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Induced expression from the Moloney murine leukemia virus long terminal repeat during differentiation of human myeloid cells is mediated through its transcriptional enhancer.

机译:莫洛尼氏鼠白血病病毒在人类骨髓细胞分化过程中长末端重复序列的诱导表达是通过其转录增强子介导的。

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摘要

Transcription from the Moloney murine leukemia virus (Mo-MuLV) long terminal repeat (LTR) is inhibited in murine stem cells and induced during maturation of these cells. We have investigated whether alterations in the activity of this viral regulatory element also occur during differentiation of human myeloid leukemia cells. The Mo-MuLV LTR and the simian virus 40 (SV40) early promoter were introduced into HL-60 promyelocytes on Epstein-Barr virus-derived chloramphenicol acetyltransferase expression vectors. When these cells were induced to terminally differentiate, transcription from the Mo-MuLV LTR was induced approximately 10-fold. Expression from the SV40 promoter remained constant during differentiation of these cells. Replacing the SV40 transcriptional enhancer with the Mo-MuLV LTR transcriptional enhancer rendered the SV40 promoter inducible during differentiation. We conclude that sequences within the transcriptional enhancer of the Mo-MuLV LTR contain cis-acting elements responsible for induction of gene expression during differentiation of human myeloid cells.
机译:莫洛尼鼠白血病病毒(Mo-MuLV)的长末端重复序列(LTR)的转录在鼠干细胞中受到抑制,并在这些细胞成熟期间被诱导。我们已经研究了在人类髓样白血病细胞分化过程中是否也发生了这种病毒调节元件活性的改变。 Mo-MuLV LTR和猿猴病毒40(SV40)早期启动子被引入到Epstein-Barr病毒衍生的氯霉素乙酰转移酶表达载体的HL-60早幼粒细胞中。当这些细胞被诱导最终分化时,从Mo-MuLV LTR的转录被诱导大约10倍。在这些细胞分化过程中,SV40启动子的表达保持恒定。用Mo-MuLV LTR转录增强子替代SV40转录增强子使得SV40启动子在分化过程中可被诱导。我们得出结论,Mo-MuLV LTR转录增强子内的序列包含顺式作用元件,负责在人类髓样细胞分化过程中诱导基因表达。

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