Fig. 8: A hypothetical model for the role of PRPF40B in BDNF-induced neuronal differentiation. | Cell Death & Disease

Fig. 8: A hypothetical model for the role of PRPF40B in BDNF-induced neuronal differentiation.

From: Regulation of NTRK2 alternative splicing by PRPF40B controls neural differentiation and synaptic plasticity

Fig. 8: A hypothetical model for the role of PRPF40B in BDNF-induced neuronal differentiation.

A In cells with normal PRPF40B expression (SH-SY5Y WT), BDNF interacts with the TRKB-FL receptor, triggering a cascade of signaling events through the MAPK/ERK and PI3K/AKT pathways to activate key genes essential for proper neuronal differentiation, synaptogenesis, and plasticity. B In cells where PRPF40B expression is silenced (SH-SY5Y G2), TRKB-T1 receptor expression is upregulated during differentiation. BDNF binds to TRKB-T1 without activating the classical signaling cascades due to the absence of the kinase domain, thereby reducing BDNF availability for TRKB-FL and impairing differentiation and synaptic maturation.

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