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c-Myc and Sp1 contribute to proviral latency by recruiting histone deacetylase 1 to the human immunodeficiency virus type 1 promoter.

c-Myc and Sp1 contribute to proviral latency by recruiting histone deacetylase 1 to the human immunodeficiency virus type 1 promoter. Research Abstract Details 

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  • c-Myc and Sp1 contribute to proviral latency by recruiting histone deacetylase 1 to the human immunodeficiency virus type 1 promoter. Abstract Text:

    guochun jiangGuochun Jiang,amy espesethAmy Espeseth,daria j hazudaDaria J Hazuda,david m margolisDavid M Margolis,guochun jiangGuochun Jiang,amy espesethAmy Espeseth,daria j hazudaDaria J Hazuda,david m margolisDavid M Margolis,

    Histone deacetylase (HDAC) inhibitors such as valproic acid (VPA) induce the expression of quiescent proviral human immunodeficiency virus type 1 (HIV-1) and may deplete proviral infection in vivo. To uncover novel molecular mechanisms that maintain HIV latency, we sought cellular mRNAs whose expression was diminished in resting CD4(+) T cells of HIV-1-infected patients exposed to VPA. c-Myc was prominent among genes markedly downregulated upon exposure to VPA. c-Myc expression repressed HIV-1 expression in chronically infected cell lines. Chromatin immunoprecipitation (ChIP) assays revealed that c-Myc and HDAC1 are coordinately resident at the HIV-1 long terminal repeat (LTR) promoter and absent from the promoter after VPA treatment in concert with histone acetylation, RNA polymerase II recruitment, and LTR expression. Sequential ChIP assays demonstrated that c-Myc, Sp1, and HDAC1 coexist in the same DNA-protein complex at the HIV promoter. Short hairpin RNA inhibition of c-Myc reduces both c-Myc and HDAC1 occupancy, blocks c-Myc repression of Tat activation, and increases LTR expression. These results expand the understanding of mechanisms that recruit HDAC and maintain the latency of HIV-1, suggesting novel therapeutic approaches against latent proviral HIV infection.

    c-Myc and Sp1 contribute to proviral latency by recruiting histone deacetylase 1 to the human immunodeficiency virus type 1 promoter. Publishing Authors By Initials

    g jiangG Jiang,a espesethA Espeseth,dj hazudaDJ Hazuda,dm margolisDM Margolis,g jiangG Jiang,a espesethA Espeseth,dj hazudaDJ Hazuda,dm margolisDM Margolis,

    For similar abstracts research abstracts see: abstracts research

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    c-Myc and Sp1 contribute to proviral latency by recruiting histone deacetylase 1 to the human immunodeficiency virus type 1 promoter. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Journal of virology

    VOLUME: 81

    Page Numbers: 10914-23

    Journal Abbreviation: J. Virol.

    ISSN: 0022-538X

    DAY: 1

    MONTH: 08

    YEAR: 2007

    c-Myc and Sp1 contribute to proviral latency by recruiting histone deacetylase 1 to the human immunodeficiency virus type 1 promoter. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 113724

    c-Myc and Sp1 contribute to proviral latency by recruiting histone deacetylase 1 to the human immunodeficiency virus type 1 promoter. Keywords Mesh Terms:

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    Grant and Affiliation Information for c-Myc and Sp1 contribute to proviral latency by recruiting histone deacetylase 1 to the human immunodeficiency virus type 1 promoter.

    AFFILIATION: Department of Medicine, University of North Carolina at Chapel Hill, 3302 Michael Hooker Research Ctr., Chapel Hill, NC 27599-7435, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIAID

    GRANT: P30 AI50410

    ACRONYM: AI

    MEDLINETA: J Virol

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    Number Hits: 0

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