ERK2 Specific Function of the CNS

ERK2 中枢神经系统的特定功能

基本信息

批准号：
6936407
负责人：
Ivy S Samuels
金额：
$ 2.66万
依托单位：
CASE WESTERN RESERVE UNIVERSITY
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：
2005-05-01 至 2007-04-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/6936407
关键词：
association learning behavior test behavioral /social science research tag biological signal transduction cell cycle developmental neurobiology genetically modified animals glial fibrillary acidic protein isozymes laboratory mouse lethal genes long term memory mitogen activated protein kinase molecular psychobiology neural plasticity predoctoral investigator tissue /cell culture

项目摘要

DESCRIPTION (provided by applicant): ERK1 and ERK2 are evolutionary conserved from yeast to human, and are ubiquitous. The activation of these proteins stimulates transcription and translation which induce essential cellular metabolic changes required for proper CMS development, function, and survival. ERK1 and ERK2 null mouse models exhibit contrasting results however, where ERK1 ablation has no overt phenotype while ERK2 null animals are embryonic lethal. Therefore, a conditional mutation of the ERK2 gene using Cre/LoxP technology was generated to investigate the specific actions of ERK2 in the CMS. Because evidence suggests that ERK1 and ERK2 have differential and specific activities in cell cycle transition events, mitogen-activated signal transduction, and synaptic plasticity, the specific aims of this proposal are to determine how a loss of ERK2 in GFAP+ cells of the CMS disrupts neural development, how the loss effects the cellular metabolic activity of cultured astrocytes, and neurons, and how it effects learning and memory. Both in vivo examination of transgenic brains and in vitro examination of cultured astrocytes and neurons will be utilized for determination of ERK2 specific function.

描述（由申请人提供）：ERK1和ERK2是从酵母到人类的进化保守的，并且无处不在。这些蛋白质的激活刺激转录和翻译，诱导正确的CMS发育，功能和生存所需的必需细胞代谢变化。 ERK1和ERK2 null小鼠模型表现出对比的结果，但是，ERK1消融没有明显的表型，而ERK2无效动物是胚胎致死的。因此，生成了使用CRE/LOXP技术的ERK2基因的条件突变，以研究CMS中ERK2的特定作用。 Because evidence suggests that ERK1 and ERK2 have differential and specific activities in cell cycle transition events, mitogen-activated signal transduction, and synaptic plasticity, the specific aims of this proposal are to determine how a loss of ERK2 in GFAP+ cells of the CMS disrupts neural development, how the loss effects the cellular metabolic activity of cultured astrocytes, and neurons, and how it effects learning and memory.体内对转基因大脑的体内检查以及对培养的星形胶质细胞和神经元的体外检查都将用于确定ERK2特异性功能。