Defective Lymphotoxin-β Receptor-Induced NF-κB Transcriptional Activity in NIK-Deficient Mice

By L. Yin, Lin Wu, H. Wesche, C. Arthur, J. White, D. Goeddel, Robert Schreiber. Science, 2001

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Transient and Selective NF-κB p65 Serine 536 Phosphorylation Induced by T Cell Costimulation Is Mediated by IκB Kinase β and Controls the Kinetics of p65 Nuclear Import 1 (2004, background): “mice show normal induction of DNA-binding, but a defective induction of NF- B target genes in response to LT (22).”
30 years of NF-κB: a blossoming of relevance to human pathobiology (2017, positive): “The phenotype of patients was different from the NIK knockout mouse because it lacked the severe structural defects in lymph nodes, Peyer’s patches, splenic and thymic structures found in the latter (Yin et al., 2001).”
TAK1 is a ubiquitin-dependent kinase of MKK and IKK (2001, background): “; however, genetic studies have shown that NIK is not involved in IKK activation by most stimuli, including IL-1&beta”
Tetrameric Oligomerization of IκB Kinase γ (IKKγ) Is Obligatory for IKK Complex Activity and NF-κB Activation (2003, background): “Furthermore, none of the MAP3K-like kinases which regulate IKK upon overexpression, such as NIK, MEKK1, and Cot/Tpl-2 (11), have been confirmed as physiological, proinflammatory IKK activators by genetic evidence (9, 37, 42 , 43).”