Role of Cell Cycle Proteins in Apoptosis
细胞周期蛋白在细胞凋亡中的作用
基本信息
- 批准号:7226655
- 负责人:
- 金额:$ 5.14万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2005
- 资助国家:美国
- 起止时间:2005-09-19 至 2007-07-31
- 项目状态:已结题
- 来源:
- 关键词:apoptosiscell growth regulationcell proliferationcyclin dependent kinasecyclinsenzyme activitygenetically modified animalsglomerulonephritisgreen fluorescent proteinskidney cellkinase inhibitorlaboratory mousemolecular pathologypostdoctoral investigatorprotein localizationprotein structure functiontissue /cell culture
项目摘要
DESCRIPTION (provided by applicant): Glomerular disease remains a leading cause of kidney failure. Injury to the glomerular mesangial cell (MC) is associated with increased proliferation and apoptosis, and the balance of these processes determines the cell number. Proliferation is controlled by cell cycle regulatory proteins, and requires the activation of specific cyclin dependent kinases (CDK). CDK-inhibitors bind to and inactivate CDKs. In this grant proposal we will show that cell cycle proteins have a critical role in regulating cell apoptosis, independent of proliferation. The first SA is designed to show that CDK2 causes MC apoptosis, that blocking CDK2 activity will prevent cell death, and the effects of CDK2 are distinct from its role in cell proliferation. We will examine mechanisms and suggest that unregulated CDK2 activity leads to catastrophic progression through the cell cycle. In the second SA, we will show that a novel function of the CDK-inhibitor, p27, is to protect cells from death. We will test the hypothesis that p27 determines the onset, magnitude and threshold to apoptosis, which is mediated by restraining CDK2 activation. Our ultimate goal is to show novel roles for specific cell cycle proteins in glomerular disease so that specific therapeutic strategies can be developed.
描述(由申请人提供):肾小球疾病仍然是肾衰竭的主要原因。对肾小球系膜细胞(MC)的损伤与增殖和凋亡的增加有关,这些过程的平衡决定了细胞数量。细胞增殖受细胞周期调节蛋白控制,需要激活特定的细胞周期蛋白依赖性激酶(CDK)。cdk抑制剂结合cdk并使其失活。在这项拨款提案中,我们将证明细胞周期蛋白在调节细胞凋亡中具有关键作用,独立于增殖。第一个SA旨在表明CDK2导致MC细胞凋亡,阻断CDK2活性将防止细胞死亡,并且CDK2的作用与其在细胞增殖中的作用不同。我们将研究机制,并提出不受管制的CDK2活性会导致细胞周期的灾难性进展。在第二个SA中,我们将展示cdk抑制剂p27的新功能是保护细胞免于死亡。我们将验证p27通过抑制CDK2激活来决定细胞凋亡的发生、大小和阈值的假设。我们的最终目标是揭示特定细胞周期蛋白在肾小球疾病中的新作用,从而开发出特定的治疗策略。
项目成果
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