Ck2β^−/− mice are protected from ischemic stroke in vivo and display less thrombotic cerebral vascular occlusions with a significantly better neurological outcome and survival after stroke. (A) Representative images of 3 corresponding coronal sections of 2,3,5-triphenyltetrazolium chloride–stained brains from ck2β^fl/fl and ck2β^−/− mice 24 hours after tMCAO (left). Arithmetic means ± standard errors of the mean (n = 11-12) of brain infarct volumes in ck2β^fl/fl (blue bar) and ck2β^−/− mice (gray bar) 24 hours after tMCAO (right). (B) Bederson score reflecting global neurological defects (0 indicates best, 5 indicates worst; left) and grip test indicating motor functional and coordination deficits (0 indicates worst, 5 indicates best; right) assessed 24 hours after tMCAO. Each dot represents 1 individual mouse. (C) Representative coronal T2-weighted magnetic resonance imaging images of hyperintense ischemic brain infarct lesions of ck2β^fl/fl and ck2β^−/− mice at day 1 and day 7 (infarct maturation) after tMCAO (n = 3-7/group). Hypointense areas (reflecting intracerebral hemorrhage) were not observed. (D) Determination of thrombosis index by quantification of thrombotic occluded vs nonoccluded vessels within the ischemic hemisphere 24 hours after tMCAO. Arithmetic means ± standard errors of the means (n = 5, right) and representative images (left) of H&E-stained cryosections are shown. Bar represents 100 μm. (E) Arithmetic means ± standard errors of the means (n = 6) of infarct volume in ck2β^fl/fl and ck2β^−/− mice 7 days after tMCAO (infarct maturation). (F) Analysis of survival of ck2β^fl/fl (blue line) and ck2β^−/− (gray line) mice 7 days after ischemic stroke (n = 13-17). Student t test in panels A-D and log-rank (Mantel-Cox) analysis in panel F. **P < .01.