Integrating cell-signalling pathways with NF-kappaB and IKK function.

By N. Perkins. Nature reviews. Molecular cell biology, 2007

1,089 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/0ed66c2d2e3b45c48bcfc9fd2593408d94477d05

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Citations in the corpus

The complexity of NF-κB signaling in inflammation and cancer (2013, background): “An alternative pathway of NF-κB activation, also designated as non-canonical pathway [34] (Figure 2B) originates from different classes of receptors including B-cell activation factor (BAFFR), lymphotoxin β-receptor (LTβR), CD40, receptor activator for nuclear factor kappa B (RANK), TNFR2 and Fn14 [”
Zinc in Infection and Inflammation (2017, background): “Activation of NF-κB requires the phosphorylation of IκBs by IκB kinase (IKK) complex, which degrades the IκB and releases NF-κB and allows it to translocate freely to the nucleus so it can induce targeted gene expression [34, 33].”
Marine omega-3 fatty acids and inflammatory processes: Effects, mechanisms and clinical relevance. (2015, background): “This allows translocation of the remaining NFκB dimer to the nucleus where it binds to response elements and upregulates gene expression [133].”
Mechanisms of action of (n-3) fatty acids. (2012, background): “IkB is then degraded, while the remaining NFkB dimer translocates to the nucleus (45).”
TBK-1 promotes autophagy-mediated antimicrobial defense by controlling autophagosome maturation (2012, unknown): “TBK-1 is a member of the IKK family of kinases that are well recognized as regulators of innate immunity (Perkins, 2007).”
Omega-3 Fatty Acids and Inflammatory Processes (2010, background): “NFB is activated as a result of a signalling cascade triggered by extracellular inflammatory stimuli and involving phosphorylation of an inhibitory subunit (inhibitory subunit of NFB (IB)) which then allows translocation of the remaining NFB dimer to the nucleus [78].”
p38MAPK is a novel DNA damage response‐independent regulator of the senescence‐associated secretory phenotype (2011, background): “Both p38MAPK and ATM are required for NF-kB activity at senescence, and NF-kB requires simultaneous phosphorylation on multiple sites for its activity (Karin, 2006; Perkins, 2007).”
Polyunsaturated fatty acids and inflammatory processes: New twists in an old tale. (2009, background): “NF-kB is activated as a result of a signalling cascade triggered by extracellular inflammatory stimuli and involving phosphorylation of an inhibitory subunit (inhibitory subunit of NF-kB (IkB)) which then allows translocation of the remaining NF-kB dimer to the nucleus [43–45].”
Off the beaten pathway: the complex cross talk between Notch and NF-κB (2008, background): “(3) Atypical or IKK-independent pathways, activated by stimuli such as hypoxia, oxidizing radicals, or UV radiation, which involve either Tyr phosphorylation of IkBa on Tyr 42 or Ser/Thr phosphorylation in its C-terminal PEST domain, leading to IkBa ubiquitination and degradation.(30)”
Oxidative Stress and Antioxidant Defense (2012, background): “Phosphorylation of IkB frees NF-kB and allows it to enter the nucleus to activate gene transcription.(139) A number of kinases have been reported to phosphorylate IkBs at the serine residues.”
NF‐κB and the link between inflammation and cancer (2012, background): “Furthermore, NF-jB modulates both the p53 and JNK signaling pathways in response to different stimuli in positive and negative manners (141, 142).”