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The RelB subunit of NFκB acts as a negative regulator of circadian gene expression
The circadian system controls a large array of physiological and metabolic functions. The molecular organization of the circadian clock is complex, involving various elements organized in feedback regulatory loops. Here we demonstrate that the RelB subunit of NFκB acts as a repressor of circadian tr...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Landes Bioscience
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3467027/ https://www.ncbi.nlm.nih.gov/pubmed/22894897 http://dx.doi.org/10.4161/cc.21669 |
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author | Bellet, Marina M. Zocchi, Loredana Sassone-Corsi, Paolo |
author_facet | Bellet, Marina M. Zocchi, Loredana Sassone-Corsi, Paolo |
author_sort | Bellet, Marina M. |
collection | PubMed |
description | The circadian system controls a large array of physiological and metabolic functions. The molecular organization of the circadian clock is complex, involving various elements organized in feedback regulatory loops. Here we demonstrate that the RelB subunit of NFκB acts as a repressor of circadian transcription. RelB physically interacts with the circadian activator BMAL1 in the presence of CLOCK to repress circadian gene expression at the promoter of the clock-controlled gene Dbp. The repression is independent of the circadian negative regulator CRY. Notably, RelB −/− fibroblasts have profound alterations of circadian genes expression. These findings reveal a previously unforeseen function for RelB as an important regulator of the mammalian circadian system in fibroblasts. |
format | Online Article Text |
id | pubmed-3467027 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Landes Bioscience |
record_format | MEDLINE/PubMed |
spelling | pubmed-34670272012-10-19 The RelB subunit of NFκB acts as a negative regulator of circadian gene expression Bellet, Marina M. Zocchi, Loredana Sassone-Corsi, Paolo Cell Cycle Report The circadian system controls a large array of physiological and metabolic functions. The molecular organization of the circadian clock is complex, involving various elements organized in feedback regulatory loops. Here we demonstrate that the RelB subunit of NFκB acts as a repressor of circadian transcription. RelB physically interacts with the circadian activator BMAL1 in the presence of CLOCK to repress circadian gene expression at the promoter of the clock-controlled gene Dbp. The repression is independent of the circadian negative regulator CRY. Notably, RelB −/− fibroblasts have profound alterations of circadian genes expression. These findings reveal a previously unforeseen function for RelB as an important regulator of the mammalian circadian system in fibroblasts. Landes Bioscience 2012-09-01 /pmc/articles/PMC3467027/ /pubmed/22894897 http://dx.doi.org/10.4161/cc.21669 Text en Copyright © 2012 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. |
spellingShingle | Report Bellet, Marina M. Zocchi, Loredana Sassone-Corsi, Paolo The RelB subunit of NFκB acts as a negative regulator of circadian gene expression |
title | The RelB subunit of NFκB acts as a negative regulator of circadian gene expression |
title_full | The RelB subunit of NFκB acts as a negative regulator of circadian gene expression |
title_fullStr | The RelB subunit of NFκB acts as a negative regulator of circadian gene expression |
title_full_unstemmed | The RelB subunit of NFκB acts as a negative regulator of circadian gene expression |
title_short | The RelB subunit of NFκB acts as a negative regulator of circadian gene expression |
title_sort | relb subunit of nfκb acts as a negative regulator of circadian gene expression |
topic | Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3467027/ https://www.ncbi.nlm.nih.gov/pubmed/22894897 http://dx.doi.org/10.4161/cc.21669 |
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