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本文引用的文献

1
Epigenetic gene silencing underlies C-fiber dysfunctions in neuropathic pain.表观遗传基因沉默是神经性疼痛中 C 纤维功能障碍的基础。
J Neurosci. 2010 Mar 31;30(13):4806-14. doi: 10.1523/JNEUROSCI.5541-09.2010.
2
Regulation of the polycomb protein Ring1B by self-ubiquitination or by E6-AP may have implications to the pathogenesis of Angelman syndrome.多梳蛋白 Ring1B 的自我泛素化或通过 E6-AP 的调控可能与 Angelman 综合征的发病机制有关。
Proc Natl Acad Sci U S A. 2010 Apr 13;107(15):6788-93. doi: 10.1073/pnas.1003108107. Epub 2010 Mar 29.
3
Polycomb group proteins as epigenetic mediators of neuroprotection in ischemic tolerance.多梳蛋白作为缺血耐受中神经保护的表观遗传介质。
Sci Signal. 2010 Mar 2;3(111):ra15. doi: 10.1126/scisignal.2000502.
4
Mechanisms of polycomb gene silencing: knowns and unknowns.多梳基因沉默的机制:已知与未知
Nat Rev Mol Cell Biol. 2009 Oct;10(10):697-708. doi: 10.1038/nrm2763. Epub 2009 Sep 9.
5
DYRK1A interacts with the REST/NRSF-SWI/SNF chromatin remodelling complex to deregulate gene clusters involved in the neuronal phenotypic traits of Down syndrome.双重特异性酪氨酸磷酸化调节激酶1A(DYRK1A)与REST/NRSF- SWI/SNF染色质重塑复合体相互作用,从而使参与唐氏综合征神经元表型特征的基因簇失调。
Hum Mol Genet. 2009 Apr 15;18(8):1405-14. doi: 10.1093/hmg/ddp047. Epub 2009 Feb 12.
6
The polycomb group gene Bmi1 regulates antioxidant defenses in neurons by repressing p53 pro-oxidant activity.多梳蛋白家族基因Bmi1通过抑制p53的促氧化活性来调节神经元中的抗氧化防御。
J Neurosci. 2009 Jan 14;29(2):529-42. doi: 10.1523/JNEUROSCI.5303-08.2009.
7
Post-ischemic brain damage: effect of ischemic preconditioning and postconditioning and identification of potential candidates for stroke therapy.缺血后脑损伤:缺血预处理和后处理的作用及中风治疗潜在候选物的鉴定
FEBS J. 2009 Jan;276(1):46-57. doi: 10.1111/j.1742-4658.2008.06769.x.
8
Genomewide analysis of PRC1 and PRC2 occupancy identifies two classes of bivalent domains.对多梳抑制复合体1(PRC1)和多梳抑制复合体2(PRC2)占据情况的全基因组分析确定了两类双价结构域。
PLoS Genet. 2008 Oct;4(10):e1000242. doi: 10.1371/journal.pgen.1000242. Epub 2008 Oct 31.
9
DYRK1A-dosage imbalance perturbs NRSF/REST levels, deregulating pluripotency and embryonic stem cell fate in Down syndrome.DYRK1A剂量失衡扰乱NRSF/REST水平,导致唐氏综合征中多能性和胚胎干细胞命运失调。
Am J Hum Genet. 2008 Sep;83(3):388-400. doi: 10.1016/j.ajhg.2008.08.012. Epub 2008 Sep 4.
10
Polycomb complexes and epigenetic states.多梳复合体与表观遗传状态。
Curr Opin Cell Biol. 2008 Jun;20(3):266-73. doi: 10.1016/j.ceb.2008.03.002. Epub 2008 Apr 23.

用细齿梳子消除神经元死亡的介质。

Eradicating the mediators of neuronal death with a fine-tooth comb.

机构信息

Dominick P. Purpura Department of Neuroscience, Rose F. Kennedy Center, Room 610, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.

出版信息

Sci Signal. 2010 Jun 8;3(125):pe20. doi: 10.1126/scisignal.3125pe20.

DOI:10.1126/scisignal.3125pe20
PMID:20530801
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3501109/
Abstract

Ischemic tolerance is an evolutionarily conserved form of cerebral plasticity in which a brief period of cerebral ischemia (called ischemic preconditioning) confers transient tolerance to a subsequent ischemic challenge in the brain. Polycomb group proteins are gene-silencing factors that are abundant and widely distributed during embryogenesis and are essential to epigenetic cellular memory, pluripotency, and stem cell self-renewal. New insight into the molecular mechanisms underlying ischemic tolerance is highlighted by the finding that ischemic preconditioning activates polycomb proteins in mature neurons. Polycomb proteins act through epigenetic gene silencing to eradicate potential mediators of neuronal death and promote cellular arrest, enabling mature neurons to survive ischemic stroke.

摘要

缺血耐受是大脑可塑性的一种进化保守形式,其中短暂的脑缺血(称为缺血预处理)赋予大脑随后的缺血性挑战短暂的耐受性。多梳组蛋白是基因沉默因子,在胚胎发生期间丰富且广泛分布,对表观遗传细胞记忆、多能性和干细胞自我更新至关重要。缺血预处理激活成熟神经元中的多梳蛋白这一发现突出了对缺血耐受相关分子机制的新认识。多梳蛋白通过表观遗传基因沉默来消除神经元死亡的潜在介质,并促进细胞停滞,使成熟神经元能够在缺血性中风中存活。