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少突胶质细胞特性的表观遗传调控。

Epigenetic regulation of oligodendrocyte identity.

机构信息

Department of Neuroscience and Genetics and Genomics, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.

出版信息

Trends Neurosci. 2010 Apr;33(4):193-201. doi: 10.1016/j.tins.2010.01.007. Epub 2010 Mar 12.

DOI:10.1016/j.tins.2010.01.007
PMID:20227775
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2849857/
Abstract

The interplay of transcription factors and epigenetic modifiers, including histone modifications, DNA methylation and microRNAs during development is essential for the acquisition of specific cell fates. Here, we review the epigenetic "programming" of stem cells into oligodendrocytes, by analyzing three sequential stages of lineage progression. The first transition from pluripotent stem cells to neural precursors is characterized by repression of pluripotency genes and restriction of the lineage potential to the neural fate. The second transition from multipotential precursors to oligodendrocyte progenitors is associated with the progressive loss of plasticity and the repression of neuronal and astrocytic genes. The last step of differentiation of oligodendrocyte progenitors into myelin-forming cells is defined by a model of derepression of myelin genes.

摘要

在发育过程中,转录因子和表观遗传修饰物(包括组蛋白修饰、DNA 甲基化和 microRNAs)的相互作用对于获得特定的细胞命运至关重要。在这里,我们通过分析谱系进展的三个连续阶段,来回顾将干细胞“编程”为少突胶质细胞的表观遗传过程。从多能干细胞到神经前体细胞的第一个转变特征是抑制多能性基因,并将谱系潜能限制为神经命运。从多潜能前体细胞到少突胶质祖细胞的第二个转变与可塑性的逐渐丧失以及神经元和星形胶质细胞基因的抑制有关。少突胶质祖细胞分化为髓鞘形成细胞的最后一步由髓鞘基因去抑制的模型定义。

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Epigenetic regulation of oligodendrocyte identity.少突胶质细胞特性的表观遗传调控。
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2
Epigenetic modifiers are necessary but not sufficient for reprogramming non-myelinating cells into myelin gene-expressing cells.表观遗传修饰物对于将非髓鞘形成细胞重编程为髓鞘基因表达细胞是必要的,但不是充分的。
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本文引用的文献

1
Chromatin states of core pluripotency-associated genes in pluripotent, multipotent and differentiated cells.多能性、多潜能和分化细胞中核心多能性相关基因的染色质状态。
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Polycomb limits the neurogenic competence of neural precursor cells to promote astrogenic fate transition.多梳蛋白限制神经前体细胞的神经发生能力以促进向星形胶质细胞命运的转变。
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Two-tier transcriptional control of oligodendrocyte differentiation.
少突胶质细胞成熟改变导致脱髓鞘的细胞死亡机制。
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Epigenetic regulation and factors that influence the effect of iPSCs-derived neural stem/progenitor cells (NS/PCs) in the treatment of spinal cord injury.表观遗传调控及影响 iPS 细胞衍生的神经干细胞/祖细胞(NS/PCs)治疗脊髓损伤效果的因素。
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The epigenetic landscape of oligodendrocyte lineage cells.少突胶质细胞谱系细胞的表观遗传学景观。
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7
In individuals with Williams syndrome, dysregulation of methylation in non-coding regions of neuronal and oligodendrocyte DNA is associated with pathology and cortical development.在患有威廉姆斯综合征的个体中,神经元和少突胶质细胞DNA非编码区的甲基化失调与病理和皮质发育有关。
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8
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少突胶质细胞分化的两层转录控制。
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SoxE function in vertebrate nervous system development.SoxE 在脊椎动物神经系统发育中的功能。
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Tubulin polymerization-promoting protein (TPPP/p25) is critical for oligodendrocyte differentiation.微管蛋白促进蛋白(TPPP/p25)对少突胶质细胞分化至关重要。
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Dysregulation of the Wnt pathway inhibits timely myelination and remyelination in the mammalian CNS.Wnt信号通路的失调会抑制哺乳动物中枢神经系统中髓鞘的及时形成和再髓鞘化。
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