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Replacement of Oct4 by Tet1 during iPSC induction reveals an important role of DNA methylation and hydroxymethylation in reprogramming.在诱导多能干细胞过程中,Tet1 取代 Oct4 揭示了 DNA 甲基化和羟甲基化在重编程中的重要作用。
Cell Stem Cell. 2013 Apr 4;12(4):453-69. doi: 10.1016/j.stem.2013.02.005. Epub 2013 Mar 14.
2
Different roles for Tet1 and Tet2 proteins in reprogramming-mediated erasure of imprints induced by EGC fusion.不同的 Tet1 和 Tet2 蛋白在胚胎干细胞融合诱导的印迹重编程中的作用。
Mol Cell. 2013 Mar 28;49(6):1023-33. doi: 10.1016/j.molcel.2013.01.032. Epub 2013 Feb 28.
3
NANOG-dependent function of TET1 and TET2 in establishment of pluripotency.NANOG 依赖的 TET1 和 TET2 功能在多能性建立中的作用。
Nature. 2013 Mar 21;495(7441):370-4. doi: 10.1038/nature11925. Epub 2013 Feb 10.
4
A molecular roadmap of reprogramming somatic cells into iPS cells.重编程体细胞为诱导多能干细胞的分子路线图。
Cell. 2012 Dec 21;151(7):1617-32. doi: 10.1016/j.cell.2012.11.039.
5
Generation of integration-free neural progenitor cells from cells in human urine.从人尿中细胞生成无整合的神经祖细胞。
Nat Methods. 2013 Jan;10(1):84-9. doi: 10.1038/nmeth.2283. Epub 2012 Dec 9.
6
Nuclear cloning and direct reprogramming: the long and the short path to Stockholm.核克隆与直接重编程:通往斯德哥尔摩的漫长与捷径。
Cell Stem Cell. 2012 Dec 7;11(6):744-7. doi: 10.1016/j.stem.2012.11.005.
7
H3K9 methylation is a barrier during somatic cell reprogramming into iPSCs.H3K9 甲基化是体细胞重编程为 iPS 细胞过程中的一个障碍。
Nat Genet. 2013 Jan;45(1):34-42. doi: 10.1038/ng.2491. Epub 2012 Dec 2.
8
Distinct metabolic flow enables large-scale purification of mouse and human pluripotent stem cell-derived cardiomyocytes.独特的代谢流可实现大规模纯化鼠和人多能干细胞来源的心肌细胞。
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9
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Nat Med. 2012 Dec;18(12):1778-85. doi: 10.1038/nm.2984. Epub 2012 Nov 11.
10
Metabolic plasticity in stem cell homeostasis and differentiation.干细胞稳态和分化中的代谢可塑性。
Cell Stem Cell. 2012 Nov 2;11(5):596-606. doi: 10.1016/j.stem.2012.10.002.

小分子在体细胞重编程中的作用。

Roles of small molecules in somatic cell reprogramming.

机构信息

Key Laboratory of Regenerative Biology, South China Institute for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou 510530, China.

出版信息

Acta Pharmacol Sin. 2013 Jun;34(6):719-24. doi: 10.1038/aps.2013.73. Epub 2013 Jun 3.

DOI:10.1038/aps.2013.73
PMID:23728722
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4002901/
Abstract

The Nobel Prize in Physiology and Medicine 2012 was awarded to Sir John B GURDON and Shinya YAMANAKA for their discovery that mature cells can be reprogrammed to become pluripotent. This event reaffirms the importance of research on cell fate plasticity and the technology progress in the stem cell field and regenerative medicine. Indeed, reprogramming technology has developed at a dazzling speed within the past 6 years, yet we are still at the early stages of understanding the mechanisms of cell fate identity. This is particularly true in the case of human induced pluripotent stem cells (iPSCs), which lack reliable standards in the evaluation of their fidelity and safety prior to their application. Along with the genetic approaches, small molecules nowadays become convenient tools for modulating endogenous protein functions and regulating key cellular processes, including the mesenchymal-to-epithelial transition, metabolism, signal transduction and epigenetics. Moreover, small molecules may affect not only the efficiency of clone formation but also the quality of the resulting cells. With increasing availability of such chemicals, we can better understand the biology of stems cells and further improve the technology of generation of stem cells.

摘要

2012 年诺贝尔生理学或医学奖授予约翰·格登爵士(Sir John B GURDON)和山中伸弥(Shinya YAMANAKA),以表彰他们发现成熟细胞可以被重新编程为多能性细胞。这一事件再次肯定了细胞命运可塑性研究以及干细胞领域和再生医学技术进步的重要性。事实上,在过去的 6 年里,重编程技术发展迅速,但我们对细胞命运身份的机制仍处于初步了解阶段。对于人类诱导多能干细胞(iPSCs)来说尤其如此,在应用之前,它们在评估其保真度和安全性方面缺乏可靠的标准。除了遗传方法外,小分子现在成为调节内源性蛋白功能和调节关键细胞过程(包括间质到上皮转化、代谢、信号转导和表观遗传学)的便捷工具。此外,小分子不仅可以影响克隆形成的效率,还可以影响产生的细胞的质量。随着这些化学物质的可用性的增加,我们可以更好地了解干细胞的生物学,并进一步改进干细胞的生成技术。