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The DOI matches its Crossref record; 18 of the 18 references it cites were found in a registry or an index.

The complexity of NF-κB signaling in inflammation and cancer

Open access
Hoesel, Bastian, Schmid, Johannes A·2013·Molecular Cancer

Abstract

The NF-κB family of transcription factors has an essential role in inflammation and innate immunity. Furthermore, NF-κB is increasingly recognized as a crucial player in many steps of cancer initiation and progression. During these latter processes NF-κB cooperates with multiple other signaling molecules and pathways. Prominent nodes of crosstalk are mediated by other transcription factors such as STAT3 and p53 or the ETS related gene ERG. These transcription factors either directly interact with NF-κB subunits or affect NF-κB target genes. Crosstalk can also occur through different kinases, such as GSK3-β, p38, or PI3K, which modulate NF-κB transcriptional activity or affect upstream signaling pathways. Other classes of molecules that act as nodes of crosstalk are reactive oxygen species and miRNAs. In this review, we provide an overview of the most relevant modes of crosstalk and cooperativity between NF-κB and other signaling molecules during inflammation and cancer.

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Metadata

Authors
Hoesel, B., & Schmid, J. A.
Venue
Molecular Cancer
Published
2013
Volume
12
Issue
1
Pages
86
ISSN
1476-4598 (ISSN-L)
OpenAlex
W2134887638
Cited by
3,165
References
18
FWCI
46.77
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: The complexity of NF-κB signaling in inflammation and cancer. https://app.cochat.ai/papers/10.1186/1476-4598-12-86
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Hoesel, B., & Schmid, J. A. (2013). The complexity of NF-κB signaling in inflammation and cancer. Molecular Cancer. https://doi.org/10.1186/1476-4598-12-86

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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.