Impaired regulation of NF-κB and increased susceptibility to colitis-associated tumorigenesis in CYLD-deficient mice
J. Clin. Invest. Jun Zhang, et al. 116:3042 doi:10.1172/JCI28746 [Go to this article.]

Figure 2
CYLD is a negative regulator of NF-κB activation in B and T cells. (A) Cellular extracts prepared from splenic B cells stimulated with anti-IgM (10 μg/ml) or CD40 agonist Ab (1 μg/ml) were analyzed by EMSA for NF-κB binding. (B) Cellular extracts prepared from splenic T cells and stimulated with anti-CD3 were analyzed by EMSA for NF-κB binding. Quantification of NF-κB activity in A and B is represented as fold change compared with unstimulated cells (set at 1.0). Ub, ubiquitin. (C) Following T cell stimulation with anti-CD3, NEMO ubiquitination was analyzed by immunoprecipitation of the proteins from denatured cellular lysates followed by immunoblotting with an anti-ubiquitin Ab. NEMO-(Ub)n, polyubiquitinylated NEMO; ns, nonspecific; SP1, specificity protein 1.