Evidence map›Paper›PMID 10918613›Full record

ArticleOncogene2000

Smad-dependent stimulation of type I collagen gene expression in human skin fibroblasts by TGF-beta involves functional cooperation with p300/CBP transcriptional coactivators.

A K Ghosh, W Yuan, Y Mori, J Varga

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
4.3field-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

94 citing papers in PubMed, 225 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Role ofInternational journal of molecular sciences · 2026
    Article
  7. Journal of functional biomaterials · 2026
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. [Research progress on collagen secretion mechanisms in scarring].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
    Review
  13. Article
  14. Article
  15. Update on the Pathogenesis of Keloid Formation.JID innovations : skin science from molecules to population health · 2024
    Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

34 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

4 authors at 1 institution in 1 country.

A K GhoshSection of Rheumatology, University of Illinois at Chicago College of Medicine, Chicago, Illinois 60607, USA.
W Yuan
Y Mori
J Varga
University of Illinois Chicago · US

Funding

REGULATION OF COLLAGEN GENE EXPRESSION BY TGF-BETAR01AR042309 · NIAMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI VARGA, JOHN · 1994 to 2014
$4.4M
CYTOKINE MODULATION OF COLLAGEN GENE EXPRESSION: SIGNALR03AR046390 · NIAMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GHOSH, ASISH K · 1999 to 2001
$155k
NIAMS NIH HHS AR-42309NIAMS NIH HHS AR-46390
6 · The paper itself

Abstract

Transforming growth factor-beta (TGF-beta) stimulation of Type I collagen gene (COL1A2) transcription involves the Smad signal transduction pathway, but the mechanisms of Smad-mediated transcriptional activation are not fully understood. We now demonstrate that the ubiquitous transcriptional coactivators p300 and CREB-binding protein (CBP) enhanced basal as well as TGF-beta- or Smad3-induced COL1A2 promoter activity, and stimulated the expression of endogenous Type I collagen. The adenoviral E1A oncoprotein abrogated stimulation of COL1A2 activity in transfected fibroblasts, and reduced the basal level of collagen gene expression. This effect was due to specific interaction of E1A with cellular p300/CBP because (a) a mutant form of E1A defective in p300 binding failed to abrogate stimulation, and (b) forced expression of p300/CBP restored the ability of TGF-beta to stimulate COL1A2 promoter activity in the presence of E1A. The effect of p300 on COL1A2 transcription appeared to be due, in part, to its intrinsic acetyltransferase activity, as stimulation induced by a histone acetyltransferase-deficient mutant p300 was substantially reduced. Transactivation of COL1A2 by p300 involved the Smad signaling pathway, as Smad4-deficient cells failed to respond to p300, and stimulation was rescued by overexpression of Smad4. Furthermore, minimal constructs containing only the Smad-binding CAGACA element of COL1A2 were transactivated by p300 in the presence of TGF-beta. These results indicate, for the first time, that the multifunctional p300/CBP coactivators play a major role in Smad-dependent TGF-beta stimulation of collagen gene expression in fibroblasts. Oncogene (2000) 19, 3546 - 3555

Indexed as

Transcriptional ActivationAdenovirus E1A ProteinsBinding SitesCells, CulturedCollagenDNA-Binding ProteinsFibroblastsGene Expression RegulationHumansNuclear ProteinsPromoter Regions, GeneticProtein BindingRecombinant Fusion ProteinsSignal TransductionSkinSmad3 ProteinAdenovirus E1A ProteinsCollagenDNA-Binding ProteinsNuclear ProteinsRecombinant Fusion ProteinsSmad3 ProteinSMAD3 protein, humanSmad4 ProteinSMAD4 protein, humanTrans-ActivatorsTransforming Growth Factor beta

Identifiers

PMID10918613
OpenAlexW2047406797

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.