Evidence map›Paper›PMID 34968289›Full record

ArticleEpigenomes2020

Implication of m6A mRNA Methylation in Susceptibility to Inflammatory Bowel Disease.

Maialen Sebastian-delaCruz, Ane Olazagoitia-Garmendia, Itziar Gonzalez-Moro, Izortze Santin, Koldo Garcia-Etxebarria, Ainara Castellanos-Rubio

Abstract read
In one paragraph

Article in Epigenomes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  10. Review
  11. The role of mGenes & diseases · 2024
    Review
  12. Review
  13. Interaction between NMolecular medicine (Cambridge, Mass.) · 2023
    Review
  14. Review
  15. Epigenetics · 2022
    Article
  16. Review
  17. Article
  18. The Role of NOxidative medicine and cellular longevity · 2022
    Review
  19. 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

6 authors.

Maialen Sebastian-delaCruzDepartment of Genetics, Physical Anthropology and Animal Fisiology, University of the Basque Country, 48940 Leioa, Spain.ORCID 0000-0003-2953-6573
Ane Olazagoitia-GarmendiaDepartment of Genetics, Physical Anthropology and Animal Fisiology, University of the Basque Country, 48940 Leioa, Spain.ORCID 0000-0002-2645-1518
Itziar Gonzalez-MoroBiocruces Bizkaia Health Research Institute, 48903 Barakaldo, Spain.ORCID 0000-0002-6504-4931
Izortze SantinBiocruces Bizkaia Health Research Institute, 48903 Barakaldo, Spain.ORCID 0000-0003-1651-6776
Koldo Garcia-EtxebarriaHepatic and Gastrointestinal Disease Area, IIS Biodonostia, 20014 Donostia, Spain.
Ainara Castellanos-RubioDepartment of Genetics, Physical Anthropology and Animal Fisiology, University of the Basque Country, 48940 Leioa, Spain.ORCID 0000-0003-3192-9544

Funding

European Foundation for the Study of Diabetes NOCORE20/06Ministerio de Ciencia, Innovación y Universidades PGC2018-097573-A-I00Osasun Saila, Eusko Jaurlaritzako 2015111068
6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract that develops due to the interaction between genetic and environmental factors. More than 160 loci have been associated with IBD, but the functional implication of many of the associated genes remains unclear. N6-Methyladenosine (m6A) is the most abundant internal modification in mRNA. m6A methylation regulates many aspects of mRNA metabolism, playing important roles in the development of several pathologies. Interestingly, SNPs located near or within m6A motifs have been proposed as possible contributors to disease pathogenesis. We hypothesized that certain IBD-associated SNPs could regulate the function of genes involved in IBD development via m6A-dependent mechanisms. We used online available GWAS, m6A and transcriptome data to find differentially expressed genes that harbored m6A-SNPs associated with IBD. Our analysis resulted in five candidate genes corresponding to two of the major IBD subtypes:

Indexed as

Crohn’s diseaseinflammationinflammatory bowel diseasem6AMETTL3SNPulcerative colitisYTHDF1

Identifiers

PMID34968289
PMCPMC8594712

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.