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. 2019 Sep 16;9:13381. doi: 10.1038/s41598-019-49821-7

Figure 2.

Figure 2

Stability of the proteins containing aminoacid changes in the VRK1 protein and detected in neuromotor syndromes associated to VRK1 mutations. Each plasmid construct expressing a VRK1 variant protein was transfected in HEK 293T cells and cell lysates were prepared at different time points after cycloheximide (CHX) addition. (a) Western blot of each individual VRK1 pathogenic variant protein. The β-actin is representative. The individual β-actin for each variant are shown in Supplementary Fig. S7. (b) Stability of the VRK1 pathogenic variant proteins representing the mean of three independent experiments for each variant. Stability of the VRK1 mutant proteins follow a polynomial regression. The correlation between different time points and protein level for each individual variant and their fit (R values) by polynomic regression analysis87 are shown in Supplementary Fig. S7. For stable protein variants, their levels do not change with time and therefore there is no correlation.