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PMID: 7777531 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

Reciprocal modulations between p53 and Tat of human immunodeficiency virus type 1.

Proceedings of the National Academy of Sciences of the United States of America ·Vol. 92 ·No. 12 ·1995-06-06 ·Pages 5461-4

Li CJ, Wang C, Friedman DJ, Pardee AB

Abstract

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.

Related Genes
Tat p53
MeSH Terms
Base Sequence DNA, Complementary Down-Regulation Gene Products, tat/genetics,physiology Genes, p53 Genes, tat HIV Long Terminal Repeat HIV-1/genetics Humans Molecular Sequence Data Promoter Regions, Genetic Transcriptional Activation Tumor Cells, Cultured Tumor Necrosis Factor-alpha/physiology Tumor Suppressor Protein p53/genetics,physiology tat Gene Products, Human Immunodeficiency Virus
Chemicals
DNA, Complementary Gene Products, tat Tumor Necrosis Factor-alpha Tumor Suppressor Protein p53 tat Gene Products, Human Immunodeficiency Virus
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Li C J
Division of Cell Growth and Regulation, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.
Wang C
Friedman D J
Pardee A B
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Article Info
Journal
Proceedings of the National Academy of Sciences of the United States of America
Abbr.
Proc Natl Acad Sci U S A
ISSN
0027-8424
DOI
10.1073/pnas.92.12.5461
Published
1995-06-06
Pages
5461-4
Language
English
Region
United States
NLM ID
7505876
PMCID
PMC41714
Subset
IM
Grants
NIAID NIH HHS · AI 35576 · United States
External Links
PubMed source DOI: 10.1073/pnas.92.12.5461 PMC Full Text View journal details
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