Evidence map›Paper›PMID 10207088›Full record

ArticleMolecular and cellular biology1999

Reciprocal modulatory interaction between human immunodeficiency virus type 1 Tat and transcription factor NFAT1.

F Macián, A Rao

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Improving HIV proteome annotation: new features of BioAfrica HIV Proteomics Resource.Database : the journal of biological databases and curation · 2016
    Article
  5. Article
  6. Epigenetics, drugs of abuse, and the retroviral promoter.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2013
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. A dimer-specific function of the transcription factor NFATp.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

F MaciánDepartment of Pathology, Harvard Medical School, and Center for Blood Research, Boston, Massachusetts 02115, USA.
A Rao
Dana-Farber/Boston Children's Cancer and Blood Disorders Center · USHarvard University · US

Funding

BZIP PROTEINS AND LYMPHOCYTE GENE INDUCTIONR37CA042471 · NCI · IMMUNE DISEASE INSTITUTE, INC. · PI RAO, ANJANA · 1999 to 2006
$3.6M
ROLE OF THE FOS ONCOGENE IN LYMPHOCYTE GROWTHR01CA042471 · NCI · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI RAO, ANJANA · 1986 to 2012
$3.1M
NCI NIH HHS CA42471NCI NIH HHS R01 CA042471NCI NIH HHS R37 CA042471
6 · The paper itself

Abstract

Human immunodeficiency virus type 1 (HIV-1) gene expression is regulated by interactions between both viral and host factors. These interactions are also responsible for changes in the expression of many host cell genes, including cytokines and other immune regulators, which may account for the state of immunological dysregulation that characterizes HIV-1 infection. We have investigated the role of a host cell protein, the transcription factor NFAT1, in HIV-1 pathogenesis. We show that NFAT1 interacts with Tat and that this interaction, which involves the major transactivation domain of NFAT1 and the amino-terminal region of Tat, results in a reciprocal modulatory interplay between the proteins: whereas Tat enhances NFAT1-driven transcription in Jurkat T cells, NFAT1 represses Tat-mediated transactivation of the HIV-1 long terminal repeat (LTR). Moreover, NFAT1 binds to the kappaB sites on the viral LTR and negatively regulates NF-kappaB-mediated activation of HIV-1 transcription, by competing with NF-kappaB1 for its binding sites on the HIV-1 LTR. Tat-mediated enhancement of NFAT1 transactivation may explain the upregulation of interleukin 2 and other cytokines that occurs during HIV-1 infection. We discuss the potentially opposing roles of NFAT1 and another family member, NFAT2, in regulating gene transcription of HIV-1 and endogenous cytokine genes.

Indexed as

Nuclear ProteinsBinding SitesCytokinesDNA-Binding ProteinsGene Expression Regulation, ViralGene Products, tatGenes, ReporterHIV-1HIV Long Terminal RepeatHumansJurkat CellsNFATC Transcription FactorsNF-kappa BProtein BindingRecombinant Proteinstat Gene Products, Human Immunodeficiency VirusCytokinesDNA-Binding ProteinsGene Products, tatNFATC2 protein, humanNFATC Transcription FactorsNF-kappa BNuclear ProteinsRecombinant Proteinstat Gene Products, Human Immunodeficiency VirusTranscription Factors

Identifiers

PMID10207088
PMCPMC84169
OpenAlexW2169824225

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.