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本文引用的文献

1
A robust and highly efficient immune cell reprogramming system.一种强大且高效的免疫细胞重编程系统。
Cell Stem Cell. 2009 Nov 6;5(5):554-66. doi: 10.1016/j.stem.2009.10.004.
2
Epigenetic chromatin states uniquely define the developmental plasticity of murine hematopoietic stem cells.表观遗传染色质状态独特地定义了小鼠造血干细胞的发育可塑性。
Blood. 2010 Jan 14;115(2):247-56. doi: 10.1182/blood-2009-07-235176. Epub 2009 Nov 3.
3
A recurrent network involving the transcription factors PU.1 and Gfi1 orchestrates innate and adaptive immune cell fates.一个涉及转录因子PU.1和Gfi1的循环网络协调先天性和适应性免疫细胞的命运。
Immunity. 2009 Oct 16;31(4):576-86. doi: 10.1016/j.immuni.2009.07.011. Epub 2009 Oct 8.
4
Self-renewal of the long-term reconstituting subset of hematopoietic stem cells is regulated by Ikaros.造血干细胞的长期重建亚群的自我更新由 Ikaros 调节。
Stem Cells. 2009 Dec;27(12):3082-92. doi: 10.1002/stem.232.
5
Distinct roles for E12 and E47 in B cell specification and the sequential rearrangement of immunoglobulin light chain loci.E12和E47在B细胞特异性及免疫球蛋白轻链基因座的顺序重排中的不同作用。
J Exp Med. 2009 Sep 28;206(10):2271-84. doi: 10.1084/jem.20090756. Epub 2009 Sep 14.
6
Genome-wide mapping of HATs and HDACs reveals distinct functions in active and inactive genes.全基因组范围内对组蛋白乙酰转移酶(HATs)和组蛋白去乙酰化酶(HDACs)的图谱绘制揭示了它们在活跃基因和非活跃基因中的不同功能。
Cell. 2009 Sep 4;138(5):1019-31. doi: 10.1016/j.cell.2009.06.049. Epub 2009 Aug 20.
7
Opposing effects of SWI/SNF and Mi-2/NuRD chromatin remodeling complexes on epigenetic reprogramming by EBF and Pax5.SWI/SNF和Mi-2/NuRD染色质重塑复合物对EBF和Pax5介导的表观遗传重编程的相反作用。
Proc Natl Acad Sci U S A. 2009 Jul 7;106(27):11258-63. doi: 10.1073/pnas.0809485106. Epub 2009 Jun 19.
8
Stepwise activation of enhancer and promoter regions of the B cell commitment gene Pax5 in early lymphopoiesis.在早期淋巴细胞生成过程中,B细胞定向分化基因Pax5的增强子和启动子区域的逐步激活。
Immunity. 2009 Apr 17;30(4):508-20. doi: 10.1016/j.immuni.2009.01.012. Epub 2009 Apr 2.
9
Genome-wide lineage-specific transcriptional networks underscore Ikaros-dependent lymphoid priming in hematopoietic stem cells.全基因组谱系特异性转录网络强调造血干细胞中依赖Ikaros的淋巴细胞启动。
Immunity. 2009 Apr 17;30(4):493-507. doi: 10.1016/j.immuni.2009.01.014. Epub 2009 Apr 2.
10
E2A proteins maintain the hematopoietic stem cell pool and promote the maturation of myelolymphoid and myeloerythroid progenitors.E2A蛋白维持造血干细胞池,并促进骨髓淋巴细胞和骨髓红系祖细胞的成熟。
Proc Natl Acad Sci U S A. 2009 Feb 10;106(6):1930-5. doi: 10.1073/pnas.0808866106. Epub 2009 Jan 30.

从造血祖细胞到 B 细胞:谱系限制和定向的机制。

From hematopoietic progenitors to B cells: mechanisms of lineage restriction and commitment.

机构信息

Integrated Department of Immunology, National Jewish Health, Denver, CO 80206, USA.

出版信息

Curr Opin Immunol. 2010 Apr;22(2):177-84. doi: 10.1016/j.coi.2010.02.003. Epub 2010 Mar 6.

DOI:10.1016/j.coi.2010.02.003
PMID:20207529
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2854230/
Abstract

The generation of B lymphocytes from hematopoietic progenitors requires lineage-specific transcription factors that progressively direct cell fate choices. Differentiation of hematopoietic stem cells to lymphoid progenitors requires Ikaros-dependent lineage priming and graded levels of PU.1, which are controlled by Ikaros and Gfi1. E2A drives expression of EBF1, which initiates B lineage specification. EBF1, in addition to Pax5, is necessary for commitment to the B cell lineage. As a model of gene activation in early B lymphopoiesis, mb-1 genes are activated sequentially by factors (e.g. EBF1) that initiate chromatin modifications before transcription. This review highlights the requisite interplay between transcription factors and epigenetic mechanisms in the context of B cell development.

摘要

B 淋巴细胞由造血祖细胞生成,需要特异性转录因子来逐步指导细胞命运选择。造血干细胞向淋巴样祖细胞的分化需要依赖 Ikaros 的谱系启动和逐渐增加的 PU.1 水平,这由 Ikaros 和 Gfi1 控制。E2A 驱动 EBF1 的表达,从而启动 B 细胞谱系的特异性。EBF1 与 Pax5 一起,对于 B 细胞谱系的确定是必需的。作为早期 B 淋巴细胞发生中基因激活的模型,mb-1 基因被(如 EBF1)等因子依次激活,这些因子在转录前引发染色质修饰。本综述强调了转录因子和表观遗传机制在 B 细胞发育过程中的必要相互作用。