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J Biol Chem, Vol. 273, Issue 12, 7088-7093, March 20, 1998
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From the Previous reports have indicated that
benzothiophenes exhibit broad anti-inflammatory properties and inhibit
human immunodeficiency virus-type 1 (HIV-1) replication. We show that
the immunosuppressant cyclosporin A (CsA) and
benzothiophene-2-carboxamide, 5-methoxy-3-(1-methyl ethoxy)-1-oxide (PD
144795) block the induction of p53 and NF- Department of Physiology and Biophysics and
Ireland Cancer Center, CWRU School of Medicine, Cleveland, Ohio 44106, the ¶ Department of Biochemistry, University of Seville School of
Medicine, 41009 Seville, Spain, the Lineberger Comprehensive
Cancer Center and Department of Biology, University of North Carolina
at Chapel Hill, Chapel Hill, North Carolina 27599, and the
** Departments of Immunopathology and Molecular Biology, Parke-Davis
Pharmaceutical Research, Division of Warner-Lambert Co.,
Ann Arbor, Michigan 48105
B binding to the HIV-1
long terminal repeat (LTR) by the T cell receptor activator
phytohemagglutinin. CsA and PD 144795 also inhibit the induction by
phytohemagglutinin of the transcription mediated by an HIV-1 LTR
fragment containing the p53 and NF-B sites. These effects of PD
144795 on HIV-1 transcription correlate with its ability to inhibit the
phosphatase activity of calcineurin and are similar to those previously
described for CsA. Moreover, a constitutive active form of calcineurin
is able to induce expression from the HIV-1 LTR in a p53- and
NF-B-dependent manner and PD 144795 is able to block
this induction. These results demonstrate that the DNA binding of p53
to the HIV-1 LTR can be modulated by calcineurin and provide a
framework to understand the anti-HIV properties of benzothiophene
derivatives.
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