Meta-analysis of differentially expressed genes in ankylosing spondylitis
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, Y. H. | - |
dc.contributor.author | Song, G. G. | - |
dc.date.accessioned | 2021-09-05T00:57:58Z | - |
dc.date.available | 2021-09-05T00:57:58Z | - |
dc.date.created | 2021-06-15 | - |
dc.date.issued | 2015 | - |
dc.identifier.issn | 1676-5680 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/96216 | - |
dc.description.abstract | The purpose of this study was to identify differentially expressed (DE) genes and biological processes associated with changes in gene expression in ankylosing spondylitis (AS). We performed a meta-analysis using the integrative meta-analysis of expression data program on publicly available microarray AS Gene Expression Omnibus (GEO) datasets. We performed Gene Ontology (GO) enrichment analyses and pathway analysis using the Kyoto Encyclopedia of Genes and Genomes. Four GEO datasets, including 31 patients with AS and 39 controls, were available for the meta-analysis. We identified 65 genes across the studies that were consistently DE in patients with AS vs controls (23 upregulated and 42 downregulated). The upregulated gene with the largest effect size (ES; -1.2628, P = 0.020951) was integral membrane protein 2A (ITM2A), which is expressed by CD4+ T cells and plays a role in activation of T cells. The downregulated gene with the largest ES (1.2299, P = 0.040075) was mitochondrial ribosomal protein S11 (MRPS11). The most significant GO enrichment was in the respiratory electron transport chain category (P = 1.67 x 10(-9)). Therefore, our meta-analysis identified genes that were consistently DE as well as biological pathways associated with gene expression changes in AS. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | FUNPEC-EDITORA | - |
dc.subject | SYSTEMIC-LUPUS-ERYTHEMATOSUS | - |
dc.subject | GENOME SCAN METAANALYSIS | - |
dc.subject | PROTEINS | - |
dc.subject | DISEASE | - |
dc.subject | CANCER | - |
dc.subject | ITM2A | - |
dc.title | Meta-analysis of differentially expressed genes in ankylosing spondylitis | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Lee, Y. H. | - |
dc.contributor.affiliatedAuthor | Song, G. G. | - |
dc.identifier.doi | 10.4238/2015.May.18.6 | - |
dc.identifier.scopusid | 2-s2.0-84929405748 | - |
dc.identifier.wosid | 000357183700237 | - |
dc.identifier.bibliographicCitation | GENETICS AND MOLECULAR RESEARCH, v.14, no.2, pp.5161 - 5170 | - |
dc.relation.isPartOf | GENETICS AND MOLECULAR RESEARCH | - |
dc.citation.title | GENETICS AND MOLECULAR RESEARCH | - |
dc.citation.volume | 14 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 5161 | - |
dc.citation.endPage | 5170 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Genetics & Heredity | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Genetics & Heredity | - |
dc.subject.keywordPlus | SYSTEMIC-LUPUS-ERYTHEMATOSUS | - |
dc.subject.keywordPlus | GENOME SCAN METAANALYSIS | - |
dc.subject.keywordPlus | PROTEINS | - |
dc.subject.keywordPlus | DISEASE | - |
dc.subject.keywordPlus | CANCER | - |
dc.subject.keywordPlus | ITM2A | - |
dc.subject.keywordAuthor | Ankylosing spondylitis | - |
dc.subject.keywordAuthor | Gene expression | - |
dc.subject.keywordAuthor | Meta-analysis | - |
dc.subject.keywordAuthor | Pathway analysis | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
(02841) 서울특별시 성북구 안암로 14502-3290-1114
COPYRIGHT © 2021 Korea University. All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.