Research Paper Volume 16, Issue 2 pp 1182—1191
Myeloid-specific knockout of Notch-1 inhibits MyD88- and TRIF-mediated TLR signaling pathways by regulating oxidative stress-SHP2 axis, thus restraining aneurysm progression
Figure 5. Notch-1 deficiency inhibited the activation of MyD88/TRIF/NF-κB signals. (A) Macrophages’ deficiency of Notch-1 inhibited the phosphorylated-MyD88, TRIF, and NF-κB and there statistical data; (B) Notch-1 cKO decreased the expression of IFN-γ, IL-1β, TNF-α expression in AAA tested by western blot. N = 6, *P < 0.05, **P < 0.01, apoE-KO/Notch-1MAC-KO group vs. apoE-KO/Notch-1WT group.