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Unless otherwise stated all data on this page refer to the human proteins. Gene information is provided for human (Hs), mouse (Mm) and rat (Rn).
NF-κB transcription factors (TFs) are homo- or heterodimeric complexes containing NFKB1/p105, NFKB1/p50, NFKB2/p52, REL, RELA/p65, and/or RELB proteins. They bind to κ-B sites in the DNA of their target genes to regulate the expression of genes that influence biological process including immune and inflammatory responses (cytokine production), development, growth, survival, and apoptosis. The different dimers are selective for κ-B sites, and act as transcriptional repressors or activators. The most abundant NF-κB transcriptional activator is the heterodimer containing NFKB1 and RELA. The RELA-REL complex is also an activator.
NF-κB activity is tightly regulated. An inactive state is maintained by interactions between transcriptionally active complexes and inhibitory proteins of the NF-κB inhibitor (I-κB) family. In turn the I-κBs are regulated by phosphorylation (catalysed by kinases IKKα and IKKβ) which promotes ubiquitin dependent degradation. Removal of the I-κBs disinhibits NF-κB TFs which then translocate into the nucleus to drive transcription of target genes. Dysregulated NF-κB pathway activity is associated with human diseases.
nuclear factor kappa B subunit 1 Show summary » |
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nuclear factor kappa B subunit 2 Show summary »
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REL proto-oncogene, NF-kB subunit Show summary » |
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RELA proto-oncogene, NF-kB subunit Show summary » |
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RELB proto-oncogene, NF-kB subunit Show summary » |
Database page citation:
NF-kappa B TF proteins. Accessed on 07/12/2024. IUPHAR/BPS Guide to PHARMACOLOGY, http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=1099.
Concise Guide to PHARMACOLOGY citation:
Alexander SPH, Kelly E, Mathie AA, Peters JA, Veale EL, Armstrong JF, Buneman OP, Faccenda E, Harding SD, Spedding M, Cidlowski JA, Fabbro D, Davenport AP, Striessnig J, Davies JA et al. (2023) The Concise Guide to PHARMACOLOGY 2023/24: Introduction and Other Protein Targets. Br J Pharmacol. 180 Suppl 2:S1-22.