Deletion of IKK2 in hepatocytes does not sensitize these cells to TNF-induced apoptosis but protects from ischemia/reperfusion injury
J. Clin. Invest. Tom Luedde, et al. 115:849 doi:10.1172/JCI23493 [Go to this article.]

Figure 1
Conditional knockout of Ikk2 and Nemo in the mouse liver. (A) Deletion in the mouse liver is shown at the DNA level by Southern blot using genomic live DNA from mice with genetic status for the floxed (f) allele and positive (+) or negative (–) cre status as indicated. (B) Deletion in cre-positive floxed Ikk2 mice (Ikk2Δhepa) was verified in comparison to cre-negative control mice (Ikk2^f/f) at the RNA level by semiquantitative RT-PCR using 1 μg of liver RNA and primers for IKK2 and GAPDH. (C) Western blot analysis with antibodies against IKK2 or α-tubulin (for loading control) from 100 μg of whole liver protein extracts from Ikk2Δhepa and Ikk2^f/f mice. (D) Immunohistochemical staining of IKK2 on liver slides from Ikk2Δhepa and Ikk2^f/f mice, showing that in Ikk2Δhepa mice, IKK2 expression is restricted to nonparenchymal liver cells such as bile duct cells (arrows). Original magnification, ×40. (E) For inducible knockout of NEMO, poly I/C was injected into both cre-positive (NemoΔ) mice and cre-negative control mice (Nemo^f/f). Efficiency of deletion in the mouse liver is shown at the RNA level by RT-PCR. (F) Western blot analysis with antibodies against NEMO and α-tubulin in NemoΔ and Nemo^f/f mice. (G) Inducible deletion of Ikk2. Deletion was induced by injection with poly I/C into Mx-cre–positive (Ikk2Δ) mice and Mx-cre–negative control mice (Ikk2^f/f). Efficiency of the deletion in the mouse liver is shown at the RNA level by RT-PCR. (H) Western blot for IKK2 or α-tubulin from Ikk2Δ and Ikk2^f/f mice.