Fig. 7: Silencing of PRPF40B elicits defects in proliferation and early neurogenesis in vivo. | Cell Death & Disease

Fig. 7: Silencing of PRPF40B elicits defects in proliferation and early neurogenesis in vivo.

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

Fig. 7: Silencing of PRPF40B elicits defects in proliferation and early neurogenesis in vivo.

A Schematic representation of mouse development depicting early and cortical neurogenesis stages at E10.5, E14.5, and E17.5. B Left: Images of WT and Prpf40b⁻/⁻ embryos at E10.5. The dotted line indicates the dissected region used for subsequent analysis. Right: Western blot analysis of Ki-67, TRKB-FL, TRKB-T1, and synaptophysin in WT and Prpf40b⁻/⁻ embryos at E10.5. C Left: Images of WT and Prpf40b⁻/⁻ embryos at E14.5. The dotted line indicates the dissected region used for analysis. Right: Western blot analysis of Ki-67, TRKB-FL, TRKB-T1, and synaptophysin in WT and Prpf40b⁻/⁻ embryos at E14.5. The arrow indicates the position of a cross-reacting protein. D Relative mRNA expression levels of TRKB-FL and TRKB-T1, normalized to total TRKB, in E10.5 and E14.5 embryos. Data represent the mean ± SEM using three (E10.5) and four (E14.5) biological replicates. Statistical significance: p ≤ 0.05.

Back to article page