Evidence map›Paper›PMID 39132043›Full record

ArticleGastro hep advances2023

Deletion of miR-150 Prevents Spontaneous T Cell Proliferation and the Development of Colitis.

Sayaka Ishihara, Masashi Sato, Haruka Miyazaki, Haruka Saito, Tsuyoshi Sato, Noriyuki Fujikado, Satoshi Sawai, Ai Kotani, Koko Katagiri

Abstract read
In one paragraph

Article in Gastro hep advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

9 authors.

Sayaka IshiharaDepartment of Biosciences, School of Science, Kitasato University, Sagamihara, Kanagawa, Japan.
Masashi SatoDepartment of Immunology, School of Medicine, Kitasato University, Sagamihara, Kanagawa, Japan.
Haruka MiyazakiDepartment of Biosciences, School of Science, Kitasato University, Sagamihara, Kanagawa, Japan.
Haruka SaitoDepartment of Biosciences, School of Science, Kitasato University, Sagamihara, Kanagawa, Japan.
Tsuyoshi SatoDepartment of Biosciences, School of Science, Kitasato University, Sagamihara, Kanagawa, Japan.
Noriyuki FujikadoDiscovery Immunology, Ferring Research Institute, Ferring Pharmaceuticals, San Diego, California.
Satoshi SawaiDepartment of Basic Science, Graduate School of Arts and Sciences, University of Tokyo, Tokyo, Japan.
Ai KotaniDepartment of Innovative Medical Science, School of Medicine, Tokai University, Isehara, Kanagawa, Japan.
Koko KatagiriDepartment of Biosciences, School of Science, Kitasato University, Sagamihara, Kanagawa, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and Aims: To examine the roles of microRNAs in the development of colitis, we conducted the RNA-sequencing studies using RNA derived from normal and colitogenic CD4+ T cells. Colitogenic CD4 Methods: We crossed miR-150 knockout mice and T-cell-specific Rap1KO mice, which is colitis model mice and spontaneously develop the colitis with tubular adenomas in microbiota-dependent manner. Results: MiR-150 silencing completely inhibited the expansion of pathogenic Th17 cells and the development of colitis. Conclusion: MiR-150 is a potential therapeutic target of inflammatory bowel diseases.

Indexed as

CD4+ T CellsColitisMir-150Rap1

Identifiers

PMID39132043
PMCPMC11308117

What OpenQuestion holds

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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.