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1.  Inhibiting caspase-3 activity blocks beta-catenin degradation after focal ischemia in rat 
Neuroreport  2008;19(8):821-824.
Beta-catenin can be cleaved by caspase-3 or degraded by activated glycogen synthase kinase-3β via phosphorylating β-catenin. We tested the hypothesis that β-catenin undergoes degradation after stroke, and its degradation is dependent on caspase activity. Stroke was generated by permanent middle cerebral artery occlusion and 1h of transient bilateral common carotid artery occlusion in rats. Active caspase-3 was expressed in the ischemic cortex from 5 to 48 h after stroke, whereas β-catenin markedly degraded at 24 and 48 h after stroke. The caspase 3-specific inhibitor, Z-DQMD-FMK, attenuated β-catenin degradation, but it did not affect phosphorylation of both β-catenin and glycogen synthase kinase-3β. In conclusion, β-catenin degraded after stroke, and its degradation was caspase-3 dependent.
doi:10.1097/WNR.0b013e3282ffda72
PMCID: PMC2744604  PMID: 18463494
β-catenin; caspase-3; focal ischemia; glycogen synthase kinase-3β; stroke

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