New Mechanisms in Axon Regeneration

轴突再生的新机制

基本信息

批准号：
9125882
负责人：
MARC HAMMARLUND
金额：
$ 36.42万
依托单位：
YALE UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2015
资助国家：
美国
起止时间：
2015-08-15 至 2020-07-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9125882
关键词：
Affect Animal Model Biological Biological Process Buffers Caenorhabditis elegans Calcium Candidate Disease Gene Cell Death Cell physiology Cells Cellular biology Clustered Regularly Interspaced Short Palindromic Repeats Data Drug Design Employee Strikes Generations Genes Genetic Genetic Transcription Genome engineering Goals Grant Health Individual Injury Knowledge Life Link MAPK1 gene Mediating Mitochondria Molecular Mus Natural regeneration Nervous system structure Neuronal Injury Neurons Outcome Output Pathway interactions Poly Adenosine Diphosphate Ribose Post-Translational Protein Processing Process Property Proteins Public Health Recovery of Function Regulation Reporter Research Signal Transduction Site Tissues Transcriptional Regulation Wallerian Degeneration Work axon injury axon regeneration axonal degeneration base fly functional loss functional restoration genetic analysis in vivo in vivo imaging inhibitor/antagonist injured insight nerve injury nervous system disorder neuron loss novel novel strategies promoter regenerative research study response response to injury trafficking transcription factor

Affect Animal Model Biological Biological Process Buffers Caenorhabditis elegans Calcium Candidate Disease Gene Cell Death Cell physiology Cells Cellular biology Clustered Regularly Interspaced Short Palindromic Repeats Data Drug Design Employee Strikes Generations Genes Genetic Genetic Transcription Genome engineering Goals Grant Health Individual Injury Knowledge Life Link MAPK1 gene Mediating Mitochondria Molecular Mus Natural regeneration Nervous system structure Neuronal Injury Neurons Outcome Output Pathway interactions Poly Adenosine Diphosphate Ribose Post-Translational Protein Processing Process Property Proteins Public Health Recovery of Function Regulation Reporter Research Signal Transduction Site Tissues Transcriptional Regulation Wallerian Degeneration Work axon injury axon regeneration axonal degeneration base fly functional loss functional restoration genetic analysis in vivo in vivo imaging inhibitor/antagonist injured insight nerve injury nervous system disorder neuron loss novel novel strategies promoter regenerative research study response response to injury trafficking transcription factor

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项目摘要

DESCRIPTION (provided by applicant): Axon regeneration is a fundamental and conserved property of nervous systems. But although axon regeneration can restore function after nerve injury, regeneration often fails. Thus, a key question in the field is to discover what determines the regenerative capacity of injured neurons. This proposal investigates new mechanisms that function in the injured neuron and that help determine whether or not regeneration occurs. The long-term goal is to gain a comprehensive understanding of the cellular functions that link neuronal injury to successful regeneration. The specific goal of this project is to analyze three novel and interrelated mechanisms that regulate axon regeneration at the genetic, cellular, and molecular level. The project uses a combination of in vivo approaches that culminate in analysis of the injury response in individual neurons. The central hypothesis is that the three novel mechanisms act in a pathway that regulates axon regeneration and the neuronal injury response. However, each Aim is independent and will result in fundamental discoveries about the cell biology of axon regeneration even if the individual mechanisms operate in parallel rather than in a linear pathway. Each Aim is supported by extensive preliminary data, as well as by novel biological concepts and experimental approaches. Completion of these Aims will describe fundamental cellular mechanisms that mediate axon regeneration.

描述（应用程序提供）：轴突再生是神经系统的基本和配置的属性。但是，尽管轴突再生可以在神经损伤后恢复功能，但再生通常会失败。这是该领域的一个关键问题是发现什么决定了受伤神经元的再生能力。该提案研究了在受伤的神经元中起作用的新机制，并有助于确定是否发生再生。长期目标是对将神经元损伤与成功再生联系起来的细胞功能有全面的了解。该项目的具体目标是分析在遗传，细胞和分子水平下调节轴突再生的三种新颖和相互关联的机制。该项目结合了体内方法的组合，在分析单个神经元的损伤反应中最终达到了最终。中心假设是三种新型机制在调节轴突再生和神经元损伤反应的途径中起作用。但是，每个目标都是独立的，即使单个机制并非在线性途径中并行运行，也会导致有关轴突再生细胞生物学的基本发现。每个目标都由广泛的初步数据以及新颖的生物学概念和实验方法支持。这些目标的完成将描述介导轴突再生的基本细胞机制。