Molecular Interactions that modulate PI3 Kinase and MAP Kinase pathways during apoptosis

细胞凋亡过程中调节 PI3 激酶和 MAP 激酶途径的分子相互作用

• 批准号: 355802-2012
• 负责人: Koeberle, Paulo
• 金额: $ 1.89万
• 依托单位: University of Toronto
• 依托单位国家: 加拿大
• 项目类别: Discovery Grants Program - Individual
• 财政年份: 2014
• 资助国家: 加拿大
• 起止时间: 2014-01-01 至 2015-12-31
• 项目状态: 已结题
• 来源: https://www.nserc-crsng.gc.ca/ase-oro/Details-Detailles_eng.asp?id=549830
• 关键词: Molecular; Interactions; modulate; PI3; Kinase

When injured, central nervous system (CNS: brain and spinal cord) neurons initiate a carefully orchestrated "suicide" program, called apoptosis. The elements that control this suicide program are conserved throughout different species and observed in a wide variety of human diseases of the CNS. Research has lead to a more complete understanding of the mechanisms of apoptosis during development of CNS in lower animals. However, relatively little is known about this process in adult mammalian CNS neurons.

当受伤时，中枢神经系统（CNS：脑和脊髓）神经元启动一个精心策划的“自杀”程序，称为细胞凋亡。控制这种自杀程序的元件在不同物种中是保守的，并且在各种各样的人类CNS疾病中观察到。研究已经导致对低等动物CNS发育过程中细胞凋亡机制的更完整的理解。然而，对成年哺乳动物中枢神经系统神经元的这一过程知之甚少。