Kusk P, John S, Fragoso G, Michelotti J, Hager G L
Laboratory of Receptor Biology and Gene Expression, NCI, National Institutes of Health, Bethesda, Maryland 20892-5055, USA.
J Biol Chem. 1996 Dec 6;271(49):31269-76. doi: 10.1074/jbc.271.49.31269.
The long terminal repeat of the mouse mammary tumor virus restricts virus expression primarily to the mammary epithelium. The extreme 5' end of the long terminal repeat contains an enhancer that has been associated with tissue-specific expression of the virus. A total of six functional cis-acting elements have been identified in the enhancer. Although proteins binding to these elements have been reported, only one has been identified; this factor, mp5, is identical or closely related to the transcription factor AP-2 (Mellentin-Michelotti, J., John, S., Pennie, W. D., Williams, T., and Hager, G. L. (1994) J. Biol. Chem. 269, 31983-31990). The other factors are hitherto unidentified and poorly described. We report here the characterization of another of the six elements, previously referred to as the F3 site (Mink, S., Hartig, E., Jennewein, P., Doppler, W., and Cato, A. C. (1992) Mol. Cell Biol. 12, 4906-4918). We show that the F3 binding activity and AP-2 act synergistically to enhance mouse mammary tumor virus-directed transcription, but only in the presence of glucocorticoid hormone. The F3 element has an NF-1-like half-site, but the activity recognizing this element has binding characteristics distinct from the NF-1/CTF family as well as the rest of the CCAAT-binding proteins. We conclude that the F3 activity represents a new member of the NF-1/CTF family.
小鼠乳腺肿瘤病毒的长末端重复序列主要将病毒表达限制在乳腺上皮细胞。长末端重复序列的最5'端包含一个与病毒组织特异性表达相关的增强子。在该增强子中总共鉴定出六个功能性顺式作用元件。尽管已报道了与这些元件结合的蛋白质，但仅鉴定出一种；这个因子mp5与转录因子AP-2相同或密切相关（Mellentin-Michelotti, J., John, S., Pennie, W. D., Williams, T., and Hager, G. L. (1994) J. Biol. Chem. 269, 31983 - 31990）。其他因子迄今尚未鉴定且描述甚少。我们在此报告对六个元件中的另一个元件的特性描述，该元件先前被称为F3位点（Mink, S., Hartig, E., Jennewein, P., Doppler, W., and Cato, A. C. (1992) Mol. Cell Biol. 12, 4906 - 4918）。我们表明，F3结合活性和AP-2协同作用以增强小鼠乳腺肿瘤病毒介导的转录，但仅在糖皮质激素存在的情况下。F3元件具有一个类似NF-1的半位点，但识别该元件的活性具有与NF-1/CTF家族以及其余CCAAT结合蛋白不同的结合特性。我们得出结论，F3活性代表NF-1/CTF家族的一个新成员。
