Fig. 5.
Fig. 5. NF-κB and cellular stress–induced apoptosis. / NF-κB activity is required for the induction of more than 150 genes involved in cell growth, differentiation, development, apoptosis, and adaptive responses to changes in cellular redox balance. NF-κB is bound by IκB, which prevents NF-κB activity. NF-κB target genes with antiapoptotic function include the IAP family, TRAF1 and TRAF2, thought to suppress caspase-8 activation, the prosurvival Bcl-2 homologs Bfl1/A1 and Bcl-XL, and nitrous oxide synthase–inducible genes. The apoptotic signaling of NF-κB may be due to the promoter activation of death receptors and ligands such as CD95, CD95-L, TNF-α, and the TRAIL receptors DR4 and DR5.

NF-κB and cellular stress–induced apoptosis.

NF-κB activity is required for the induction of more than 150 genes involved in cell growth, differentiation, development, apoptosis, and adaptive responses to changes in cellular redox balance. NF-κB is bound by IκB, which prevents NF-κB activity. NF-κB target genes with antiapoptotic function include the IAP family, TRAF1 and TRAF2, thought to suppress caspase-8 activation, the prosurvival Bcl-2 homologs Bfl1/A1 and Bcl-XL, and nitrous oxide synthase–inducible genes. The apoptotic signaling of NF-κB may be due to the promoter activation of death receptors and ligands such as CD95, CD95-L, TNF-α, and the TRAIL receptors DR4 and DR5.

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