How Ephexin Signaling Promotes Neuronal Stability
Ephexin 信号如何促进神经元稳定性
基本信息
- 批准号:8012026
- 负责人:
- 金额:$ 24.9万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2008
- 资助国家:美国
- 起止时间:2008-07-15 至 2013-02-28
- 项目状态:已结题
- 来源:
- 关键词:AffectAntibodiesBindingBiochemicalBiological AssayCalcium ChannelCaliforniaCommitCyclin-Dependent Kinase 5DataDiseaseDrosophila genusEnvironmentEph Family ReceptorsEphA ReceptorsEquilibriumFacultyFamilyFellowshipFibroblast Growth Factor ReceptorsFinancial compensationG-Protein-Coupled ReceptorsGTP-Binding ProteinsGoalsGrowth ConesGuanine Nucleotide Exchange FactorsGuanosine Triphosphate PhosphohydrolasesHome environmentHomeostasisHomologous GeneInstitutionK-Series Research Career ProgramsLaboratoriesLeadLigandsLinkMediatingMentorsModelingMolecularMutationNervous system structureNeuromuscular JunctionNeuronsNeurophysiology - biologic functionP-Q type voltage-dependent calcium channelPathway interactionsPhasePlayPositioning AttributeProtein Kinase CProteinsPublishingReagentRegulationResearchResearch PersonnelRoleSan FranciscoSignal PathwaySignal TransductionSignaling MoleculeStaining methodStainsStructureSynapsesSynaptic TransmissionSystemTestingTrainingUniversitiesVertebratesWorkbasedesignephexininterestmeetingsmembernervous system disorderneuroregulationneurotransmissionpresynapticrelating to nervous systemresearch studyretinal rodsrhorho GTP-Binding Proteinssrc-Family Kinasesyeast two hybrid system
项目摘要
PROJECT SUMMARY: The causes and progression of several neurological diseases are influenced by
factors that control the stability of neural function. Yet the mechanisms that dictate neural excitation and
inhibition are poorly understood. Many studies indicate that homeostatic signaling mechanisms participate in
the regulation of neural function - in paricular by modulating the strength of synaptic connections. This
proposal aims to clarify the mechanisms of synaptic homeostatic signaling.
Prior work defined a role for a presynaptic CaV2.1 calcium channel in synaptic homeostasis. New
data show that the cytoplasmic signaling molecule, Ephexin, is also essential for synaptic homeostasis, and
it may act via CaV2.1 regulation. In vertebrates, the Ephrin ligand and EphA receptor act upstream of
Ephexin, and Rho-type GTPases act downstream of Ephexin to control growth cone dynamics. We
hypothesize that all of these molecules are involved in a homeostatic signaling pathway in the presynaptic
neuron. The proposed experiments for the K99 mentored phase will test this hypothesis. The results should
define the role Ephexin signaling plays in the context of synaptic homeostasis. For the ROD independent
phase, candidate molecules already known to regulate calcium channel function and Eph/Ephexin/GTPase
signaling will be tested for roles in synaptic homeostasis. The long-term goal of this research is to define
signaling mechisms with direct relevance to the cause and progression of neural disease.
CANDIDATE: The K99 portion of this reserach will be conducted in the laboratory of Dr. Graeme W. Davis
at UCSF. In this environment, I will continue to augment my training, both in the lab as well as in seminars,
professional meetings, and one-on-one meetings with UCSF faculty. I am committed to attaining a faculty
position at a major research institution. As an independent investigator, I would like to continue my research
into the regulation of neural activity.
RELEVANCE: Many neurological diseases result from nervous system instability, but it is not understood
exactly how neural stability is normally maintained. Data show that a molecule called Ephexin helps to direct
neural stability. This proposal is designed to clarify exactly how Ephexin performs this function; the results
may ultimately lead to a better understanding of the cause, progression, and treatment of neural diseases.
