Research Paper Volume 12, Issue 10 pp 9726—9744
NF2 deficiency accelerates neointima hyperplasia following vascular injury via promoting YAP-TEAD1 interaction in vascular smooth muscle cells
Figure 7. The hypothesis of NF2/YAP/TEAD1 signaling axis in VSMC after PDGF-BB stimuli. PDGF-BB excretion after vascular injury induces nuclear NF2 phosphorylation, thereby causing inactivation of NF2. Decreased active NF2 led to dephosphorylation of YAP and subsequent nuclear translocation of YAP. Increased nuclear YAP binds to TEAD1 and positively regulates relative target gene expression.