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本文引用的文献

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Robust Axonal Regeneration Occurs in the Injured CAST/Ei Mouse CNS.在受伤的CAST/Ei小鼠中枢神经系统中发生了强大的轴突再生。
Neuron. 2015 Jun 3;86(5):1215-27. doi: 10.1016/j.neuron.2015.05.005. Epub 2015 May 21.
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Metallothionein-I/II Promotes Axonal Regeneration in the Central Nervous System.金属硫蛋白-I/II促进中枢神经系统轴突再生。
J Biol Chem. 2015 Jun 26;290(26):16343-56. doi: 10.1074/jbc.M114.630574. Epub 2015 May 6.
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Growth control mechanisms in neuronal regeneration.神经元再生中的生长控制机制。
FEBS Lett. 2015 Jun 22;589(14):1669-77. doi: 10.1016/j.febslet.2015.04.046. Epub 2015 May 1.
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Does repair of spinal cord injury follow the evolutionary theory?脊髓损伤的修复是否遵循进化理论?
Neural Regen Res. 2012 Apr 15;7(11):849-52. doi: 10.3969/j.issn.1673-5374.2012.11.009.
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Conditional genetic deletion of PTEN after a spinal cord injury enhances regenerative growth of CST axons and motor function recovery in mice.脊髓损伤后条件性基因敲除PTEN可增强小鼠皮质脊髓束轴突的再生生长及运动功能恢复。
Exp Neurol. 2015 Apr;266:147-60. doi: 10.1016/j.expneurol.2015.02.012. Epub 2015 Feb 20.
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Overexpression of Sox11 promotes corticospinal tract regeneration after spinal injury while interfering with functional recovery.Sox11的过表达促进脊髓损伤后皮质脊髓束的再生,但会干扰功能恢复。
J Neurosci. 2015 Feb 18;35(7):3139-45. doi: 10.1523/JNEUROSCI.2832-14.2015.
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Methods of integrating data to uncover genotype-phenotype interactions.整合数据以揭示基因型-表型相互作用的方法。
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8
Transcriptional profiling at whole population and single cell levels reveals somatosensory neuron molecular diversity.全群体和单细胞水平的转录组分析揭示了体感神经元的分子多样性。
Elife. 2014 Dec 19;3:e04660. doi: 10.7554/eLife.04660.
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Defining the nociceptor transcriptome.定义伤害感受器转录组。
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10
cAMP-responsive element-binding protein (CREB) and cAMP co-regulate activator protein 1 (AP1)-dependent regeneration-associated gene expression and neurite growth.环磷酸腺苷反应元件结合蛋白(CREB)与环磷酸腺苷共同调节活化蛋白1(AP1)依赖性再生相关基因的表达及神经突生长。
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神经修复的转录组学方法

Transcriptomic Approaches to Neural Repair.

作者信息

Dulin Jennifer N, Antunes-Martins Ana, Chandran Vijayendran, Costigan Michael, Lerch Jessica K, Willis Dianna E, Tuszynski Mark H

机构信息

Department of Neurosciences, University of California, San Diego, La Jolla, California 92093,

Wolfson Centre for Age-Related Disease, King's College London, London SE1 1UL, United Kingdom.

出版信息

J Neurosci. 2015 Oct 14;35(41):13860-7. doi: 10.1523/JNEUROSCI.2599-15.2015.

DOI:10.1523/JNEUROSCI.2599-15.2015
PMID:26468186
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4604224/
Abstract

UNLABELLED

Understanding why adult CNS neurons fail to regenerate their axons following injury remains a central challenge of neuroscience research. A more complete appreciation of the biological mechanisms shaping the injured nervous system is a crucial prerequisite for the development of robust therapies to promote neural repair. Historically, the identification of regeneration associated signaling pathways has been impeded by the limitations of available genetic and molecular tools. As we progress into an era in which the high-throughput interrogation of gene expression is commonplace and our knowledge base of interactome data is rapidly expanding, we can now begin to assemble a more comprehensive view of the complex biology governing axon regeneration. Here, we highlight current and ongoing work featuring transcriptomic approaches toward the discovery of novel molecular mechanisms that can be manipulated to promote neural repair.

SIGNIFICANCE STATEMENT

Transcriptional profiling is a powerful technique with broad applications in the field of neuroscience. Recent advances such as single-cell transcriptomics, CNS cell type-specific and developmental stage-specific expression libraries are rapidly enhancing the power of transcriptomics for neuroscience applications. However, extracting biologically meaningful information from large transcriptomic datasets remains a formidable challenge. This mini-symposium will highlight current work using transcriptomic approaches to identify regulatory networks in the injured nervous system. We will discuss analytical strategies for transcriptomics data, the significance of noncoding RNA networks, and the utility of multiomic data integration. Though the studies featured here specifically focus on neural repair, the approaches highlighted in this mini-symposium will be of broad interest and utility to neuroscientists working in diverse areas of the field.

摘要

未标注

理解成年中枢神经系统神经元在损伤后为何无法再生轴突仍是神经科学研究的核心挑战。更全面地认识塑造受损神经系统的生物学机制,是开发促进神经修复的有效疗法的关键前提。从历史上看,可用的遗传和分子工具的局限性阻碍了再生相关信号通路的识别。随着我们进入一个基因表达高通量检测已很常见且我们的相互作用组数据知识库迅速扩展的时代,我们现在可以开始对控制轴突再生的复杂生物学形成更全面的认识。在此,我们重点介绍当前和正在进行的工作,这些工作采用转录组学方法来发现可被操纵以促进神经修复 的新分子机制。

意义声明

转录谱分析是一种强大的技术,在神经科学领域有广泛应用。诸如单细胞转录组学、中枢神经系统细胞类型特异性和发育阶段特异性表达文库等最新进展正在迅速增强转录组学在神经科学应用中的能力。然而,从大型转录组数据集中提取具有生物学意义的信息仍然是一项艰巨的挑战。本次小型研讨会将重点介绍当前使用转录组学方法识别受损神经系统中调控网络的工作。我们将讨论转录组学数据的分析策略、非编码RNA网络的意义以及多组学数据整合的效用。尽管此处介绍的研究特别关注神经修复,但本次小型研讨会强调的方法将引起该领域不同领域的神经科学家的广泛兴趣并具有实用性。