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TNF induced inhibition of Cirbp expression depends on RelB NF-κB signalling pathway

The circadian clock is required for the rhythmic expression of a plethora of genes that orchestrate metabolism, sleep-wake behaviour and the immune response to pathogens. The cold-inducible RNA binding protein (CIRBP) is required for high amplitude expression of clock genes. Moreover, CIRBP protects...

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Detalles Bibliográficos
Autores principales: Lopez, Martin A., Meier, Daniel, Wong, W.Wei-Lynn, Fontana, Adriano
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5600431/
https://www.ncbi.nlm.nih.gov/pubmed/28955803
http://dx.doi.org/10.1016/j.bbrep.2015.11.007
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author Lopez, Martin A.
Meier, Daniel
Wong, W.Wei-Lynn
Fontana, Adriano
author_facet Lopez, Martin A.
Meier, Daniel
Wong, W.Wei-Lynn
Fontana, Adriano
author_sort Lopez, Martin A.
collection PubMed
description The circadian clock is required for the rhythmic expression of a plethora of genes that orchestrate metabolism, sleep-wake behaviour and the immune response to pathogens. The cold-inducible RNA binding protein (CIRBP) is required for high amplitude expression of clock genes. Moreover, CIRBP protects the expression of clock genes from the inhibitory effects of tumour necrosis factor (TNF). However, since TNF represses Cirbp expression, the protective effect of CIRBP is lost. Here, we show that the TNF effect on Cirbp requires the non-canonical NF-κB signalling pathway. While a knock down of RelA does not alter the effects of TNF on Cirbp, a knock down of RelB represses this effect. In addition, the data indicate that p50 and p52 are required in the TNF induced inhibition of Cirbp. These results show that Cirbp expression in TNF treated cells is regulated via the non-canonical NF-κB pathway.
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spelling pubmed-56004312017-09-27 TNF induced inhibition of Cirbp expression depends on RelB NF-κB signalling pathway Lopez, Martin A. Meier, Daniel Wong, W.Wei-Lynn Fontana, Adriano Biochem Biophys Rep Research Article The circadian clock is required for the rhythmic expression of a plethora of genes that orchestrate metabolism, sleep-wake behaviour and the immune response to pathogens. The cold-inducible RNA binding protein (CIRBP) is required for high amplitude expression of clock genes. Moreover, CIRBP protects the expression of clock genes from the inhibitory effects of tumour necrosis factor (TNF). However, since TNF represses Cirbp expression, the protective effect of CIRBP is lost. Here, we show that the TNF effect on Cirbp requires the non-canonical NF-κB signalling pathway. While a knock down of RelA does not alter the effects of TNF on Cirbp, a knock down of RelB represses this effect. In addition, the data indicate that p50 and p52 are required in the TNF induced inhibition of Cirbp. These results show that Cirbp expression in TNF treated cells is regulated via the non-canonical NF-κB pathway. Elsevier 2015-11-14 /pmc/articles/PMC5600431/ /pubmed/28955803 http://dx.doi.org/10.1016/j.bbrep.2015.11.007 Text en © 2015 The Authors http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Research Article
Lopez, Martin A.
Meier, Daniel
Wong, W.Wei-Lynn
Fontana, Adriano
TNF induced inhibition of Cirbp expression depends on RelB NF-κB signalling pathway
title TNF induced inhibition of Cirbp expression depends on RelB NF-κB signalling pathway
title_full TNF induced inhibition of Cirbp expression depends on RelB NF-κB signalling pathway
title_fullStr TNF induced inhibition of Cirbp expression depends on RelB NF-κB signalling pathway
title_full_unstemmed TNF induced inhibition of Cirbp expression depends on RelB NF-κB signalling pathway
title_short TNF induced inhibition of Cirbp expression depends on RelB NF-κB signalling pathway
title_sort tnf induced inhibition of cirbp expression depends on relb nf-κb signalling pathway
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5600431/
https://www.ncbi.nlm.nih.gov/pubmed/28955803
http://dx.doi.org/10.1016/j.bbrep.2015.11.007
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