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横纹肌肉瘤中肌分化抗原(MyoD)活性及肌生成所需因子的缺乏。

Deficiency in rhabdomyosarcomas of a factor required for MyoD activity and myogenesis.

作者信息

Tapscott S J, Thayer M J, Weintraub H

机构信息

Fred Hutchinson Cancer Research Center, Seattle, WA 98104.

出版信息

Science. 1993 Mar 5;259(5100):1450-3. doi: 10.1126/science.8383879.

DOI:10.1126/science.8383879
PMID:8383879
Abstract

Rhabdomyosarcoma cells express the myogenic helix-loop-helix proteins of the MyoD family but do not differentiate into skeletal muscle cells. Gel shift and transient transfection assays revealed that MyoD in the rhabdomyosarcoma cells was capable of binding DNA but was relatively nonfunctional as a transcriptional activator. Heterokaryon formation with fibroblasts resulted in the restoration of transcriptional activation by MyoD and the differentiation of the rhabdomyosarcoma cells into skeletal muscle cells. These results suggest that rhabdomyosarcomas are deficient in a factor required for MyoD activity.

摘要

横纹肌肉瘤细胞表达MyoD家族的生肌螺旋-环-螺旋蛋白,但不会分化为骨骼肌细胞。凝胶迁移和瞬时转染分析表明,横纹肌肉瘤细胞中的MyoD能够结合DNA,但作为转录激活因子相对无功能。与成纤维细胞形成异核体导致MyoD恢复转录激活,横纹肌肉瘤细胞分化为骨骼肌细胞。这些结果表明,横纹肌肉瘤缺乏MyoD活性所需的一种因子。

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Deficiency in rhabdomyosarcomas of a factor required for MyoD activity and myogenesis.横纹肌肉瘤中肌分化抗原(MyoD)活性及肌生成所需因子的缺乏。
Science. 1993 Mar 5;259(5100):1450-3. doi: 10.1126/science.8383879.
2
Transcriptional activation domain of the muscle-specific gene-regulatory protein myf5.肌肉特异性基因调控蛋白Myf5的转录激活结构域。
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Comparison of genome-wide binding of MyoD in normal human myogenic cells and rhabdomyosarcomas identifies regional and local suppression of promyogenic transcription factors.比较正常人类成肌细胞和横纹肌肉瘤中 MyoD 的全基因组结合,确定了促成肌转录因子的局部和区域抑制。
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Regulatory elements that control the lineage-specific expression of myoD.
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Repression of c-fos promoter by MyoD on muscle cell differentiation.在肌肉细胞分化过程中,MyoD对c-fos启动子的抑制作用。
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Transcriptional activation of the myogenin gene by MEF2-mediated recruitment of myf5 is inhibited by adenovirus E1A protein.腺病毒E1A蛋白可抑制MEF2介导的myf5募集对肌细胞生成素基因的转录激活作用。
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Mutation of Thr115 in MyoD positively regulates function in murine fibroblasts and human rhabdomyosarcoma cells.MyoD中苏氨酸115位点的突变正向调控小鼠成纤维细胞和人横纹肌肉瘤细胞的功能。
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DNA binding and transcriptional regulatory activity of mammalian achaete-scute homologous (MASH) proteins revealed by interaction with a muscle-specific enhancer.通过与肌肉特异性增强子相互作用揭示的哺乳动物无刚毛-小盾片同源(MASH)蛋白的DNA结合和转录调控活性
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Rhabdomyosarcomas do not contain mutations in the DNA binding domains of myogenic transcription factors.横纹肌肉瘤在生肌转录因子的DNA结合结构域中不含有突变。
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Cell-cell interaction modulates myoD-induced skeletal myogenesis of pluripotent P19 cells in vitro.细胞间相互作用在体外调节多能性P19细胞中MyoD诱导的骨骼肌生成。
Exp Cell Res. 1999 Aug 25;251(1):79-91. doi: 10.1006/excr.1999.4567.

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