Evidence map›Paper›PMID 9436983›Full record

ArticleGenes & development1998

p300 and ATF-2 are components of the DRF complex, which regulates retinoic acid- and E1A-mediated transcription of the c-jun gene in F9 cells.

H Kawasaki, J Song, R Eckner, H Ugai, R Chiu, K Taira, Y Shi, N Jones, K K Yokoyama

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
–field-weighted citation impact
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

45 citing papers in PubMed, 89 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Functional cDNA expression cloning: pushing it to the limit.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2012
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Suppressor role of activating transcription factor 2 (ATF2) in skin cancer.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  16. Article
  17. Article
  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

9 authors at 7 institutions in 5 countries.

H KawasakiTsukuba Life Science Center, The Institute of Physical and Chemical Research (RIKEN), Tsukuba 305, Japan.
J Song
R Eckner
H Ugai
R Chiu
K Taira
Y Shi
N Jones
K K Yokoyama
Life Science Institute · JPHarvard University · USNational Institute for Interdisciplinary Science and Technology · INNational Institute of Advanced Industrial Science and Technology · JPThe Honourable Society of Lincoln's Inn · GBUniversity of California, Los Angeles · USUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcriptional activation of the c-jun gene is a critical event in the differentiation of F9 cells. In our previous studies we characterized an element [differentiation response element (DRE)] in the c-jun promoter that is both necessary and sufficient to confer the capacity for differentiation-dependent up-regulation. This element binds the differentiation regulatory factor (DRF) complex, of which one component is the adenovirus E1A-associated protein p300. We have now identified activation transcription factor-2 (ATF-2) as a DNA-binding subunit of the DRF complex. p300 and ATF-2 interact with each other in vivo and in vitro. The bromodomain and the C/H2 domain of p300 mediate the binding to ATF-2, which in turn requires a proline-rich region between amino acids 112 and 350 for its interaction with p300. The phosphorylation of the serine residue at position 121 of ATF-2 appears to be induced by protein kinase C alpha (PKC alpha) after treatment of cells with retinoic acid (RA) or induction with E1A. In cotransfection assays, wild-type ATF-2 enhanced the transcription of an E2/tk-luciferase construct, in conjunction with p300-E2. However, a mutant form of ATF-2 with a mutation at position 121 (pCMVATF-2(Ser121-Ala)) did not. These results suggest that ATF-2 and p300 cooperate in the control of transcription by forming a protein complex that is responsive to differentiation-inducing signals, such as RA or E1A, and moreover, that the phosphorylation of ATF-2 by PKC alpha is probably a signaling event in the pathway that leads to the transactivation of the c-jun gene in F9 cells.

Indexed as

Trans-ActivatorsActivating Transcription Factor 2AnimalsCell DifferentiationCell LineCyclic AMP Response Element-Binding ProteinE1A-Associated p300 ProteinGene Expression RegulationGenes, junGenes, ViralIsoenzymesMiceNuclear ProteinsPhosphorylationPromoter Regions, GeneticProtein Kinase CActivating Transcription Factor 2Atf2 protein, mouseCyclic AMP Response Element-Binding ProteinE1A-Associated p300 ProteinEp300 protein, mouseIsoenzymesNuclear ProteinsPrkca protein, mouseProtein Kinase CProtein Kinase C-alphaRecombinant Fusion ProteinsTrans-ActivatorsTranscription FactorsTretinoin

Identifiers

PMID9436983
PMCPMC316443
OpenAlexW2112468983

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.