴，我们相信它将活性氧与血小板信号事件联系起来。这为预防异常凝血的治疗开辟了新的途径。