Evidence map›Paper›PMID 9882329›Full record

ArticleJournal of virology1999

Expression of the human endogenous retrovirus HTDV/HERV-K is enhanced by cellular transcription factor YY1.

M Knössl, R Löwer, J Löwer

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.9field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Review
  3. YY1 is a transcriptional activator of mouse LINE-1 Tf subfamily.bioRxiv : the preprint server for biology · 2024
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Endogenous retrovirus-K and nervous system diseases.Current neurology and neuroscience reports · 2014
    Review
  17. Article
  18. Review
  19. Review
  20. Review
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

3 authors at 1 institution in 1 country.

M KnösslVirology Department, Paul-Ehrlich-Institut, D-63225 Langen, Germany.
R Löwer
J Löwer
Paul Ehrlich Institut · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human endogenous retrovirus HTDV/HERV-K, which resides in moderate copy numbers in the human genome, is expressed in a cell-type-specific manner, predominantly in teratocarcinoma cells. We have analyzed the regulatory potential of the 5' enhancer of the HERV-K long terminal repeat. Protein extracts of HERV-K-expressing teratocarcinoma cell lines (GH and Tera2) and nonexpressing HeLa and HepG2 cells form different protein complexes on the enhancer sequence as detected by electrophoretic mobility shift assays (EMSA). Using competition EMSAs, DNase I footprinting, and supershift experiments, we localized the binding site of these complexes to a 20-bp sequence within the enhancer and showed that the transcription factor YY1 is one component of the HERV-K enhancer complex. Replacement of the YY1 binding site with unrelated sequences reduced expression of the luciferase gene as a reporter in transient-transfection assays.

Indexed as

Enhancer Elements, GeneticGene Expression Regulation, ViralDNA-Binding ProteinsEndogenous RetrovirusesErythroid-Specific DNA-Binding FactorsHeLa CellsHumansTranscription FactorsTumor Cells, CulturedYY1 Transcription FactorDNA-Binding ProteinsErythroid-Specific DNA-Binding FactorsTranscription FactorsYY1 protein, humanYY1 Transcription Factor

Identifiers

PMID9882329
PMCPMC103948
OpenAlexW1822739362

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.