Evidence map›Paper›PMID 31586032›Full record

ArticleThe Journal of biological chemistry2019

The transcription factor PU.1 mediates enhancer-promoter looping that is required for IL-1β eRNA and mRNA transcription in mouse melanoma and macrophage cell lines.

Soon-Duck Ha, Woohyun Cho, Rodney P DeKoter, Sung Ouk Kim

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

23 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
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  6. The LIM-domain-only protein LMO2 and its binding partner LDB1 are differentially required for class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  9. CRISPRi screens identify the lncRNA,Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Article
  11. Article
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  13. Article
  14. 1,25(OH)Nutrients · 2022
    Article
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  16. Review
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  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

4 authors at 1 institution in 1 country.

Soon-Duck HaDepartment of Microbiology and Immunology and Infectious Diseases Research Group, Siebens-Drake Research Institute, University of Western Ontario, London, Ontario N6G 2V4, Canada.
Woohyun ChoDepartment of Microbiology and Immunology and Infectious Diseases Research Group, Siebens-Drake Research Institute, University of Western Ontario, London, Ontario N6G 2V4, Canada.
Rodney P DeKoterDepartment of Microbiology and Immunology and Infectious Diseases Research Group, Siebens-Drake Research Institute, University of Western Ontario, London, Ontario N6G 2V4, Canada.
Sung Ouk KimDepartment of Microbiology and Immunology and Infectious Diseases Research Group, Siebens-Drake Research Institute, University of Western Ontario, London, Ontario N6G 2V4, Canada skim283@uwo.ca.ORCID 0000-0002-0282-6661
Western University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The DNA-binding protein PU.1 is a myeloid lineage-determining and pioneering transcription factor due to its ability to bind "closed" genomic sites and maintain "open" chromatin state for myeloid lineage-specific genes. The precise mechanism of PU.1 in cell type-specific programming is yet to be elucidated. The melanoma cell line B16BL6, although it is nonmyeloid lineage, expressed Toll-like receptors and activated the transcription factor NF-κB upon stimulation by the bacterial cell wall component lipopolysaccharide. However, it did not produce cytokines, such as IL-1β mRNA. Ectopic PU.1 expression induced remodeling of a novel distal enhancer (located ∼10 kbp upstream of the IL-1β transcription start site), marked by nucleosome depletion, enhancer-promoter looping, and histone H3 lysine 27 acetylation (H3K27ac). PU.1 induced enhancer-promoter looping and H3K27ac through two distinct PU.1 regions. These PU.1-dependent events were independently required for subsequent signal-dependent and co-dependent events: NF-κB recruitment and further H3K27ac, both of which were required for enhancer RNA (eRNA) transcription. In murine macrophage RAW264.7 cells, these PU.1-dependent events were constitutively established and readily expressed eRNA and subsequently IL-1β mRNA by lipopolysaccharide stimulation. In summary, this study showed a sequence of epigenetic events in programming IL-1β transcription by the distal enhancer priming and eRNA production mediated by PU.1 and the signal-dependent transcription factor NF-κB.

Indexed as

AnimalsCell Line, TumorEpigenesis, GeneticGene Expression Regulation, NeoplasticInterleukin-1betaMelanoma, ExperimentalMicePromoter Regions, GeneticProto-Oncogene ProteinsProto-Oncogene Protein Spi-1RAW 264.7 CellsRNA, MessengerTrans-ActivatorsTranscriptional ActivationIL1B protein, mouseInterleukin-1betaProto-Oncogene ProteinsProto-Oncogene Protein Spi-1RNA, MessengerTrans-Activatorschromatin modificationDNA loopingenhancereRNAgene expressionhistone acetylationIL-1betainterleukin 1 (IL-1)macrophagemelanomamelanoma cellsPU.1transcription factor

Identifiers

PMID31586032
PMCPMC6873190
OpenAlexW2979180857

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.