Crosstalk via the NF-κB signaling system
Open accessAbstract
The nuclear factor kappaB (NF-kappaB) family of transcription factors consists of 15 possible dimers whose activity is controlled by a family of inhibitor proteins, known as IkappaBs. A variety of cellular stimuli, many of them transduced by members of the tumor necrosis factor receptor (TNFR) superfamily, induce degradation of IkappaBs to activate an overlapping subset of NF-kappaB dimers. However, generation and stimulus-responsive activation of NF-kappaB dimers are intimately linked via various cross-regulatory mechanisms that allow crosstalk between different signaling pathways through the NF-kappaB signaling system. In this review, we summarize these mechanisms and discuss physiological and pathological consequences of crosstalk between apparently distinct inflammatory and developmental signals. We argue that a systems approach will be valuable for understanding questions of specificity and emergent properties of highly networked cellular signaling systems.
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NF-κB translocated into the nucleus activates transcription of target genes.
“NF-κB translocated into the nucleus activates the transcription of target genes (Basak and Hoffmann 2008).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Basak and Hoffmann 2008
The canonical NF-κB activation pathway is triggered through site-specific phosphorylation by an IKK complex in response to microbes and proinflammatory cytokines.
“The canonical activation pathway is triggered through the site-specific phosphorylation by an IκB-kinase (IKK) complex in response to microbes, and proinflammatory cytokines.”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Basak and Hoffmann 2008
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- Authors
- Basak, S., & Hoffmann, A.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Basak, Soumen
- Hoffmann, Alexander
- Venue
- Cytokine & Growth Factor Reviews
- Publisher
- Elsevier BV
- Published
- 2008-06
- Volume
- 19
- Issue
- 3-4
- Pages
- 187-197
- ISSN
- 1359-6101 (ISSN-L)
- PMC
- PMC2675004
- OpenAlex
- W2054072076
- Cited by
- 177
- References
- 64
- Citations by year
- 2026: 5 · 2025: 12 · 2024: 5 · 2023: 6 · 2022: 2 · 2021: 9 · 2020: 10 · 2019: 5 · 2018: 13 · 2017: 6 · 2016: 10 · 2015: 8 · 2014: 12 · 2013: 13 · 2012: 8
- FWCI
- 1.26
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Cytokine & Growth Factor Reviews (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of General Medical Sciences (P01GM071862, R01GM071573)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- NF-κB signaling, signaling crosstalk, IκB degradation, TNF receptor superfamily, inflammatory signaling, developmental signaling
- MeSH terms
- Animals, Immunity, Inflammation, Lymphoid Tissue, Signal Transduction, NF-kappa B, Receptors, Tumor Necrosis Factor, Growth and Development, Mice, Transcription Factor RelA, NF-kappa B p50 Subunit
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