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The nuclear factor-κB (NF-κB) signalling pathway serves a crucial role in regulating the transcriptional responses of physiological processes that include cell division, cell survival, differentiation, immunity and inflammation. Here we outline studies using mouse models in which the core components of the NF-κB pathway, namely the IκB kinase subunits (IKKα, IKKβ and NEMO), the IκB proteins (IκBα, IκBβ, IκBɛ and Bcl-3) and the five NF-κB transcription factors (NF-κB1, NF-κB2, c-Rel, RelA and RelB), have been genetically manipulated using transgenic and knockout technology.Oncogene (2006) 25, 6781–6799. doi:10.1038/sj.onc.1209944 [ABSTRACT FROM AUTHOR]

The article presents a discussion about the loss of the BH3-only protein Bid. The BH3-only members of the Bcl-2 protein family are considered as important initiators of developmentally programmed cell death and stress-induced apoptosis, by acting as molecular sensors for intracellular stress signals. The BH3-only protein Bid is capable of activating through proteolytic cleavage by caspases or other proteases.

A letter to the editor is presented in response to the article "Bcl-2 transgene expression fails to prevent fatal hepatocyte apoptosis induced by endogenous TNFα in mice lacking RelA" that was published online in February 17, 2006.