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dc.contributor.authorYoshinaga, Masanorien
dc.contributor.authorTakeuchi, Osamuen
dc.contributor.alternative吉永, 正憲ja
dc.contributor.alternative竹内, 理ja
dc.date.accessioned2024-03-22T00:08:10Z-
dc.date.available2024-03-22T00:08:10Z-
dc.date.issued2024-03-15-
dc.identifier.urihttp://hdl.handle.net/2433/287448-
dc.description.abstractInflammation orchestrates a finely balanced process crucial for microorganism elimination and tissue injury protection. A multitude of immune and non-immune cells, alongside various proinflammatory cytokines and chemokines, collectively regulate this response. Central to this regulation is post-transcriptional control, governing gene expression at the mRNA level. RNA-binding proteins such as tristetraprolin, Roquin, and the Regnase family, along with RNA modifications, intricately dictate the mRNA decay of pivotal mediators and regulators in the inflammatory response. Dysregulated activity of these factors has been implicated in numerous human inflammatory diseases, underscoring the significance of post-transcriptional regulation. The increasing focus on targeting these mechanisms presents a promising therapeutic strategy for inflammatory and autoimmune diseases. This review offers an extensive overview of post-transcriptional regulation mechanisms during inflammatory responses, delving into recent advancements, their implications in human diseases, and the strides made in therapeutic exploitation.en
dc.language.isoeng-
dc.publisherSpringer Natureen
dc.publisherBMCen
dc.rights© The Author(s) 2024.en
dc.rightsThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder.en
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/-
dc.subjectPost-transcriptional regulationen
dc.subjectmRNA decayen
dc.subjectAutoimmune diseasesen
dc.subjectmRNA methylationen
dc.subjectRNA-binding proteinsen
dc.subjectRegnase familyen
dc.subjectTherapeutic interventionen
dc.titleRegulation of inflammatory diseases via the control of mRNA decayen
dc.typejournal article-
dc.type.niitypeJournal Article-
dc.identifier.jtitleInflammation and Regenerationen
dc.identifier.volume44-
dc.relation.doi10.1186/s41232-024-00326-5-
dc.textversionpublisher-
dc.identifier.artnum14-
dc.identifier.pmid38491500-
dcterms.accessRightsopen access-
datacite.awardNumber18H05278-
datacite.awardNumber16H06279-
datacite.awardNumber23H00402-
datacite.awardNumber20K22737-
datacite.awardNumber21K15372-
datacite.awardNumber23H04777-
datacite.awardNumber.urihttps://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18H05278/-
datacite.awardNumber.urihttps://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16H06279/-
datacite.awardNumber.urihttps://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23H00402/-
datacite.awardNumber.urihttps://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20K22737/-
datacite.awardNumber.urihttps://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21K15372/-
datacite.awardNumber.urihttps://kaken.nii.ac.jp/grant/KAKENHI-PUBLICLY-23H04777/-
dc.identifier.eissn1880-8190-
jpcoar.funderName日本学術振興会ja
jpcoar.funderName日本学術振興会ja
jpcoar.funderName日本学術振興会ja
jpcoar.funderName日本学術振興会ja
jpcoar.funderName日本学術振興会ja
jpcoar.funderName日本学術振興会ja
jpcoar.awardTitlemRNA代謝が司る免疫制御機構の解明ja
jpcoar.awardTitle先進ゲノム解析研究推進プラットフォームja
jpcoar.awardTitlemRNA結合タンパク質による免疫制御機構の解明ja
jpcoar.awardTitle鉄代謝におけるRNA修飾を介した転写後調節機構の解明ja
jpcoar.awardTitleRNA修飾を介した赤芽球分化制御機構の解明ja
jpcoar.awardTitleRNAメチル化修飾破綻による自己指向性免疫応答の解明ja
出現コレクション:学術雑誌掲載論文等

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