| First Author | Kumar V | Year | 2018 |
| Journal | BMC Neurosci | Volume | 19 |
| Issue | 1 | Pages | 76 |
| PubMed ID | 30497386 | Mgi Jnum | J:318555 |
| Mgi Id | MGI:6860128 | Doi | 10.1186/s12868-018-0479-z |
| Citation | Kumar V, et al. (2018) PKCepsilon phosphorylation regulates the mitochondrial translocation of ATF2 in ischemia-induced neurodegeneration. BMC Neurosci 19(1):76 |
| abstractText | 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 (PKCepsilon) 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 PKCepsilon-ATF2 signaling in neurodegeneration. RESULTS: Phosphorylation of ATF2 at Thr-52 was reduced in the hippocampus of PKCepsilon null mice, suggesting that ATF2 is a phosphorylation substrate of PKCepsilon. PKCepsilon 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 PKCepsilon regulates phosphorylation and nuclear sequestration of ATF2 in hippocampal neurons during ischemia-induced neurodegeneration. |