项目概述:几种神经系统疾病的原因和进展受到以下因素的影响:
控制神经功能稳定性的因素。然而,决定神经兴奋和
对抑制作用了解很少。许多研究表明,稳态信号机制参与了
调节神经功能--特别是通过调节突触连接的强度。这
该提案旨在阐明突触稳态信号传导的机制。
先前的工作定义了突触前CaV2.1钙通道在突触稳态中的作用。新
数据显示,细胞质信号分子Ephexin也是突触稳态所必需的,
它可能通过CaV2.1调节起作用。在脊椎动物中,Ephrin配体和EphA受体作用于EphA受体的上游。
Ephexin和Rho型GTP酶作用于Ephexin下游以控制生长锥动力学。我们
假设所有这些分子都参与了突触前的稳态信号通路,
neuron. K99指导阶段的拟议实验将检验这一假设。结果应
定义Ephexin信号在突触稳态中的作用。对于独立的ROD
阶段,候选分子已经知道调节钙通道功能和Eph/Ephexin/GT3
将测试信号传导在突触稳态中的作用。这项研究的长期目标是确定
与神经疾病的起因和进展直接相关的信号机制。
候选人:本研究的K99部分将在Graeme W.戴维斯
在UCSF在这种环境下,我将继续加强我的训练,无论是在实验室还是在研讨会上,
专业会议,以及与UCSF教师的一对一会议。我致力于成为一名
在一家大型研究机构工作。作为一名独立调查员,我想继续我的研究
神经活动的调节。
相关性:许多神经系统疾病是由神经系统不稳定引起的,但目前尚不清楚。
神经系统的稳定性是如何维持的数据显示,一种名为Ephexin的分子有助于指导
神经稳定性该提案旨在明确Ephexin如何执行此功能;结果
可能最终导致更好地了解神经疾病的原因,进展和治疗。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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{{ truncateString('CARL ANDREW FRANK', 18)}}的其他基金
How discrete homeostatic signals stabilize synapse function across time
离散稳态信号如何随时间稳定突触功能
- 批准号:
10706581 - 财政年份:2022
- 资助金额:
$ 24.9万 - 项目类别:
How discrete homeostatic signals stabilize synapse function across time
离散稳态信号如何随时间稳定突触功能
- 批准号:
10568507 - 财政年份:2022
- 资助金额:
$ 24.9万 - 项目类别:
Synaptic signals that drive the long-term maintenance of homeostatic neuroplasticity
驱动长期维持稳态神经可塑性的突触信号
- 批准号:
10059270 - 财政年份:2016
- 资助金额:
$ 24.9万 - 项目类别:
Synaptic signals that drive the long-term maintenance of homeostatic neuroplasticity
驱动长期维持稳态神经可塑性的突触信号
- 批准号:
10088612 - 财政年份:2016
- 资助金额:
$ 24.9万 - 项目类别:
How Ephexin Signaling Promotes Neuronal Stability
Ephexin 信号如何促进神经元稳定性
- 批准号:
7509540 - 财政年份:2008
- 资助金额:
$ 24.9万 - 项目类别:
How Ephexin Signaling Promotes Neuronal Stability
Ephexin 信号如何促进神经元稳定性
- 批准号:
8231539 - 财政年份:2008
- 资助金额:
$ 24.9万 - 项目类别:
How Ephexin Signaling Promotes Neuronal Stability
Ephexin 信号如何促进神经元稳定性
- 批准号:
7652330 - 财政年份:2008
- 资助金额:
$ 24.9万 - 项目类别:
How Ephexin Signaling Promotes Neuronal Stability
Ephexin 信号如何促进神经元稳定性
- 批准号:
8032421 - 财政年份:2008
- 资助金额:
$ 24.9万 - 项目类别:
Identifying genes that maintain stable neural activity
识别维持稳定神经活动的基因
- 批准号:
7115022 - 财政年份:2004
- 资助金额:
$ 24.9万 - 项目类别:
Identifying genes that maintain stable neural activity
识别维持稳定神经活动的基因
- 批准号:
6946808 - 财政年份:2004
- 资助金额:
$ 24.9万 - 项目类别:
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