Fig. 3: ELK1 inhibited the SYVN1-mediated ubiquitination and degradation of PS1.

a Coimmunoprecipitation (Co-IP) of endogenous PS1 and SYVN1 in N2A^APP cells was performed using antibodies to PS1 and SYVN1 (n = 3 in each group). b Co-IP of exogenous PS1 and SYVN1 in HEK293 cells cotransfected with PS1-Flag and SYVN1-HA was performed using antibodies to Flag and HA (n = 3–4 in each group). c The HEK293 cells were transfected with or without SYVN1, followed by exposure to CHX (100 μg ml⁻¹) for the indicated time. PS1 was determined by western blot (WB) to evaluate its degradation (n = 4 in each group). *P < 0.05, determined by two-way ANOVA. d PS1-Flag and Ub-HA, along with or without SYVN1, were transfected to HEK293 cells. PS1 ubiquitination was evaluated by Co-IP as described above (n = 3 in each group). e WB of PS1 in N2A^APP cells treated with different concentrations of LS-102 (n = 7 in each group). *P < 0.05 and ***P < 0.001, determined by one-way ANOVA. f ELK1 or sh_ELK1 plasmid was transfected to 2EB2 cells. SYVN1 was determined by WB 48 h later (n = 4 in each group). *P < 0.05, determined by one-way ANOVA. g Co-IP of exogenous PS1 and ELK1 in HEK293 cells cotransfected with PS1-Flag and ELK1-HA was performed using antibodies to Flag and HA (n = 3 in each group). h PS1-Flag and SYVN1-HA, along with or without ELK1, were transfected to the HEK293 cells. Co-IP of exogenous PS1 and SYVN1 was performed as described above (n = 3–4 in each group). i PS1-Flag, Ub-HA and SYVN1, along with or without ELK1, were transfected to HEK293 cells. PS1 ubiquitination was evaluated by Co-IP as described above (n = 3 in each group). j WB of ELK1 and PS1 in N2A^APP cells transfected with sh_ELK1, along with or without LS-102 treatment (1 μM for 48 h) (n = 4 in each group). **P < 0.01 and ***P < 0.001, determined by one-way ANOVA. ns, not significant.