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T细胞白血病蛋白SCL/tal-1在血管发育中存在未被发现的作用。

Unsuspected role for the T-cell leukemia protein SCL/tal-1 in vascular development.

作者信息

Visvader J E, Fujiwara Y, Orkin S H

机构信息

Division of Hematology-Oncology, Children's Hospital and the Dana Farber Cancer Center, Department of Pediatrics, and the Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.

出版信息

Genes Dev. 1998 Feb 15;12(4):473-9. doi: 10.1101/gad.12.4.473.

DOI:10.1101/gad.12.4.473
PMID:9472016
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC316527/
Abstract

The transcription factor SCL/tal-1 is essential for blood cell development. Though it is also expressed in vascular endothelium, SCL has been considered dispensable for vessel formation. Through transgenic rescue of hematopoietic defects of SCL-/- embryos and analysis of chimeras generated with SCL-/- ES cells tagged with a transgene expressed in vascular endothelial cells, we show that SCL is essential for angiogenic remodeling of the yolk sac capillary network into complex vitelline vessels. These findings establish a role for SCL in embryonic angiogenesis and argue for critical functions in both embryonic blood and vascular cells, the descendents of the presumptive hemangioblast.

摘要

转录因子SCL/tal-1对血细胞发育至关重要。尽管它也在血管内皮中表达,但SCL一直被认为对血管形成是可有可无的。通过对SCL-/-胚胎造血缺陷的转基因拯救以及对用在血管内皮细胞中表达的转基因标记的SCL-/-胚胎干细胞产生的嵌合体进行分析,我们发现SCL对于将卵黄囊毛细血管网络重塑为复杂的卵黄管是血管生成所必需的。这些发现确立了SCL在胚胎血管生成中的作用,并表明其在胚胎血液和血管细胞(假定成血管细胞的后代)中具有关键功能。

相似文献

1
Unsuspected role for the T-cell leukemia protein SCL/tal-1 in vascular development.T细胞白血病蛋白SCL/tal-1在血管发育中存在未被发现的作用。
Genes Dev. 1998 Feb 15;12(4):473-9. doi: 10.1101/gad.12.4.473.
2
An SCL 3' enhancer targets developing endothelium together with embryonic and adult haematopoietic progenitors.一个SCL 3'增强子与胚胎和成年造血祖细胞一起靶向发育中的内皮细胞。
Development. 1999 Sep;126(17):3891-904. doi: 10.1242/dev.126.17.3891.
3
Selective rescue of early haematopoietic progenitors in Scl(-/-) mice by expressing Scl under the control of a stem cell enhancer.通过在干细胞增强子的控制下表达Scl,选择性拯救Scl(-/-)小鼠中的早期造血祖细胞。
Development. 2001 Dec;128(23):4815-27. doi: 10.1242/dev.128.23.4815.
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The bHLH TAL-1/SCL regulates endothelial cell migration and morphogenesis.bHLH转录因子TAL-1/SCL调节内皮细胞迁移和形态发生。
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Hematopoietic-specific genes are not induced during in vitro differentiation of scl-null embryonic stem cells.造血特异性基因在scl基因缺失的胚胎干细胞体外分化过程中未被诱导表达。
Blood. 1997 Aug 15;90(4):1435-47.
6
A mutant receptor tyrosine phosphatase, CD148, causes defects in vascular development.一种突变的受体酪氨酸磷酸酶CD148会导致血管发育缺陷。
Mol Cell Biol. 2003 Mar;23(5):1817-31. doi: 10.1128/MCB.23.5.1817-1831.2003.
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The SCL/TAL-1 gene is expressed in progenitors of both the hematopoietic and vascular systems during embryogenesis.SCL/TAL-1基因在胚胎发育过程中于造血系统和血管系统的祖细胞中表达。
Blood. 1994 Mar 1;83(5):1200-8.
8
Lmo2 and Scl/Tal1 convert non-axial mesoderm into haemangioblasts which differentiate into endothelial cells in the absence of Gata1.Lmo2和Scl/Tal1将非轴中胚层转化为成血管细胞,在缺乏Gata1的情况下,这些成血管细胞会分化为内皮细胞。
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Absence of yolk sac hematopoiesis from mice with a targeted disruption of the scl gene.scl基因靶向破坏的小鼠中卵黄囊造血功能缺失。
Proc Natl Acad Sci U S A. 1995 Jul 18;92(15):7075-9. doi: 10.1073/pnas.92.15.7075.
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The T cell leukemia oncoprotein SCL/tal-1 is essential for development of all hematopoietic lineages.T细胞白血病癌蛋白SCL/tal-1对所有造血谱系的发育至关重要。
Cell. 1996 Jul 12;86(1):47-57. doi: 10.1016/s0092-8674(00)80076-8.

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本文引用的文献

1
Yolk sac angiogenic defect and intra-embryonic apoptosis in mice lacking the Ets-related factor TEL.缺乏Ets相关因子TEL的小鼠的卵黄囊血管生成缺陷和胚胎内凋亡
EMBO J. 1997 Jul 16;16(14):4374-83. doi: 10.1093/emboj/16.14.4374.
2
An upstream, DNase I hypersensitive region of the hematopoietic-expressed transcription factor GATA-1 gene confers developmental specificity in transgenic mice.造血表达转录因子GATA-1基因的一个上游DNase I超敏区域赋予转基因小鼠发育特异性。
Proc Natl Acad Sci U S A. 1997 Jul 22;94(15):7976-81. doi: 10.1073/pnas.94.15.7976.
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A requirement for Flk1 in primitive and definitive hematopoiesis and vasculogenesis.原始造血、定向造血及血管生成过程中对Flk1的需求。
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4
Abnormal angiogenesis and responses to glucose and oxygen deprivation in mice lacking the protein ARNT.缺乏蛋白质ARNT的小鼠的异常血管生成以及对葡萄糖和氧剥夺的反应。
Nature. 1997 Mar 27;386(6623):403-7. doi: 10.1038/386403a0.
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Mechanisms of angiogenesis.血管生成的机制。
Nature. 1997 Apr 17;386(6626):671-4. doi: 10.1038/386671a0.
6
Disruption of overlapping transcripts in the ROSA beta geo 26 gene trap strain leads to widespread expression of beta-galactosidase in mouse embryos and hematopoietic cells.ROSA βgeo 26基因捕获品系中重叠转录本的破坏导致β-半乳糖苷酶在小鼠胚胎和造血细胞中广泛表达。
Proc Natl Acad Sci U S A. 1997 Apr 15;94(8):3789-94. doi: 10.1073/pnas.94.8.3789.
7
Uniform vascular-endothelial-cell-specific gene expression in both embryonic and adult transgenic mice.在胚胎期和成年转基因小鼠中均有一致的血管内皮细胞特异性基因表达。
Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):3058-63. doi: 10.1073/pnas.94.7.3058.
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Initiation of murine embryonic erythropoiesis: a spatial analysis.小鼠胚胎红细胞生成的起始:空间分析
Blood. 1997 Feb 15;89(4):1154-64.
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Vascular system defects and impaired cell chemokinesis as a result of Galpha13 deficiency.由于Gα13缺乏导致的血管系统缺陷和细胞趋化性受损。
Science. 1997 Jan 24;275(5299):533-6. doi: 10.1126/science.275.5299.533.
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Vascular dysmorphogenesis caused by an activating mutation in the receptor tyrosine kinase TIE2.受体酪氨酸激酶TIE2激活突变引起的血管发育异常。
Cell. 1996 Dec 27;87(7):1181-90. doi: 10.1016/s0092-8674(00)81814-0.