1: J Immunol. 1999 May 15;162(10):5986-92. 

USF/c-Myc enhances, while Yin-Yang 1 suppresses, the promoter activity of CXCR4,
a coreceptor for HIV-1 entry.

Moriuchi M, Moriuchi H, Margolis DM, Fauci AS.

Laboratory of Immunoregulation, National Institute of Allergy and Infectious
Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Baltimore, MD
21201, USA.

Transcription factors USF1 and USF2 up-regulate gene expression (i.e. , HIV-1
long terminal repeats) via interaction with an E box on their target promoters,
which is also a binding site for c-Myc. The c-Myc oncoprotein is important in
control of cellular proliferation and differentiation, while Yin-Yang 1 (YY1)
has been shown to control the expression of a number of cellular and viral
genes. These two proteins physically interact with each other and mutually
inhibit their respective biological functions. In this study, we show that
USF/c-Myc up-regulates, while YY1 down-regulates the promoter activity of CXCR4,
a coreceptor for T cell-tropic HIV-1 entry. We have identified an E box around
-260 and a YY1 binding site around -300 relative to the transcription start
site. Mutation of the E box abolished USF/c-Myc-mediated up-regulation of CXCR4
promoter activity, and mutation of the YY1 binding site was associated with
unresponsiveness to YY1-mediated inhibition. These data suggest that USF/c-Myc
and YY1 may play an important role in the HIV-1-replicative cycle, by modulating
both the viral fusion/entry process and viral expression.

PMID: 10229837 [PubMed - indexed for MEDLINE]


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2: J Biol Chem. 1998 Oct 2;273(40):26130-7. 

Cloning and characterization of the 5'-flanking region for the human
topoisomerase III gene.

Kim JC, Yoon JB, Koo HS, Chung IK.

Department of Biology, College of Science, Bioproducts Research Center, Yonsei
University, Seoul 120-749, Korea.

The human DNA topoisomerase III (hTOP3) gene encodes a topoisomerase homologous
to the Escherichia coli DNA topoisomerase I subfamily. To understand the
mechanisms responsible for regulating hTOP3 expression, we have cloned the
5'-flanking region of the gene coding for the hTOP3 and analyzed its promoter
activity. The presence of a single transcription initiation site was suggested
by primer extension analysis. The hTOP3 gene promoter is moderately high in GC
content and lacks a canonical TATA box, suggesting that hTOP3 promoter has
overall similarity to promoters of a number of housekeeping genes. Examination
of the promoter sequence indicated the presence of four Sp-1 consensus binding
sequences and a putative initiator element surrounding the transcription
initiation site. Transient expression of a luciferase reporter gene under the
control of serially deleted 5'-flanking sequences revealed that the 52-base pair
region from -326 to -275 upstream of the transcription initiation site includes
a positive cis-acting element(s) for the efficient expression of hTOP3 gene. On
the basis of gel mobility shift and supershift assays, we demonstrated that both
YY1 and USF1 transcription factors can bind to the 52-base pair region. When
HeLa cells were transiently transfected with a mutant construct which had
disabled both YY1- and USF1-binding sites, the luciferase activity was greatly
reduced, suggesting that these binding elements play a functional role in the
basal activation of the hTOP3 promoter. Transfection studies with mutations that
selectively impaired YY1 or USF1 binding suggested that both YY1 and USF1
function as activators in the hTOP3 promoter.

PMID: 9748294 [PubMed - indexed for MEDLINE]


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