Evidence map›Paper›PMID 10644332›Full record

ArticleJournal of virology2000

The human immunodeficiency virus type 1 Tat protein up-regulates the promoter activity of the beta-chemokine monocyte chemoattractant protein 1 in the human astrocytoma cell line U-87 MG: role of SP-1, AP-1, and NF-kappaB consensus sites.

S P Lim, A Garzino-Demo

Abstract read
In one paragraph

Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

32 citing papers in PubMed, 95 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Immunomodulatory properties of kappa opioids and synthetic cannabinoids in HIV-1 neuropathogenesis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Rebuilding synaptic architecture in HIV-1 associated neurocognitive disease: a therapeutic strategy based on modulation of mixed lineage kinase.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2010
    Review
  18. Article
  19. Article
  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 2 countries.

S P LimInstitute of Molecular and Cell Biology, Singapore 117609, Singapore.
A Garzino-Demo
Institute of Molecular and Cell Biology · SGUniversity of Maryland, Baltimore · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been shown that the human immunodeficiency virus type 1 (HIV-1) Tat protein can specifically enhance expression and release of monocyte chemoattractant protein 1 (MCP-1) from human astrocytes. In this study, we show evidence that Tat-induced MCP-1 expression is mediated at the transcriptional level. Transient transfection of an expression construct encoding the full-length Tat into the human glioblastoma-astrocytoma cell line U-87 MG enhances reporter gene activity from cotransfected deletion constructs of the MCP-1 promoter. HIV-1 Tat exerts its effect through a minimal construct containing 213 nucleotides upstream of the translational start site. Site-directed mutagenesis studies indicate that an SP1 site (located between nucleotides -123 and -115) is critical for both constitutive and Tat-enhanced expression of the human MCP-1 promoter, as mutation of this SP1 site significantly diminished reporter gene expression in both instances. Gel retardation experiments further demonstrate that Tat strongly enhances the binding of SP1 protein to its DNA element on the MCP-1 promoter. Moreover, we also observe an increase in the binding activities of transcriptional factors AP1 and NF-kappaB to the MCP-1 promoter following Tat treatment. Mutagenesis studies show that an upstream AP1 site and an adjacent NF-kappaB site (located at -128 to -122 and -150 to -137, respectively) play a role in Tat-mediated transactivation. In contrast, a further upstream AP1 site (-156 to -150) does not appear to be crucial for promoter activity. We postulate that a Tat-mediated increase in SP1 binding activities augments the binding of AP1 and NF-kappaB, leading to synergistic activation of the MCP-1 promoter.

Indexed as

HIV-1Promoter Regions, GeneticUp-RegulationAstrocytomaChemokine CCL2Consensus SequenceDNAGene Products, tatHumansMutagenesisNF-kappa BRecombinant Fusion ProteinsSp1 Transcription Factortat Gene Products, Human Immunodeficiency VirusTranscriptional ActivationTranscription Factor AP-1Chemokine CCL2DNAGene Products, tatNF-kappa BRecombinant Fusion ProteinsSp1 Transcription Factortat Gene Products, Human Immunodeficiency VirusTranscription Factor AP-1

Identifiers

PMID10644332
PMCPMC111637
OpenAlexW2136505680

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.