Evidence map›Paper›PMID 29386516›Full record

ArticleScientific reports2018

The effect of PU.1 knockdown on gene expression and function of mast cells.

Yoshihito Oda, Kazumi Kasakura, Izumi Fujigaki, Azusa Kageyama, Ko Okumura, Hideoki Ogawa, Takuya Yashiro, Chiharu Nishiyama

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Role of the IRE1α-XBP1 Axis in IgE-Dependent Activation of Mast Cells.International journal of molecular sciences · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. ETS Transcription Factors in Immune Cells and Immune-Related Diseases.International journal of molecular sciences · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Anaphylaxis: Focus on Transcription Factor Activity.International journal of molecular sciences · 2021
    Review
  11. Review
  12. Cooperative Regulation of the Mucosal Mast Cell-Specific Protease GenesJournal of immunology (Baltimore, Md. : 1950) · 2020
    Article
  13. 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

8 authors at 2 institutions in 1 country.

Yoshihito OdaDepartment of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.
Kazumi KasakuraDepartment of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.
Izumi FujigakiDepartment of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.
Azusa KageyamaDepartment of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.
Ko OkumuraAtopy (Allergy) Research Center, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Hideoki OgawaAtopy (Allergy) Research Center, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Takuya YashiroDepartment of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.
Chiharu NishiyamaDepartment of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan. chinishi@rs.tus.ac.jp.ORCID http://orcid.org/0000-0002-4082-9097
Tokyo University of Science · JPJuntendo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PU.1 is a hematopoietic cell-specific transcription factor. In the current study, we investigated the role of PU.1 in the gene expression and the function of mouse mast cells (MCs) in vitro and in vivo. When PU.1 siRNA was introduced into bone marrow-derived MCs (BMMCs), IgE-mediated activation was reduced, and the Syk and FcεRIβ mRNA levels were significantly decreased. As the regulatory mechanism of the Syk gene is largely unknown, we performed promoter analysis and found that PU.1 transactivated the Syk promoter through direct binding to a cis-element in the 5'-untranslated region. The involvement of PU.1 in the Syk promoter was also observed in mouse dendritic cells and human MCs, suggesting that the relationship between PU.1 and Syk is common in mammals and in hematopoietic lineages. When antigen was administrated intravenously after the transfusion of siRNA-transfected BMMCs in the mouse footpad, the footpad thickening was significantly suppressed by PU.1 knockdown. Finally, administration of the immunomodulator pomalidomide suppressed passive systemic anaphylaxis of mice. Taken together, these results indicate that PU.1 knockdown might be an efficacious strategy for the prevention of MC-mediated allergic diseases.

Indexed as

AnaphylaxisAnimalsCells, CulturedDendritic CellsGene Knockdown TechniquesHEK293 CellsHumansImmunologic FactorsMast CellsMiceMice, Inbred C57BLPromoter Regions, GeneticProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Receptors, IgESyk KinaseImmunologic FactorspomalidomideProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Receptors, IgESyk KinaseSyk protein, mouseThalidomideTrans-Activators

Identifiers

PMID29386516
PMCPMC5792452
OpenAlexW2805423286

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.