| First Author | Culmsee C | Year | 2001 |
| Journal | Brain Res Mol Brain Res | Volume | 87 |
| Issue | 2 | Pages | 257-62 |
| PubMed ID | 11245929 | Mgi Jnum | J:109293 |
| Mgi Id | MGI:3628682 | Doi | 10.1016/s0169-328x(01)00008-0 |
| Citation | Culmsee C, et al. (2001) Hippocampal neurons of mice deficient in DNA-dependent protein kinase exhibit increased vulnerability to DNA damage, oxidative stress and excitotoxicity. Brain Res Mol Brain Res 87(2):257-62 |
| abstractText | DNA damage has been documented in neurodegenerative conditions ranging from Alzheimer's disease to stroke. DNA-dependent protein kinase (DNA-PK) is involved in V(D)J recombination and DNA double strand break repair, and may play a role in cell death induced by DNA damage. We now report that cultured hippocampal neurons from severe combined immunodeficient (scid) mice which lack DNA-PK activity are hypersensitive to apoptosis induced by exposure to topoisomerase inhibitors, amyloid beta peptide (A beta) and glutamate. A similar increased vulnerability of hippocampal CA1 and CA3 neurons was observed in adult scid mice after kainate-induced seizures. Our results suggest that DNA-PK activity is important for neuron survival under conditions that may occur in neurological disorders. |
