Evidence map›Paper›PMID 33478486›Full record

ArticleRespiratory research2021

Potential interactions between the TBX4-FGF10 and SHH-FOXF1 signaling during human lung development revealed using ChIP-seq.

Justyna A Karolak, Tomasz Gambin, Przemyslaw Szafranski, Paweł Stankiewicz

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  6. Loss ofAmerican journal of respiratory cell and molecular biology · 2025
    Article
  7. Review
  8. Article
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  10. Article
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  12. Molecular Function and Contribution ofAmerican journal of respiratory and critical care medicine · 2023
    Review
  13. Article
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  16. Transcriptome and Immunohistochemical Analyses inAmerican journal of respiratory cell and molecular biology · 2022
    Article
  17. Long Non-Coding RNAGenes · 2021
    Review
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 2 countries.

Justyna A KarolakDepartment of Molecular & Human Genetics, Baylor College of Medicine, One Baylor Plaza, Rm ABBR-R809, Houston, TX, 77030, USA.
Tomasz GambinDepartment of Molecular & Human Genetics, Baylor College of Medicine, One Baylor Plaza, Rm ABBR-R809, Houston, TX, 77030, USA.
Przemyslaw SzafranskiDepartment of Molecular & Human Genetics, Baylor College of Medicine, One Baylor Plaza, Rm ABBR-R809, Houston, TX, 77030, USA.
Paweł StankiewiczDepartment of Molecular & Human Genetics, Baylor College of Medicine, One Baylor Plaza, Rm ABBR-R809, Houston, TX, 77030, USA. pawels@bcm.edu.
Baylor College of Medicine · US

Funding

Epigenomic dysfunction at 16q24.1 vascular defects and perinatal consequencesR01HL137203 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI STANKIEWICZ, PAWEL · 2017 to 2020
$2.0M
NHLBI NIH HHS R01 HL137203The US National Institutes of Health (NIH), National Heart Lung and Blood Institute (NHLBI) R01HL137203
6 · The paper itself

Abstract

backgroundThe epithelial-mesenchymal signaling involving SHH-FOXF1, TBX4-FGF10, and TBX2 pathways is an essential transcriptional network operating during early lung organogenesis. However, precise regulatory interactions between different genes and proteins in this pathway are incompletely understood.

methodsTo identify TBX2 and TBX4 genome-wide binding sites, we performed chromatin immunoprecipitation followed by next-generation sequencing (ChIP-seq) in human fetal lung fibroblasts IMR-90.

resultsWe identified 14,322 and 1,862 sites strongly-enriched for binding of TBX2 and TBX4, respectively, 43.95% and 18.79% of which are located in the gene promoter regions. Gene Ontology, pathway enrichment, and DNA binding motif analyses revealed a number of overrepresented cues and transcription factor binding motifs relevant for lung branching that can be transcriptionally regulated by TBX2 and/or TBX4. In addition, TBX2 and TBX4 binding sites were found enriched around and within FOXF1 and its antisense long noncoding RNA FENDRR, indicating that the TBX4-FGF10 cascade may directly interact with the SHH-FOXF1 signaling.

conclusionsWe highlight the complexity of transcriptional network driven by TBX2 and TBX4 and show that disruption of this crosstalk during morphogenesis can play a substantial role in etiology of lung developmental disorders.

Indexed as

Chromatin Immunoprecipitation SequencingFetal DevelopmentFibroblast Growth Factor 10Forkhead Transcription FactorsHedgehog ProteinsHumansLungProtein BindingT-Box Domain ProteinsFGF10 protein, humanFibroblast Growth Factor 10Forkhead Transcription FactorsFOXF1 protein, humanHedgehog ProteinsSHH protein, humanT-Box Domain ProteinsTBX4 protein, humanLung morphogenesisMotif enrichmentTranscriptional regulation

Identifiers

PMID33478486
PMCPMC7818749
OpenAlexW3125014944

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.