NF-kappaB regulation in the immune system.

By Qiutang Li, Inder M. Verma. Nature reviews. Immunology, 2002

1,584 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/3f47558e839157a538658b8af91e1ce9f5986319

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Citations in the corpus

Role of tumor-associated macrophages in tumor progression and invasion (2006, background): “TNF-α, is a proinflammatory cytokine generally produced by macrophages in response to pro-inflammatory signals [59, 60].”
NF-κB activation as a pathological mechanism of septic shock and inflammation (2006, unknown): “In the Th1 response, induction of intrinsic NF- B activity is required for postdifferentiation IFN- production and clonal expansion (53, 139).”
The IκB Kinase Complex and NF-κB Actas Master Regulators of Lipopolysaccharide-Induced Gene Expressionand Control Subordinate Activation ofAP-1 (2004, background): “NF- B activation is initiated through cytokine signaling, innate or adaptive immune responses, morphological signals, or environmental stress (14, 18, 28).”
The Yin‐Yang of tumor‐associated macrophages in neoplastic progression and immune surveillance (2008, background): “TNF-a is a proinflammatory cytokine generally produced by macrophages in response to proinflammatory signals (27, 28).”
NF-κB in biology and targeted therapy: new insights and translational implications (2024, background): “79 Persistent activation of the NF-κ B pathway is frequently implicated in in ﬂ ammatory conditions like rheumatoid arthritis, in ﬂ ammatory bowel disease, multiple sclerosis (MS), and asthma.”
NF-κB and AP-1 Connection: Mechanism of NF-κB-Dependent Regulation of AP-1 Activity (2004, background): “The subsequent proteasome-mediated degradation of I B exposes the nuclear localization signal (NLS) of NF- B, which releases the NF- B proteins to be translocated to the nucleus, where they regulate the transcription of specific genes (5, 48).”
Molecular Mechanisms of Treg-Mediated T Cell Suppression (2012, background): “The NF-κB complex itself can be phosphorylated and acetylated , which regulates its transcriptional activity and association with other transcription factors (Li and Verma, 2002; Perkins, 2006).”
Obesity, Inflammation, Toll-Like Receptor 4 and Fatty Acids (2018, background): “The IκB proteins bind to different NF-κB dimers, although they have different affinities and specificities; therefore, besides the different NF-κB dimers that are found in a specific cell type, there are a large number of combinations of the IκB and the NF-κB dimers [82,83].”
NF-κB, an Active Player in Human Cancers (2014, unknown): “The activated IKK complex is responsible for the phosphorylation of I κ B, marking it for degradation through the β -transducin repeat-containing protein ( β -TrCP)-dependent E3 ubiquitin ligase-mediated proteasomal degradation machinery (2, 3).”
The NF-κB pathway (2005, background): “B transcription factor regulates expression of numerous components of the immune system (Li and Verma, 2002).”
Transcription Factors in Long-Term Memory and Synaptic Plasticity (2009, unknown): “A critical function of NF B was first found in the immune system, where NF B-dependent gene expression is critical during inflammation and host defense (141).”
oPOSSUM: identification of over-represented transcription factor binding sites in co-expressed genes (2005, background): “The NF-kB/Rel family of TFs, which includes RELA (p65), NF-kB1 (p50, p105), NF-kB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response (27).”
NF-kappaB Signaling Pathways in Neurological Inflammation: A Mini Review (2015, background): “NF-κB exerts effects on almost all cell types in the body, playing an important function in inflammation, immune responses, cell cycle, and cell survival (Sen and Baltimore, 1986; Li and Verma, 2002; Kaltschmidt et al., 2005; Mattson, 2005; Ledoux and Perkins, 2014).”