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Regulation of neuronal survival by gamma protocadherins

γ 原钙粘蛋白对神经元存活的调节

基本信息

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
起止时间：
2012-09-15 至 2015-08-31
项目状态：
已结题

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

项目摘要

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.

描述（由申请人提供）：神经元死亡不仅在形成发育中的神经系统的大小和连接性方面至关重要，而且在神经退行性疾病和中风的发病机制中也有重要作用。越来越多的遗传学证据表明，成簇原钙粘蛋白（Pcdhs）在神经元存活的调节中起着重要作用。我们的初步数据表明，PDCD 10，也被称为CCM 3，一个致病的遗传缺陷，脑海绵状血管畸形在人类，行为下游的Pcdh-？s来调节此功能。为了更好地了解Pcdhs调节神经元存活的分子途径，我们将通过使用遗传修饰的小鼠模型评估PDCD 10蛋白相互作用网络中单个组分的作用来定义PDCD 10下游的分子途径。