γ 原钙粘蛋白对神经元存活的调节-猫眼课题宝

γ 原钙粘蛋白对神经元存活的调节

批准号：

8543779

负责人：

XIAOZHONG ALEC WANG

金额：

$18.64万

依托单位：

NORTHWESTERN UNIVERSITY

依托单位国家：

美国

项目类别：

财政年份：

2012

资助国家：

美国

项目状态：

已结题

起止时间：

2012-09-15 至 2015-08-31

来源：

https://reporter.nih.gov/project-details/8543779

关键词：

Acute Adaptor Signaling Protein Adult Affect Alleles Alzheimer&apos s Disease Apoptosis Apoptotic Attenuated Binding Cavernous Malformation Cell surface Cells Cerebral Ischemia Cerebrum Cessation of life Chickens Chronic Cytoplasmic Tail Data Development Dominant-Negative Mutation Ectopic Expression Ensure Experimental Models Family Genetic Human In Vitro Individual Interneurons Investigation Knockout Mice MAP Kinase Gene MAPK14 gene Mediating Membrane Mitochondria Modeling Molecular Mus Mutation Nature Nerve Degeneration Nervous system structure Neurodegenerative Disorders Neurons Pathogenesis Pathway interactions Phosphorylation Play Population Process Protein Isoforms Proteins Reactive Oxygen Species Regulation Retinal Ganglion Cells Role Shapes Signal Pathway Signal Transduction Spinal Spinal Cord Stroke Synapses Testing Work attenuation excitotoxicity in vivo in vivo Model mouse model nervous system development neurodevelopment neuron apoptosis neuronal cell body neuronal survival neurotrophic factor postsynaptic presynaptic protein aggregate protein complex protein protein interaction research study spinal pathway

中文摘要

翻译

描述(由申请人提供)：神经元死亡不仅对形成发育中的神经系统的大小和连通性至关重要，而且对神经退行性疾病和中风的发病机制也有重要影响。越来越多的遗传学证据表明，聚集型原钙粘附素(Pcdhs)在神经元存活的调控中发挥着重要作用。我们的初步数据表明，PDCD10，也被称为CCM3，是人类脑海绵状血管畸形的致病基因缺陷，在PcdH-？S的下游起调节作用。为了更好地了解Pcdhs调控神经元存活的分子途径，我们将通过使用转基因小鼠模型评估PDCD10蛋白相互作用网络中单个成分的作用来定义PDCD10下游的分子途径。

英文摘要

DESCRIPTION (provided by applicant): Neuronal death is not only essential in shaping the size and connectivity of the developing nervous system, but also contributes significantly to the pathogenesis of neurodegenerative diseases and stroke. Accumulating genetic evidence shows that clustered protocadherins (Pcdhs) play an important role in the regulation of neuronal survival. Our preliminary data show that PDCD10, also known as CCM3, a causative genetic defect for Cerebral Cavernous Malformations in human, acts downstream of Pcdh-?s to mediate this function. To better understand molecular pathways by which Pcdhs regulate neuronal survival, we will define the molecular pathways downstream of PDCD10 by evaluating the role of individual components in PDCD10 protein interaction network using genetically modified mouse models.

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