Evidence map›Paper›PMID 8657141›Full record

ArticleMolecular and cellular biology1996

Interaction of Sp1 with the growth- and cell cycle-regulated transcription factor E2F.

J Karlseder, H Rotheneder, E Wintersberger

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed
18.6field-weighted citation impact, top 1% 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

113 citing papers in PubMed, 342 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Beyond HAT Adaptor: TRRAP Liaisons with Sp1-Mediated Transcription.International journal of molecular sciences · 2021
    Review
  6. Article
  7. AlteredEpigenetics · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Positional specificity of different transcription factor classes within enhancers.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

53 more citing papers are in PubMed but not listed here.

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.

J KarlsederInstitut Für Molekularbiologie, Universität Wien, Austria, USA.
H Rotheneder
E Wintersberger
Institute of Molecular Biotechnology · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Within the region around 150 bp upstream of the initiation codon, which was previously shown to suffice for growth-regulated expression, the murine thymidine kinase gene carries a single binding site for transcription factor Sp1; about 10 bp downstream of this site, there is a binding motif for transcription factor E2F. The latter protein appears to be responsible for growth regulation of the promoter. Mutational inactivation of either the Sp1 or the E2F site almost completely abolishes promoter activity, suggesting that the two transcription factors interact directly in delivering an activation signal to the basic transcription machinery. This was verified by demonstrating with the use of glutathione S-transferase fusion proteins that E2F and Sp1 bind to each other in vitro. For this interaction, the C-terminal part of Sp1 and the N terminus of E2F1, a domain also present in E2F2 and E2F3 but absent in E2F4 and E2F5, were essential. Accordingly, E2F1 to E2F3 but not E2F4 and E2F5 were found to bind sp1 in vitro. Coimmunoprecipitation experiments showed that complexes exist in vivo, and it was estabilished that the distance between the binding sites for the two transcription factors was critical for optimal promoter activity. Finally, in vivo footprinting experiments indicated that both the sp1 and E2F binding sites are occupied throughout the cell cycle. Mutation of either binding motif abolished binding of both transcription factors in vivo, which may indicate cooperative binding of the two proteins to chromatin-organized DNA. Our data are in line with the hypothesis that E2F functions as a growth- and cell cycle regulated tethering factor between Sp1 and the basic transcription machinery.

Indexed as

Carrier ProteinsGene Expression Regulation3T3 CellsAnimalsBase SequenceBinding SitesCell Cycle ProteinsDNA-Binding ProteinsE2F1 Transcription FactorE2F3 Transcription FactorE2F4 Transcription FactorE2F5 Transcription FactorE2F Transcription FactorsMiceMolecular Sequence DataPromoter Regions, GeneticArid4a protein, mouseCarrier ProteinsCell Cycle ProteinsDNA-Binding ProteinsE2f1 protein, mouseE2F1 Transcription FactorE2F3 Transcription FactorE2f4 protein, mouseE2F4 Transcription FactorE2F5 Transcription FactorE2F Transcription FactorsRetinoblastoma-Binding Protein 1RNA, MessengerSp1 Transcription FactorThymidine KinaseTranscription Factor DP1Transcription Factors

Identifiers

PMID8657141
PMCPMC231152
OpenAlexW1753047181

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.