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Updated: Aug 15, 2026

Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells
Published on: March 9, 2012
TFII-I and USF (RBF-2) regulate Ras/MAPK-responsive HIV-1 transcription in T cells
Ivan Sadowski1, David A Mitchell
1Department of Biochemistry and Molecular Biology, University of British Columbia, 2146 Health Sciences Mall, Vancouver, BC, Canada V6T 1Z3. sadowski@interchange.ubc.ca
Abstract:
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.
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