Missing pieces in the NF-kappaB puzzle.

By S. Ghosh, M. Karin. Cell, 2002

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CYLD is a deubiquitinating enzyme that negatively regulates NF-κB activation by TNFR family members (2003, background): “Activation of NF-κB by cytokines depends on the activity of the IκB kinase (IKK) complex, which mediates phosphorylation of the NF-κB inhibitor Iκ”
Is NF-κB a good target for cancer therapy? Hopes and pitfalls (2009, neutral): “RELA–p50 dimers are subsequently released and translocate to the nucleus where they activate the transcription of various target gene”
Curcumin: A review of anti-cancer properties and therapeutic activity in head and neck squamous cell carcinoma (2011, background): “NF- B is a heterodimeric protein composed of five subunits: RelA (p65), RelB, c-Rel, NF- B1 (p50 and p105) and NF- B2 (p52) [68].”
Innate immunity gone awry: linking microbial infections to chronic inflammation and cancer. (2006, background): “…upon receptor engagement, activate several effector pathways, the most important of which include mitogen-activated protein kinases (MAPK), especially JNK (Karin and Gallagher, 2005) and p38 MAPK (Zarubin and Han, 2005), as well as IkB kinases (IKK) and their relatives (Ghosh and Karin, 2002).”
Current Understanding of RANK Signaling in Osteoclast Differentiation and Maturation (2017, neutral): “ubiquitination to achieve optimal activation (Duran et al., 2004; Ghosh and Karin, 2002; Mizukami et al., 2002).”