Research Paper Volume 11, Issue 1 pp 127—159

Premature aging and cancer development in transgenic mice lacking functional CYLD


Figure 7. Overactivation of the NF-κB, and other pro-aging pathways, along with increased IL6 and TNF-α expression in the skin of the K5-CYLDC/S mice. (A) p65 and IκBα phosphorylation kinetics in the back skin of 3-day-old Control and transgenic mice treated with TNF-α for the indicated times. (B) WB showing over-activation of the classical NF-κB signaling pathway (P-p65 and P-IκBα) in the skin of 20-month-old transgenic mice. (C) Increased expression of the inflammatory cytokines TNF-α and IL6 in the skin of the K5-CYLDC/S mice. (D-F) WB showing the hyperactivation (phosphorylation) of Akt (D), JNK (E) and c-Myc (F) in the skin of adult K5-CYLDC/S mice. Graphic representations of the densitometric analysis of western blots corresponding to extracts from 5-7 animals of each genotype are shown. Mann-Whitney U test was used for statistical analysis. (*p<0.05; **p<0.01; ***p<0.001).