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Genetic Analysis of AMPK-alpha in Astrocytes during Normal and Energetic Stress

Genetic Analysis of AMPK-alpha in Astrocytes during Normal and Energetic Stress
正常和能量应激期间星形胶质细胞 AMPK-α 的遗传分析
批准号:
9332686
负责人:
Tyisha Williams
金额:
$34.99万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2016
资助国家:
美国
项目状态:
已结题
起止时间:
2016-08-16 至 2020-05-31

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Abstract An Academic Research Enhancement Award (AREA) award to promote research at primarily undergraduate institutions (PUIs) –(R15) will greatly impact both my career goals and my undergraduate students and fully meet the intended purpose of this award. Specifically, this award would 1) allow me to pursue my continuing interest in metabolism as it relates to the normal and diseased brain, 2) expose students to relevant research, and 3) support the commitment Trinity University has for scientific research and discovery. During this award period students in my lab will be afforded an exceptional opportunity to obtain training in the field of mouse genetics, cortical development and culturing primary neurons as well as astrocytes, which will enhance their interest in molecular and cellular neuroscience. As a junior faculty member, this award will positively impact the achievement of my long term goals. As a new assistant professor, securing a prestigious award will be pivotal in launching a successful career trajectory as a neurobiology researcher and professor at a PUI. My proposal focuses on AMPK in the nervous system. AMPK is a trimer composed of a catalytic subunit, α, and two regulatory subunits, β and γ. As an energy sensor and regulator of metabolism, AMPK would be expected to play a vital function during neuronal development, maintenance, and survival. However, to date the genetic analysis of AMPKα function in the mammalian nervous system has not been explored. Therefore, this proposal aims to identify molecular mechanisms AMP-activated protein kinase may play in the mammalian nervous system. We will specifically evaluate the in vitro effects of AMPKα1/α2 genetically null astrocytes in autophagy and apoptosis
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