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. 2009 Nov 25;29(47):14779–14789. doi: 10.1523/JNEUROSCI.4161-09.2009

Figure 1.

Figure 1.

The activity and protein levels of the CK2 subunits are changed in oxidative stress-induced neuronal cell death. Brain lysates were obtained from the cerebral cortex and striatum of mouse brains 1, 3, 6, 12, 24, and 48 h after ischemia and reperfusion. A, Samples from shams or from mice 24 h after ischemia and reperfusion used to measure relative CK2 activity (#p < 0.05; n = 8 per group). B, Western blot was performed with antibodies against CK2α, CK2α′, CK2β, and β-tubulin (used as a loading control). C, A graph showing the changes in the CK2α subunit after ischemia/reperfusion. D, A graph showing the changes in the CK2α′ subunit after ischemia/reperfusion. E, A graph showing the changes in the CK2β subunit after ischemia/reperfusion compared with sham controls (n = 4 per each time course). F, Primary cortical neurons underwent OGD for 4 h and were allowed 24 h of reoxygenation. Samples were obtained 24 h after reoxygenation. Western blot was performed with antibodies against CK2α, CK2α′, CK2β, and β-tubulin. G, Summary graph showing the changes in the CK2 subunits (#p < 0.05 compared with controls; n = 4). I/R, Ischemic reperfusion; S, sham; O.D., optical density; Con, control; R, reoxygenation. Error bars indicate SEM.