Activated NTRK2 signals through FYN

In mouse brain, Fyn activation downstream of Bdnf-induced Ntrk2 (TrkB) signaling results in increased protein levels of AMPA receptor subunits Gria2 (GluR2), Gria3 (GluR3) and Gria1 (GluR1) without change in mRNA levels (Narisawa-Saito et al. 1999).<p>BDNF-mediated activation of NTRK2 increases phosphorylation of voltage gated sodium channels by FYN, resulting in decrease of sodium currents (Ahn et al. 2007).<p>FYN activation downstream of NTRK2 is implicated in olygodendrocyte myelination and contributes to BDNF-induced activation of ERK1/2 (MAPK3/1) through an unknown mechanism (Peckham et al. 2015).<p>Besides acting downstream of NTRK2, FYN and other SRC kinases, activated by other receptors such as GPCRs, may phosphorylate NTRK2 and enhance its catalytic activity (Rajagopal and Chao 2006, Huang and McNamara 2010).

在鼠脑中，Bdnf诱导的Ntrk2（TrkB）信号通路下游的Fyn激活导致AMPA受体亚基Gria2（GluR2）、Gria3（GluR3）和Gria1（GluR1）的蛋白质水平增加，而mRNA水平保持不变（Narisawa-Saito等，1999年）。<p>BDNF介导的NTRK2激活通过FYN增加电压门控钠通道的磷酸化，导致钠电流减少（Ahn等，2007年）。<p>FYN在NTRK2下游的激活与少突胶质细胞的髓鞘形成有关，并通过一种未知的机制促进BDNF诱导的ERK1/2（MAPK3/1）的激活（Peckham等，2015年）。<p>除了在NTRK2下游发挥作用外，FYN和其他由GPCRs等受体激活的SRC激酶，也可能磷酸化NTRK2并增强其催化活性（Rajagopal和Chao，2006年，Huang和McNamara，2010年）。