Abstract
Human immunodeficiency virus type 1 (HIV-1) Tat repressed the p53-dependent gene expression through its C-terminal domain of Tat (amino acid residues 73-86) independent of the involvement of NF-kappaB and coactivator CBP/p300. Although Tat did not directly bind to p53, this repression required the N-terminal domain of p53. In contrast, Tat and p53 cooperated in the activation of HIV-1 gene expression. Thus, the cross-talk between Tat and p53 may be linked with cellular transformation by HIV-1 infection or activation of HIV-1 replication.
Copyright 2001 Academic Press.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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COS Cells
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Gene Expression / drug effects
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Gene Expression / physiology
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Gene Products, tat / chemistry
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Gene Products, tat / pharmacology*
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Gene Silencing
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HIV Long Terminal Repeat / physiology
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HIV-1 / chemistry*
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HIV-1 / physiology
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NF-kappa B / metabolism
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Protein Structure, Tertiary
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Transcriptional Activation / drug effects
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / metabolism*
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Virus Replication
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tat Gene Products, Human Immunodeficiency Virus
Substances
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Gene Products, tat
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NF-kappa B
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Tumor Suppressor Protein p53
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tat Gene Products, Human Immunodeficiency Virus