GTP-bound RAC contributes to JNK activation

Ras-related C3 botulinum toxin substrate 1 (RAC1) activation was described as essential for p75NTR to induce MAPK8 (aka JNK) and apoptosis in cortical oligodendrocytes (Bazenet et al. 1998). The simultaneous activation of TRKA counteracts the apoptotic action of p75, by modulating the kinetics of p75-mediated RAC activation.

Ras相关C3肉毒杆菌毒素底物1（RAC1）的激活被描述为p75NTR诱导皮质少突胶质细胞中MAPK8（亦称JNK）及细胞凋亡的必要条件（Bazenet等，1998年）。TRKA的同时激活通过调节p75介导的RAC激活的动力学，抵消了p75的细胞凋亡作用。