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. Author manuscript; available in PMC: 2021 Jul 3.
Published in final edited form as: Mol Psychiatry. 2020 Jan 3;26(8):3723–3736. doi: 10.1038/s41380-019-0635-6

Fig. 2. Sustained expression of MET disrupts synapse proteins and neuronal growth mechanisms.

Fig. 2.

a. VC proteins were harvested at P25–28 in ctg+;tTA+ mice with sustained Metctg from P14 and control littermates. Representative blots showed decreased GluA1, GluN2A and increased GluB2B proteins. b. Among many synaptic proteins detected, sustained Metctg decreased Homer1 and vGlut1. c. Metctg leads to persistent activation of small GTPases cdc42 and rac1, and enhanced phosphorylation of PAK1/2 (T423/402), LIMK1 (T508), and cofilin (Ser 3). d. Decreased GluA1 and vGlut1 levels were verified using immunohistochemistry staining and confocal imaging. e-g. Quantification of Western blot (a-d) protein band intensity from 4–6 independent experiments. * p < 0.05, ** p < 0.01 (increase); # p < 0.05, ## p < 0.01 (decrease). cdc42-GTP, rac1-GTP and p-cofilin were normalized to cdc42, rac1 and cofilin, respectively, and expressed as percent of control levels.