Priority Research Paper Volume 12, Issue 6 pp 4688—4710

ATM is a key driver of NF-κB-dependent DNA-damage-induced senescence, stem cell dysfunction and aging

Figure 7. ATM and NF-κB activation are downregulated in Ercc1-/Δ mice heterozygous for Atm. (A) Livers were collected at 12 weeks of age from WT, Ercc1-/Δ and Ercc1-/ΔAtm+/- mic (n=3 per genotype) and lysates analyzed by western blot for activation of ATM and its downstream effectors. (B) Same liver lysates were used to measure phosphorylation of p65 and IκBα. (C) Western blot analysis of livers from 16-week-old WT, Ercc1-/Δ and Ercc1-/ΔAtm+/-mice (n=3 per genotype) probed for activation of ATM. GAPDH was used as a loading control. (D) Same liver lysates used to measure activation of NF-κB. (E) Fourteen-week-old livers from Ercc1-/Δ and Ercc1-/Δp65+/- mice (n=3 per genotype) were analyzed by western blot for activation of ATM (F) and NF-κB.