Reciprocal modulations between p53 and Tat of human immunodeficiency virus type 1.
Infection by human immunodeficiency virus type 1 (HIV-1) causes acquired immunodeficiency syndrome (AIDS) after a long clinical latency. This disease is associated with a spectrum of cancers. Here we report that wild-type p53 is a potent suppressor of Tat, a major transactivator of HIV-1. Reciprocally, Tat inhibits the transcription of p53. Downregulation of p53 by upregulated tat may be important for the establishment of productive viral infection in a cell and also may be involved in the development of AIDS-related malignancies.
Li
C J
CJ
Division of Cell Growth and Regulation, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.
Wang
C
C
Friedman
D J
DJ
Pardee
A B
AB
D001483:Base Sequence; D018076:DNA, Complementary; D015536:Down-Regulation; D015696:Gene Products, tat / Q000235:genetics / Q000502:physiology*; D016158:Genes, p53; D015756:Genes, tat; D016325:HIV Long Terminal Repeat; D015497:HIV-1 / Q000235:genetics*; D006801:Humans; D008969:Molecular Sequence Data; D011401:Promoter Regions, Genetic; D015533:Transcriptional Activation; D014407:Tumor Cells, Cultured; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000502:physiology*; D054322:tat Gene Products, Human Immunodeficiency Virus
D018076:DNA, Complementary; D015696:Gene Products, tat; D014409:Tumor Necrosis Factor-alpha; D016159:Tumor Suppressor Protein p53; D054322:tat Gene Products, Human Immunodeficiency Virus