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Fig. 4 | Molecular Autism

Fig. 4

From: Targeting the RHOA pathway improves learning and memory in adult Kctd13 and 16p11.2 deletion mouse models

Fig. 4

Detection of RHOA (a, b) and of the phoshorylated form of MLC (P-MLC, c, d) by western blots in heterozygous Kctd13+/− (a, c) and the 16p11.2 Del/+ (b, d) hippocampal lysates and their control (wt) littermate. a The quantification of the western blot (an example is shown below the graph) revealed no changes in RHOA protein levels in the Kctd13+/− (A) or in the 16p11.2 Del/+, b mutant lines compared to their wt littermates. Fasudil treatment did not cause changes in RHOA protein levels in the two mutant lines [non-treated wt (n = 22), treated wt (n = 11), non-treated Kctd13+/− (n = 21) and treated Kctd13+/− (n = 7); and non-treated wt (n = 17), treated wt (n = 8), non-treated Del/+ (n = 11) and treated Del/+ (n = 11)]. However, Kctd13 deficient mice showed an increase in the levels of phosphorylated MLC protein (c) and the loss of a copy of 16p11.2 region caused an increase in the levels of phosphorylated MLC protein (d). The treatment with fasudil reversed this alteration in Kctd13+/− and in the Del/+ mutant line. (*p < 0.05; **p < 0.01)

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