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c-myb原癌基因产物的转录反式抑制作用。

Transcriptional trans-repression by the c-myb proto-oncogene product.

作者信息

Nakagoshi H, Nagase T, Ueno Y, Ishii S

机构信息

Laboratory of Molecular Genetics, Institute of Physical and Chemical Research (RIKEN), Ibaraki, Japan.

出版信息

Nucleic Acids Res. 1989 Sep 25;17(18):7315-24. doi: 10.1093/nar/17.18.7315.

Abstract

We report that the c-myb protein binds to another site, MBS-II, in the SV40 enhancer with low affinity. In co-transfection experiments with a c-myb expression plasmid, tandem repeats of the sequence containing the MBS-II site induced c-myb-dependent transcriptional repression. Results of mutational analyses of the sequence around the MBS-II site suggested that the c-myb protein represses transcription by competing with another trans-activator. These results indicate that c-myb protein can regulate transcription not only positively but also negatively.

摘要

我们报告称,c-myb蛋白以低亲和力与SV40增强子中的另一个位点MBS-II结合。在与c-myb表达质粒的共转染实验中,含有MBS-II位点的序列串联重复诱导了c-myb依赖性的转录抑制。对MBS-II位点周围序列的突变分析结果表明,c-myb蛋白通过与另一种反式激活因子竞争来抑制转录。这些结果表明,c-myb蛋白不仅可以正向调节转录,还可以负向调节转录。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4768/334811/19b9022f33a5/nar00135-0178-a.jpg

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