Circuitry of nuclear factor κB signaling
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Summary: Over the past few years, the transcription factor nuclear factor (NF)‐κB and the proteins that regulate it have emerged as a signaling system of pre‐eminent importance in human physiology and in an increasing number of pathologies. While NF‐κB is present in all differentiated cell types, its discovery and early characterization were rooted in understanding B‐cell biology. Significant research efforts over two decades have yielded a large body of literature devoted to understanding NF‐κB's functioning in the immune system. NF‐κB has been found to play roles in many different compartments of the immune system during differentiation of immune cells and development of lymphoid organs and during immune activation. NF‐κB is the nuclear effector of signaling pathways emanating from many receptors, including those of the inflammatory tumor necrosis factor and Toll‐like receptor superfamilies. With this review, we hope to provide historical context and summarize the diverse physiological functions of NF‐κB in the immune system before focusing on recent advances in elucidating the molecular mechanisms that mediate cell type‐specific and stimulus‐specific functions of this pleiotropic signaling system. Understanding the genetic regulatory circuitry of NF‐κB functionalities involves system‐wide measurements, biophysical studies, and computational modeling.
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In the NF-κB system, NF-κB is normally held inactive in the cytoplasm by binding to an inhibitor IκB; pro-inflammatory cytokines such as TNF-α, LPS and IL-1 act by binding to receptors at the cell surface and initiating signalling pathways that lead to activation of IKK; IKK phosphorylates IκB causing its release and degradation, allowing NF-κB to translocate to the nucleus where it can activate a
“In the NF-κB system (e.g. [2020-2024]) (Fig 8), NF-κB is normally held inactive in the cytoplasm by binding to an inhibitor IκB (often IκBα). Pro-inflammatory cytokines such as TNF-α, LPS [2025-2030] and IL-1 [2031] act by binding to receptors at the cell surface and initiating signalling pathways that lead to the activation of a particular kinase, IκB kinase or IKK. This kinase phosphorylates the”
From Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases (2009) · cites this paper as [2023]
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Sorted by citations
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Pulsatile Stimulation Determines Timing and Specificity of NF-κB-Dependent Transcription
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Crosstalk via the NF-κB signaling system
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Self-citationZinc Triggers Microglial Activation
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- Authors
- Hoffmann, A., & Baltimore, D.
- Affiliations
- University of California San Diego (US)
- California Institute of Technology (US)
- Corresponding author
- Hoffmann, Alexander
- Venue
- Immunological Reviews
- Publisher
- Wiley
- Published
- 2006-03-28
- Volume
- 210
- Issue
- 1
- Pages
- 171-186
- ISSN
- 0105-2896 (ISSN-L)
- 1600-065X
- OpenAlex
- W1694093395
- Cited by
- 907
- References
- 92
- Citations by year
- 2026: 16 · 2025: 29 · 2024: 32 · 2023: 30 · 2022: 34 · 2021: 30 · 2020: 31 · 2019: 42 · 2018: 56 · 2017: 50 · 2016: 36 · 2015: 59 · 2014: 50 · 2013: 65 · 2012: 59
- FWCI
- 4.08
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Immunological Reviews (publishedVersion)
- PubMed (publishedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Keywords
- NF-κB signaling, transcription factor regulation, immune system, B cell biology, Toll-like receptors, TNF-α, immune cell differentiation, lymphoid organ development, immune activation, cell type-specific signaling
- MeSH terms
- Humans, Immune System, Immunity, Innate, Protein Conformation, Signal Transduction, NF-kappa B
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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