Figure 1: Increased GluK2 levels in brain tissues from the PARK2 mouse model parkin-Q311X and from patients with PARK2 mutations.
From: Parkin regulates kainate receptors by interacting with the GluK2 subunit
(a) Western blottings of glutamate receptor subunits in substantia nigra lysates from controls (n=7) and littermate parkin-Q311X mice (n=6). All mice were 3 to 4 weeks old. Samples were run in parallel gels, each gel contained wt and parkin-Q311X samples. Western blottings were blotted and developed contemporaneously. Results derive from three independent experiments. The densitometer analysis shows that GluK2 protein is significantly increased in parkin-Q311X mice as compared with littermate controls (unpaired t-test, **P=0.0010, t=4.424). No statistically significant differences were found for the other AMPA, NMDA and KAR subunits analysed (unpaired t-test, P>0.05). No GluK1 and GluN1 expression was detectable. Error bars indicate±s.e.m. (b) Western blottings for glutamate receptor subunits in frontal cortex brain lysates from control subjects (n=5) and PARK2 patients (n=4). No GluK1 expression was detectable. Results derive from three independent experiments. The densitometer analysis shows that GluK2 protein is significantly increased in brain tissues from patients with PARK2 mutations (unpaired t-test; ***P=0.0002; t=7.259) and that GluA1 decreases in brain tissues from patients with PARK2 mutations (unpaired t-test; ***P=0.0001; t=7.826). Error bars indicate±s.e.m.
