Implication of m6A mRNA Methylation in Susceptibility to Inflammatory Bowel Disease
dc.contributor.author | Sebastián de la Cruz, Maialen | |
dc.contributor.author | Olazagoitia Garmendia, Ane | |
dc.contributor.author | González Moro, Itziar | |
dc.contributor.author | Santín Gómez, Izortze | |
dc.contributor.author | García Etxebarria, Koldo | |
dc.contributor.author | Castellanos Rubio, Ainara | |
dc.date.accessioned | 2020-10-01T09:20:40Z | |
dc.date.available | 2020-10-01T09:20:40Z | |
dc.date.issued | 2020-08-03 | |
dc.identifier.citation | Epigenomes 4(3) : (2020) // Article ID 16 | es_ES |
dc.identifier.issn | 2075-4655 | |
dc.identifier.uri | http://hdl.handle.net/10810/46329 | |
dc.description.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: UBE2L3 and SLC22A4 for Crohn’s Disease and TCF19, C6orf47 and SNAPC4 for Ulcerative Colitis. Further analysis using in silico predictions and co-expression analyses in combination with in vitro functional studies showed that our candidate genes seem to be regulated by m6A-dependent mechanisms. These findings provide the first indication of the implication of RNA methylation events in IBD pathogenesis. | es_ES |
dc.description.sponsorship | This work was supported by Spanish Ministry of Science, Innovation and Universities (grant PGC2018-097573-A-I00) to A.C.-R. I.S. was funded by research project grant 2015111068 of the Basque Department of Health and a Research Grant from the European Foundation for the Study of Diabetes. M.S.-d. and I.G.-M. are predoctoral fellows funded by grants from the University of Basque Country and A.O.-G. is a predoctoral fellow funded by Basque Department of Education, Universities and Research. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | MDPI | es_ES |
dc.rights | info:eu-repo/semantics/openAccess | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es/ | |
dc.subject | inflammatory bowel disease | es_ES |
dc.subject | Crohn’s disease | es_ES |
dc.subject | ulcerative colitis | es_ES |
dc.subject | m6A | es_ES |
dc.subject | SNP | es_ES |
dc.subject | METTL3 | es_ES |
dc.subject | YTHDF1 | es_ES |
dc.subject | inflammation | es_ES |
dc.title | Implication of m6A mRNA Methylation in Susceptibility to Inflammatory Bowel Disease | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.date.updated | 2020-09-25T13:26:15Z | |
dc.rights.holder | 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). | es_ES |
dc.relation.publisherversion | https://www.mdpi.com/2075-4655/4/3/16 | es_ES |
dc.identifier.doi | 0.3390/epigenomes4030016 | |
dc.departamentoes | Genética, antropología física y fisiología animal | |
dc.departamentoes | Bioquímica y biología molecular |
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Except where otherwise noted, this item's license is described as 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).