Evidence map›Paper›PMID 18583319›Full record

ArticleThe American journal of pathology2008

Cross talk between Id1 and its interactive protein Dril1 mediate fibroblast responses to transforming growth factor-beta in pulmonary fibrosis.

Ling Lin, Zhihong Zhou, Liang Zheng, Sean Alber, Simon Watkins, Prabir Ray, Naftali Kaminski, Yingze Zhang, Danielle Morse

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
  5. Article
  6. Article
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  9. Article
  10. Leucine-richPhysiological reports · 2017
    Article
  11. Article
  12. Article
  13. Arid3a regulates mesoderm differentiation in mouse embryonic stem cells.Journal of stem cell therapy and transplantation · 2017
    Article
  14. Article
  15. Review
  16. 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

9 authors at 1 institution in 1 country.

Ling LinDivision of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15217, USA.
Zhihong Zhou
Liang Zheng
Sean Alber
Simon Watkins
Prabir Ray
Naftali Kaminski
Yingze Zhang
Danielle Morse
University of Pittsburgh · US

Funding

Inhibitor of differentiation-1 mediates antifibrotic effects of carbon monoxideR01HL087122 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MORSE, ERIN DANIELLE · 2008 to 2012
$1.9M
NHLBI NIH HHS R01 HL087122NHLBI NIH HHS R01HL087122-01
6 · The paper itself

Abstract

The presence of activated fibroblasts or myofibroblasts represents a hallmark of progressive lung fibrosis. Because the transcriptional response of fibroblasts to transforming growth factor-beta(1) (TGF-beta(1)) is a determinant of disease progression, we investigated the role of the transcriptional regulator inhibitor of differentiation-1 (Id1) in the setting of lung fibrosis. Mice lacking the gene for Id1 had increased susceptibility to bleomycin-induced lung fibrosis, and fibroblasts lacking Id1 exhibited enhanced responses to TGF-beta(1). Because the effect of Id1 on fibrosis could not be explained by known mechanisms, we performed protein interaction screening and identified a novel binding partner for Id1, known as dead ringer-like-1 (Dril1). Dril1 shares structural similarities with Id1 and was recently implicated in TGF-beta(1) signaling during embryogenesis. To date, little is known about the function of Dril1 in humans. Although it has not been previously implicated in fibrotic disease, we found that Dril1 was highly expressed in lungs from patients with idiopathic pulmonary fibrosis and was regulated by TGF-beta(1) in human fibroblasts. Dril1 enhanced activation of TGF-beta(1) target genes, whereas Id1 decreased expression of these same molecules. Id1 inhibited DNA binding by Dril1, and the two proteins co-localized in vitro and in vivo, providing a potential mechanism for suppression of fibrosis by Id1 through inhibition of the profibrotic function of Dril1.

Indexed as

AnimalsBleomycinCells, CulturedDNA-Binding ProteinsFibroblastsHumansInhibitor of Differentiation Protein 1LungMiceMice, KnockoutOncogenesProtein BindingPulmonary FibrosisTrans-ActivatorsTranscription FactorsTransforming Growth Factor betaARID3A protein, humanArid3a protein, mouseBleomycinDNA-Binding ProteinsID1 protein, humanIdb1 protein, mouseInhibitor of Differentiation Protein 1Trans-ActivatorsTranscription FactorsTransforming Growth Factor beta

Identifiers

PMID18583319
PMCPMC2475772
OpenAlexW2067008993

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.