PKCε phosphorylation regulates the mitochondrial translocation of ATF2 in ischemia-induced neurodegeneration.

BACKGROUND:Global cerebral ischemia triggers neurodegeneration in the hippocampal CA1 region, but the mechanism of neuronal death remains elusive. The epsilon isoform of protein kinase C has recently been identified as a master switch that controls the nucleocytoplasmic trafficking of ATF2 and the survival of melanoma cells. It is of interest to assess the role of signaling in neurodegeneration. RESULTS:Phosphorylation of ATF2 at Thr-52 was reduced in the hippocampus of null mice, suggesting that ATF2 is a phosphorylation substrate of duanyu1531ε protein concentrations were significantly reduced 4, 24, 48 and 72 h after transient global cerebral ischemia, resulting in translocation of nuclear ATF2 to the mitochondria. Degenerating neurons staining positively with Fluoro-Jade C exhibited cytoplasmic ATF2. CONCLUSIONS:Our results support the hypothesis that duanyu1531ε regulates phosphorylation and nuclear sequestration of ATF2 in hippocampal neurons during ischemia-induced neurodegeneration.

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