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Cells 2016, 5(2), 23; doi:10.3390/cells5020023

The Ubiquitination of NF-κB Subunits in the Control of Transcription

Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8TA, UK
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Academic Editor: Alexander E. Kalyuzhny
Received: 15 March 2016 / Revised: 3 May 2016 / Accepted: 6 May 2016 / Published: 12 May 2016
(This article belongs to the Special Issue Cellular and Molecular Biology of NF-κB)
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Abstract

Nuclear factor (NF)-κB has evolved as a latent, inducible family of transcription factors fundamental in the control of the inflammatory response. The transcription of hundreds of genes involved in inflammation and immune homeostasis require NF-κB, necessitating the need for its strict control. The inducible ubiquitination and proteasomal degradation of the cytoplasmic inhibitor of κB (IκB) proteins promotes the nuclear translocation and transcriptional activity of NF-κB. More recently, an additional role for ubiquitination in the regulation of NF-κB activity has been identified. In this case, the ubiquitination and degradation of the NF-κB subunits themselves plays a critical role in the termination of NF-κB activity and the associated transcriptional response. While there is still much to discover, a number of NF-κB ubiquitin ligases and deubiquitinases have now been identified which coordinate to regulate the NF-κB transcriptional response. This review will focus the regulation of NF-κB subunits by ubiquitination, the key regulatory components and their impact on NF-κB directed transcription. View Full-Text
Keywords: ubiquitination; NF-κB; transcription ubiquitination; NF-κB; transcription
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Collins, P.E.; Mitxitorena, I.; Carmody, R.J. The Ubiquitination of NF-κB Subunits in the Control of Transcription. Cells 2016, 5, 23.

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