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Fig. 3 | Molecular Neurodegeneration

Fig. 3

From: Modifying Rap1-signalling by targeting Pde6δ is neuroprotective in models of Alzheimer’s disease

Fig. 3

REM reduces toxicity and [Ca2+]i by selectively abrogating the interaction of Rap1 with Pde6δ. a Affinity purification coupled with mass spectrometry assay to identify interactors associating with Pde6δ in a REM dependent fashion. Signals for each interactor were normalised to the vehicle condition (n = 3; Treatment: P = 0.01; DF = 1; F (1, 32)=7.508; Rap1A: P < 0.0001; t = 5.284; DF = 32). b Left, the impact of genetic silencing of RAP1A in the toxicity assay in function of increasing concentrations REM (n = 6). Box at the right, efficiency of silencing validated by Western analysis (representative immunoblots; immunostaining of GAPDH was determined as a loading control; Rap1A expression was reduced on average by 66% ± 8%; Average ± SEM). (One-way ANOVA (REM treatment); siNC: P = 0.0004; F = 4.615; DF = 8; siRAP1A: n.s.). c Concentration-response curve of deltarasin in the toxicity assay (EC50 = 480 nM; n = 3). d The impact of genetic silencing of PDE6δ or RAP1A in the neuroblastoma cells on cytosolic Ca2+ levels in the toxicity assay in function of increasing REM concentrations (n = 2 per concentration; one representative experiment of three is shown)

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