Targeted ablation of IKK2 improves skeletal muscle strength, maintains mass, and promotes regeneration
J. Clin. Invest. Foteini Mourkioti, et al. 116:2945 doi:10.1172/JCI28721 [Go to this article.]

Figure 1
Comparison of NF-κB activation in Ikk2^f/f and Ikk2^mko muscles. (A) Deletion of the floxed alleles only in Ikk2^mko skeletal muscles as shown by Southern blot analysis on genomic DNA isolated from different tissues. (B) Decreased expression of IKK2 in different Ikk2^mko muscles, shown by immunoblotting of total muscle extracts. The other subunits, IKK1 and NEMO, remain intact. (C) Unchanged levels of IKK proteins in other tissues. H, heart; G, gastrocnemius; T, TA; D, diaphragm; S, soleus; B, brain; K, kidney; Sp, spleen; C, control from brain-specific IKK2 deletion. (D) IP in 300 μg of whole-muscle extracts from Ikk2^f/f and Ikk2^mko mice was performed with a polyclonal antibody against NEMO, followed by Western blot (WB) analysis with a monoclonal antibody against IKK1 or IKK2 as indicated. MEF, mouse embryonic fibroblasts. (E) Nuclear translocation of NF-κB was demonstrated by EMSA. (F) Evaluation of IKK activity. Total protein (300 μg) from normal or challenged (injured or denervated) muscles was IP with a NEMO antibody and subjected to a kinase assay using a truncated glutathione S-transferase–IκBa (aa residues 1–54) protein as substrate. DN, denervated; NDN, nondenervated.