NTRK2 activates RAC1

DOCK3-mediated activation of RAC1 downstream of BDNF-induced signaling by NTRK2 (TRKB) plays a role in axonal growth and regeneration. DOCK3 can be recruited to the plasma membrane to activate RAC1 by binding to NTRK-associated FYN (Namekata et al. 2010). Alternatively, DOCK3 can, upon poorly elucidated RHOG activation by the BDNF:NTRK2 complex, bind to the RHOG:GTP complex and activate RAC1 in an ELMO1-dependent manner (Namekata et al. 2012).

DOCK3介导的RAC1在BDNF诱导的NTRK2（TRKB）信号通路下游的激活在轴突生长和再生中发挥着作用。DOCK3可通过与NTRK相关联的FYN（Namekata等，2010年）结合，被招募至质膜上激活RAC1。另辟蹊径，在BDNF:NTRK2复合物对RHOG的复杂激活机制尚不明确的情况下，DOCK3能够与RHOG:GTP复合物结合，并在ELMO1依赖性途径中激活RAC1（Namekata等，2012年）。