| First Author | Kerr LE | Year | 2004 |
| Journal | Cell Death Differ | Volume | 11 |
| Issue | 10 | Pages | 1102-11 |
| PubMed ID | 15153940 | Mgi Jnum | J:101696 |
| Mgi Id | MGI:3604831 | Doi | 10.1038/sj.cdd.4401449 |
| Citation | Kerr LE, et al. (2004) Mice overexpressing human caspase 3 appear phenotypically normal but exhibit increased apoptosis and larger lesion volumes in response to transient focal cerebral ischaemia. Cell Death Differ 11(10):1102-11 |
| abstractText | Caspase 3 activation has been implicated in cell death following a number of neurodegenerative insults. To determine whether caspase genes can affect the susceptibility of cells to neurodegeneration, a transgenic mouse line was created, expressing human caspase 3 under control of its own promoter. The human gene was regulated by the murine homeostatic machinery and human procaspase 3 was expressed in the same tissues as mouse caspase 3. These novel transgenic mice appeared phenotypically and developmentally normal and survived in excess of 2 years. Behavioural assessment using the 5-choice serial reaction time task found no differences from wild-type littermates. Caspase activity was found to be tightly regulated under physiological conditions, however, significantly larger lesions were obtained when transgenic mice were subjected to focal cerebral ischaemia/reperfusion injury compared to wild-type littermates. These data demonstrate that mice overexpressing human caspase 3 are essentially normal, however, they have increased susceptibility to degenerative insults. |
