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 1
Pancreas-specific truncation of RelA/p65 using a Cre-loxP system. (A) Two identically oriented loxP sites (triangles) flank exons 7 and 10 of the rela gene. loxP_mod, modified loxP site. (B) Recombination of genomic DNA from the pancreata of rela^Δ/Δ mice was detected by Southern blot analysis using a probe external to the 5′ end of the targeting construct. No recombination was detected in the other organs. (C) Deletion of rela (exons 7–10) in the mouse pancreas was demonstrated at the protein level by Western blot of isolated acini from mice with the floxed allele in the presence or absence of Cre as indicated. In contrast to rela^flox/flox mice, rela^Δ/Δ mice display a truncated form of RelA/p65 (Δp65). Pancreas protein extracts (40 μg) were analyzed using antibodies against p50, IκBα, and β-actin (as a loading control). The protein marker (PM) indicates the size of detected protein bands.