Model for BAZF-containing, CUL3-based E3 ligase complex as a silencer of Notch signaling for angiogenic quiescence-to-sprouting transition. (A) Degradation of CBF1 leads to silencing Notch signal and supports angiogenic sprouting. Notch signaling maintains angiogenic quiescence. Notch1 signaling is transmitted via N1ICD to CBF1. CBF1-N1ICD recruits coactivators for expression of anti-angiogenic genes. (B) BAZF-containing, CUL3-based E3 ligase complex induces CBF1 polyubiquitination. VEGF-A induces BAZF expression, and make a complex with CUL3 and CBF1 for CBF1 polyubiquitination. BAZF binding to CBF1 does not compete with N1ICD binding. However, in this step it is still unclear whether BAZF coexists with N1ICD on CBF1. (C) Degradation of polyubiquitinated CBF1. Polyubiquitinated CBF1 is released from DNA, and is degraded by proteasomes. Degradation of CBF1 leads to silencing Notch signal and supports angiogenic sprouting.