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Arid5a Regulation and the Roles of Arid5a in the Inflammatory Response and Disease
Abnormal gene expression patterns underlie many diseases that represent major public health concerns and robust therapeutic challenges. Posttranscriptional gene regulation by RNA-binding proteins (RBPs) is well-recognized, and the biological functions of RBPs have been implicated in many diseases, s...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6906145/ https://www.ncbi.nlm.nih.gov/pubmed/31867000 http://dx.doi.org/10.3389/fimmu.2019.02790 |
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author | Nyati, Kishan Kumar Agarwal, Riddhi Girdhar Sharma, Praveen Kishimoto, Tadamitsu |
author_facet | Nyati, Kishan Kumar Agarwal, Riddhi Girdhar Sharma, Praveen Kishimoto, Tadamitsu |
author_sort | Nyati, Kishan Kumar |
collection | PubMed |
description | Abnormal gene expression patterns underlie many diseases that represent major public health concerns and robust therapeutic challenges. Posttranscriptional gene regulation by RNA-binding proteins (RBPs) is well-recognized, and the biological functions of RBPs have been implicated in many diseases, such as autoimmune diseases, inflammatory diseases, and cancer. However, a complete understanding of the regulation mediated by several RBPs is lacking. During the past few years, a novel role of AT-rich interactive domain-containing protein 5a (Arid5a) as an RBP is being investigated in the field of immunology owing to binding of Arid5a protein to the 3′ untranslated region (UTR) of Il-6 mRNA. Indeed, Arid5a is a dynamic molecule because upon inflammation, it translocates to the cytoplasm and stabilizes a variety of inflammatory mRNA transcripts, including Il-6, Stat3, Ox40, T-bet, and IL-17-induced targets, and contributes to the inflammatory response and a variety of diseases. TLR4-activated NF-κB and MAPK pathways are involved in regulating Arid5a expression from synthesis to degradation, and even a slight alteration in these pathways can lead to intense production of inflammatory molecules, such as IL-6, which may further contribute to the development of inflammatory diseases such as sepsis and experimental autoimmune encephalomyelitis. This review highlights the regulation of the Arid5a expression and function. Additionally, recent findings on Arid5a are discussed to further our understanding of this molecule, which may be a promising therapeutic target for inflammatory diseases. |
format | Online Article Text |
id | pubmed-6906145 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-69061452019-12-20 Arid5a Regulation and the Roles of Arid5a in the Inflammatory Response and Disease Nyati, Kishan Kumar Agarwal, Riddhi Girdhar Sharma, Praveen Kishimoto, Tadamitsu Front Immunol Immunology Abnormal gene expression patterns underlie many diseases that represent major public health concerns and robust therapeutic challenges. Posttranscriptional gene regulation by RNA-binding proteins (RBPs) is well-recognized, and the biological functions of RBPs have been implicated in many diseases, such as autoimmune diseases, inflammatory diseases, and cancer. However, a complete understanding of the regulation mediated by several RBPs is lacking. During the past few years, a novel role of AT-rich interactive domain-containing protein 5a (Arid5a) as an RBP is being investigated in the field of immunology owing to binding of Arid5a protein to the 3′ untranslated region (UTR) of Il-6 mRNA. Indeed, Arid5a is a dynamic molecule because upon inflammation, it translocates to the cytoplasm and stabilizes a variety of inflammatory mRNA transcripts, including Il-6, Stat3, Ox40, T-bet, and IL-17-induced targets, and contributes to the inflammatory response and a variety of diseases. TLR4-activated NF-κB and MAPK pathways are involved in regulating Arid5a expression from synthesis to degradation, and even a slight alteration in these pathways can lead to intense production of inflammatory molecules, such as IL-6, which may further contribute to the development of inflammatory diseases such as sepsis and experimental autoimmune encephalomyelitis. This review highlights the regulation of the Arid5a expression and function. Additionally, recent findings on Arid5a are discussed to further our understanding of this molecule, which may be a promising therapeutic target for inflammatory diseases. Frontiers Media S.A. 2019-12-05 /pmc/articles/PMC6906145/ /pubmed/31867000 http://dx.doi.org/10.3389/fimmu.2019.02790 Text en Copyright © 2019 Nyati, Agarwal, Sharma and Kishimoto. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Nyati, Kishan Kumar Agarwal, Riddhi Girdhar Sharma, Praveen Kishimoto, Tadamitsu Arid5a Regulation and the Roles of Arid5a in the Inflammatory Response and Disease |
title | Arid5a Regulation and the Roles of Arid5a in the Inflammatory Response and Disease |
title_full | Arid5a Regulation and the Roles of Arid5a in the Inflammatory Response and Disease |
title_fullStr | Arid5a Regulation and the Roles of Arid5a in the Inflammatory Response and Disease |
title_full_unstemmed | Arid5a Regulation and the Roles of Arid5a in the Inflammatory Response and Disease |
title_short | Arid5a Regulation and the Roles of Arid5a in the Inflammatory Response and Disease |
title_sort | arid5a regulation and the roles of arid5a in the inflammatory response and disease |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6906145/ https://www.ncbi.nlm.nih.gov/pubmed/31867000 http://dx.doi.org/10.3389/fimmu.2019.02790 |
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