Evidence map›Paper›PMID 20185820›Full record

ArticleThe Journal of biological chemistry2010

Foxp1/2/4-NuRD interactions regulate gene expression and epithelial injury response in the lung via regulation of interleukin-6.

Ann L Chokas, Chinmay M Trivedi, Min Min Lu, Philip W Tucker, Shanru Li, Jonathan A Epstein, Edward E Morrisey

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

41 citing papers in PubMed, 74 citations in OpenAlex.

  1. Peripheral blood mononuclear cell gene expression in chronic obstructive pulmonary disease.American journal of respiratory cell and molecular biology · 2013
    Trial
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  12. Review
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  15. Review
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  18. FOXP transcription factors in vertebrate brain development, function, and disorders.Wiley interdisciplinary reviews. Developmental biology · 2020
    Review
  19. GATAD2B-associated neurodevelopmental disorder (GAND): clinical and molecular insights into a NuRD-related disorder.Genetics in medicine : official journal of the American College of Medical Genetics · 2020
    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

7 authors at 3 institutions in 1 country.

Ann L ChokasDepartment of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Chinmay M Trivedi
Min Min Lu
Philip W Tucker
Shanru Li
Jonathan A Epstein
Edward E Morrisey
University of Pennsylvania · USCalifornia Institute for Regenerative Medicine · USThe University of Texas at Austin · US

Funding

Winged-helix repressors and lung developmentR01HL071589 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI MORRISEY, EDWARD E · 2003 to 2015
$4.6M
THE ROLE OF GATA6 IN LUNG DEVELOPMENTR01HL064632 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI MORRISEY, EDWARD E · 2000 to 2013
$4.6M
NHLBI NIH HHS HL064632NHLBI NIH HHS HL071589NHLBI NIH HHS R01 HL064632NHLBI NIH HHS R01 HL071589
6 · The paper itself

Abstract

To determine the underlying mechanism of Foxp1/2/4-mediated transcriptional repression, a yeast two-hybrid screen was performed that identified p66beta, a transcriptional repressor and component of the NuRD chromatin-remodeling complex. We show that direct interactions between Foxp1/4 and p66beta are mediated by the CR2 domain within p66beta and the zinc finger/leucine zipper repression domain found in Foxp1/2/4. These direct interactions are functionally relevant as overexpression of p66beta in combination with Foxp factors cooperatively represses Foxp target gene expression, whereas loss of p66 and Foxp factors results in de-repression of endogenous Foxp target genes in lung epithelial cells. Moreover, the NuRD components HDAC1/2 associate in a macromolecular complex with Foxp proteins, and loss of expression or inhibition of HDAC1/2 activity leads to de-repression of Foxp target gene expression. Importantly, we show in vivo that Foxp1 and HDAC2 act cooperatively to regulate expression of the cytoprotective cytokine interleukin-6, which results in increased resistance to hyperoxic lung injury in Foxp1/HDAC2 compound mutant animals. These data reveal an important interaction between the Foxp transcription factors and the NuRD chromatin-remodeling complex that modulates transcriptional repression critical for the lung epithelial injury response.

Indexed as

AnimalsForkhead Transcription FactorsGene Expression RegulationHistone Deacetylase 1Histone Deacetylase 2HumansHyperoxiaInterleukin-6LungMi-2 Nucleosome Remodeling and Deacetylase ComplexMiceMice, Mutant StrainsNIH 3T3 CellsRepressor ProteinsRespiratory MucosaTwo-Hybrid System TechniquesForkhead Transcription FactorsFoxp1 protein, mouseFoxp2 protein, mouseFoxp4 protein, mouseHdac1 protein, mouseHdac2 protein, mouseHistone Deacetylase 1Histone Deacetylase 2Interleukin-6Mi-2 Nucleosome Remodeling and Deacetylase ComplexRepressor Proteins

Identifiers

PMID20185820
PMCPMC2857082
OpenAlexW2028694476

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.