Circuitry of nuclear factor κB signaling
By Alexander Hoffmann, David Baltimore. 2006
627 citations recorded by the source corpus.
Subfields: Cancer Research, Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/78aec7c2683846634a31a26abc9cc21cce6e1c64
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In Cancer Research
In Immunology
In Oncology
Citations in the corpus
- Control of the senescence-associated secretory phenotype by NF-κB promotes senescence and enhances chemosensitivity. (2011, background): “In all of these settings, Bcl-2 translocations enforce a strong apoptotic block, and recent transcriptome analyses of GCB-DLBCL indeed suggest that low NF-kB activity correlates with poor treatment outcome in patients harboring lymphomas of this subtype (Jing et al. 2011).”
- Mutations of multiple genes cause deregulation of NF-kB in diffuse large B-cell lymphoma (2009, neutral): “8){ 2/20 (10) TNFRSF11A (RANK) 3/37 (8.”
- Transcriptional regulation via the NF-κB signaling module (2006, background): “Since then, high throughput technologies have revealed that the vast majority of the inflammatory gene expression program is NF-kBdependent (Hoffmann and Baltimore, 2006), and that DNA-bound NF-kB can be detected at many chromosomal locations (Martone et al., 2003; Schreiber et al, 2006).”
- Osteoarthritis: pathogenic signaling pathways and therapeutic targets (2023, background): “Lacking TAD, the dimers formed only by p50 and p52, either homodimers or heterodimers, could not drive the transcription.(181) In contrast, the heterodimers of cRel:p50, p65:p50, and RelB:p52 could function as transcriptional activators.”