The nuclear receptor 4A family members: mediators in human disease and autophagy

The Nuclear receptor 4A (NR4A) subfamily, which belongs to the nuclear receptor (NR) superfamily, has three members: NR4A1 (Nur77), NR4A2 (Nurr1) and NR4A3 (Nor1). They are gene regulators with broad involvement in various signaling pathways and human disease responses, including autophagy. Here, we...

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Autores principales: Chen, Liqun, Fan, Fengtian, Wu, Lingjuan, Zhao, Yiyi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Review Letter
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7640683/
https://www.ncbi.nlm.nih.gov/pubmed/33292165
http://dx.doi.org/10.1186/s11658-020-00241-w
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author Chen, Liqun
Fan, Fengtian
Wu, Lingjuan
Zhao, Yiyi
author_facet Chen, Liqun
Fan, Fengtian
Wu, Lingjuan
Zhao, Yiyi
author_sort Chen, Liqun
collection PubMed
description The Nuclear receptor 4A (NR4A) subfamily, which belongs to the nuclear receptor (NR) superfamily, has three members: NR4A1 (Nur77), NR4A2 (Nurr1) and NR4A3 (Nor1). They are gene regulators with broad involvement in various signaling pathways and human disease responses, including autophagy. Here, we provide a concise overview of the current understanding of the role of the NR4A subfamily members in human diseases and review the research into their regulation of cell autophagy. A deeper understanding of these mechanisms has potential to improve drug development processes and disease therapy.
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spelling pubmed-76406832020-11-04 The nuclear receptor 4A family members: mediators in human disease and autophagy Chen, Liqun Fan, Fengtian Wu, Lingjuan Zhao, Yiyi Cell Mol Biol Lett Review Letter The Nuclear receptor 4A (NR4A) subfamily, which belongs to the nuclear receptor (NR) superfamily, has three members: NR4A1 (Nur77), NR4A2 (Nurr1) and NR4A3 (Nor1). They are gene regulators with broad involvement in various signaling pathways and human disease responses, including autophagy. Here, we provide a concise overview of the current understanding of the role of the NR4A subfamily members in human diseases and review the research into their regulation of cell autophagy. A deeper understanding of these mechanisms has potential to improve drug development processes and disease therapy. BioMed Central 2020-11-03 /pmc/articles/PMC7640683/ /pubmed/33292165 http://dx.doi.org/10.1186/s11658-020-00241-w Text en © The Author(s) 2020 Open AccessThis 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. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Review Letter
Chen, Liqun
Fan, Fengtian
Wu, Lingjuan
Zhao, Yiyi
The nuclear receptor 4A family members: mediators in human disease and autophagy
title The nuclear receptor 4A family members: mediators in human disease and autophagy
title_full The nuclear receptor 4A family members: mediators in human disease and autophagy
title_fullStr The nuclear receptor 4A family members: mediators in human disease and autophagy
title_full_unstemmed The nuclear receptor 4A family members: mediators in human disease and autophagy
title_short The nuclear receptor 4A family members: mediators in human disease and autophagy
title_sort nuclear receptor 4a family members: mediators in human disease and autophagy
topic Review Letter
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7640683/
https://www.ncbi.nlm.nih.gov/pubmed/33292165
http://dx.doi.org/10.1186/s11658-020-00241-w
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