Pancreas-specific RelA/p65 truncation increases susceptibility of acini to inflammation-associated cell death following cerulein pancreatitis
J. Clin. Invest. Hana Algül, et al. 117:1490 doi:10.1172/JCI29882 [Go to this article.]

Figure 2
Inhibition of nuclear translocation of RelA/p65 in the pancreas following cerulein stimulation. (A) rela^flox/flox and rela^Δ/Δ mice were injected i.p. with 50 μg/kg cerulein at hourly intervals. Pancreatic nuclear protein extracts (10 μg) at the indicated time points were subjected to gel retardation assays with an NF-κB consensus probe. (B) Kinetics of IκBα degradation in rela^flox/flox and rela^Δ/Δ mice were assessed by Western blot analyzing the protein content of 40 μg of pancreatic whole-cell protein lysates using an antibody against IκBα. Phosphorylated IκBα (p-IκBα; Ser32) was monitored by Western blotting using a phosphospecific antibody.