Evidence map›Paper›PMID 7862639›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1995

Cooperative action of cellular proteins YB-1 and Pur alpha with the tumor antigen of the human JC polyomavirus determines their interaction with the viral lytic control element.

N N Chen, C F Chang, G L Gallia, D A Kerr, E M Johnson, C P Krachmarov, S M Barr, R J Frisque, B Bollag, K Khalili

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 94 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Host-Immune Interactions in JC Virus Reactivation and Development of Progressive Multifocal Leukoencephalopathy (PML).Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Molecular regulation of JC virus tropism: insights into potential therapeutic targets for progressive multifocal leukoencephalopathy.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 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

10 authors at 3 institutions in 1 country.

N N ChenDepartment of Biochemistry and Molecular Biology, Thomas Jefferson University, Philadelphia, PA 19107.
C F Chang
G L Gallia
D A Kerr
E M Johnson
C P Krachmarov
S M Barr
R J Frisque
B Bollag
K Khalili
Thomas Jefferson University · USIcahn School of Medicine at Mount Sinai · USPennsylvania State University · US

Funding

TRANSCRIPTION OF HIV-1 PROMOTER IN CENTRAL NERVOUS SYSTEM DERIVED CELLSP01NS030916 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI KHALILI, KAMEL · 1993 to 2009
$10.6M
JC VIRUS: PATHOGENIC POTENTIAL AND MECHANISMSR01CA044970 · NCI · PENNSYLVANIA STATE UNIVERSITY-UNIV PARK · PI FRISQUE, RICHARD J · 1987 to 1999
–
NCI NIH HHS CA 44970NCI NIH HHS CA 5549NINDS NIH HHS NS 30916
6 · The paper itself

Abstract

Human JC polyomavirus (JCV) is the etiologic agent of the neurodegenerative disease progressive mulifocal leukoencephalopathy. By using JCV as a model, we investigated the role of the viral early protein tumor antigen (TAg) in the binding of two cellular proteins, Pura alpha and YB-1, to JCV regulatory sequences. Results from band-shift assays with purified YB-1, Pur alpha, and TAg indicated that efficient binding of Pur alpha, a strong activator of early gene transcription, to a single-stranded target sequence corresponding to the viral lytic control element, is diminished in the presence of the late gene activator YB-1, which recognizes the opposite strand of the Pur alpha binding site. Of particular interest was the ability of Pur alpha and TAg to enhance binding of YB-1 to DNA molecules without being associated with this complex. Binding studies using a mutant peptide encompassing the N terminus of YB-1 indicated that the C terminus of YB-1 is important for its DNA binding activity. The ability of Pur alpha and TAg to increase binding of YB-1 to DNA is independent of the YB-1 C terminus. Similarly, results from band-shift assays using Pur alpha variants indicated that two distinct regions of this protein contribute either to its ability to bind DNA or to its ability to enhance YB-1 DNA binding activity. Based on the interaction of Pur alpha, YB-1, and TAg, and their binding to DNA, a model is proposed for the role of these proteins in transcription of viral early and late genes during the lytic cycle.

Indexed as

CCAAT-Enhancer-Binding ProteinsCyclic AMP Response Element-Binding ProteinRegulatory Sequences, Nucleic AcidTranscription FactorsAnimalsCells, CulturedDNA-Binding ProteinsDNA, ViralGenes, ViralJC VirusNFI Transcription FactorsNuclear ProteinsNucleopolyhedrovirusesSpodopteraTranscription, GeneticViral ProteinsCCAAT-Enhancer-Binding ProteinsCyclic AMP Response Element-Binding ProteinDNA-Binding ProteinsDNA, ViralNFI Transcription FactorsNuclear ProteinsTranscription FactorsViral ProteinsY-Box-Binding Protein 1YBX1 protein, human

Identifiers

PMID7862639
PMCPMC42642
OpenAlexW1999839712

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.