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Cited by 717

The DOI matches its Crossref record; 118 of the 118 references it cites were found in a registry or an index.

The Regulation of NF-κB Subunits by Phosphorylation

Open access
Christian, Frank, Smith, Emma, Carmody, Ruaidhrí·2016·Cells

Abstract

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.

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Crossref · 10.3390/cells5010012

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Metadata

Authors
Christian, F., Smith, E., & Carmody, R.
Venue
Cells
Publisher
MDPI AG
Published
2016-03-18
Volume
5
Issue
1
Pages
12
ISSN
2073-4409 (ISSN-L)
OpenAlex
W2302524766
Cited by
717
References
118
FWCI
20.14
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: The Regulation of NF-κB Subunits by Phosphorylation. https://app.cochat.ai/papers/10.3390/cells5010012
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Christian, F., Smith, E., & Carmody, R. (2016). The Regulation of NF-κB Subunits by Phosphorylation. Cells. https://doi.org/10.3390/cells5010012

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.