4.7 Article

TFII-I and USF (RBF-2) regulate Ras/MAPK-responsive HIV-1 transcription in T cells

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EUROPEAN JOURNAL OF CANCER
卷 41, 期 16, 页码 2528-2536

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ELSEVIER SCI LTD
DOI: 10.1016/j.ejca.2005.08.011

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transcription; Ras; USF1; USF2; TFII-I; HIV-1; chromatin; T cells

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The HIV-1 long terminal repeat (LTR) is stringently controlled by T cell activation signals, and binds a variety of transcription factors whose activities are regulated downstream of the T cell receptor. One of the most highly conserved cis-elements on the LTR, designated RBEIII, binds the factor RBF-2 which is comprised of a USF-1/USF-2 heterodimer and a co-factor TFII-I. RBF-2 is necessary for transcription from the LTR in response to RAS-MAPK activation through T cell receptor engagement, but is also required for repression of viral expression in unstimulated cells. Considering the defined activities of USF and TFII-I, RBF-2 may be responsible for regulating promoter context by controlling chromatin organisation, thereby coordinating opportunity for transcriptional activation by additional factors bound to the enhancer region. (c) 2005 Elsevier Ltd. All rights reserved.

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