Evidence map›Paper›PMID 11371641›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2001

c-Jun interacts with the corepressor TG-interacting factor (TGIF) to suppress Smad2 transcriptional activity.

M Pessah, C Prunier, J Marais, N Ferrand, A Mazars, F Lallemand, J M Gauthier, A Atfi

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

35 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Cytotechnology · 2021
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. The role of TGF-β/SMAD4 signaling in cancer.International journal of biological sciences · 2018
    Review
  10. Article
  11. Article
  12. Elevated expression of TGIF is involved in lung carcinogenesis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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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

8 authors at 4 institutions in 1 country.

M PessahInstitut National de la Santé et de la Recherche Médicale U 482, Hôpital Saint-Antoine, 184 Rue du Faubourg Saint-Antoine, 75571, Paris Cedex 12, France.
C Prunier
J Marais
N Ferrand
A Mazars
F Lallemand
J M Gauthier
A Atfi
Hôpital Saint-Antoine · FRHybrigenics (France) · FRInserm · FRSorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Sma and Mad related (Smad) family proteins are critical mediators of the transforming growth factor-beta (TGF-beta) superfamily signaling. After TGF-beta-mediated phosphorylation and association with Smad4, Smad2 moves to the nucleus and activates expression of specific genes through cooperative interactions with DNA-binding proteins, including members of the winged-helix family of transcription factors, forkhead activin signal transducer (FAST)-1 and FAST2. TGF-beta has also been described to activate other signaling pathways, such as the c-Jun N-terminal Kinase (JNK) pathway. Here, we show that activation of JNK cascade blocked the ability of Smad2 to mediate TGF-beta-dependent activation of the FAST proteins. This inhibitory activity is mediated through the transcriptional factor c-Jun, which enhances the association of Smad2 with the nuclear transcriptional corepressor TG-interacting factor (TGIF), thereby interfering with the assembly of Smad2 and the coactivator p300 in response to TGF-beta signaling. Interestingly, c-Jun directly binds to the nuclear transcriptional corepressor TGIF and is required for TGIF-mediated repression of Smad2 transcriptional activity. These studies thus reveal a mechanism for suppression of Smad2 signaling pathway by JNK cascade through transcriptional repression.

Indexed as

Gene Expression RegulationMAP Kinase Kinase 4MAP Kinase Kinase Kinase 1AnimalsChlorocebus aethiopsCOS CellsDNA-Binding ProteinsForkhead Transcription FactorsHomeodomain ProteinsHumansJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesProtein Serine-Threonine KinasesRepressor ProteinsSignal TransductionDNA-Binding ProteinsForkhead Transcription FactorsFOXH1 protein, humanFoxh1 protein, mouseHomeodomain ProteinsJNK Mitogen-Activated Protein KinasesMAP2K4 protein, humanMAP3K1 protein, humanMAP Kinase Kinase 4MAP Kinase Kinase Kinase 1Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesProtein Serine-Threonine KinasesRepressor ProteinsSmad2 ProteinSMAD2 protein, humanTGIF1 protein, humanTrans-ActivatorsTranscription FactorsTransforming Growth Factor beta

Identifiers

PMID11371641
PMCPMC33445
OpenAlexW2014046803

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.