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Hypoxia Induced NF-κB

The Regulation of NF-κB Subunits by Phosphorylation

Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8TA, UK
Author to whom correspondence should be addressed.
Academic Editor: Alexander E. Kalyuzhny
Cells 2016, 5(1), 12;
Received: 26 February 2016 / Revised: 9 March 2016 / Accepted: 14 March 2016 / Published: 18 March 2016
(This article belongs to the Special Issue Cellular and Molecular Biology of NF-κB)
The NF-κB transcription factor is the master regulator of the inflammatory response and is essential for the homeostasis of the immune system. NF-κB regulates the transcription of genes that control inflammation, immune cell development, cell cycle, proliferation, and cell death. The fundamental role that NF-κB plays in key physiological processes makes it an important factor in determining health and disease. The importance of NF-κB in tissue homeostasis and immunity has frustrated therapeutic approaches aimed at inhibiting NF-κB activation. However, significant research efforts have revealed the crucial contribution of NF-κB phosphorylation to controlling NF-κB directed transactivation. Importantly, NF-κB phosphorylation controls transcription in a gene-specific manner, offering new opportunities to selectively target NF-κB for therapeutic benefit. This review will focus on the phosphorylation of the NF-κB subunits and the impact on NF-κB function. View Full-Text
Keywords: NF-κB; phosphorylation; kinase; transcription factor NF-κB; phosphorylation; kinase; transcription factor
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MDPI and ACS Style

Christian, F.; Smith, E.L.; Carmody, R.J. The Regulation of NF-κB Subunits by Phosphorylation. Cells 2016, 5, 12.

AMA Style

Christian F, Smith EL, Carmody RJ. The Regulation of NF-κB Subunits by Phosphorylation. Cells. 2016; 5(1):12.

Chicago/Turabian Style

Christian, Frank, Emma L. Smith, and Ruaidhrí J. Carmody. 2016. "The Regulation of NF-κB Subunits by Phosphorylation" Cells 5, no. 1: 12.

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