| First Author | Selimi F | Year | 2000 |
| Journal | C R Acad Sci III | Volume | 323 |
| Issue | 11 | Pages | 967-73 |
| PubMed ID | 11144029 | Mgi Jnum | J:298287 |
| Mgi Id | MGI:6479493 | Doi | 10.1016/s0764-4469(00)01243-9 |
| Citation | Selimi F, et al. (2000) Bax and p53 are differentially involved in the regulation of caspase-3 expression and activation during neurodegeneration in Lurcher mice. C R Acad Sci III 323(11):967-73 |
| abstractText | Intrinsic Purkinje cell death in heterozygous Lurcher (Grid2Lc/+) mice is accompanied by the target-related death of granule cells and olivary neurons. The expression of pro-caspase-3 is increased in Grid2Lc/+ Purkinje cells and activated caspase-3 is detected in all three cell types before their death. Bax inactivation in Grid2Lc/+ mutants rescues granule cells but not Purkinje cells. Here, we show that, while Bax inactivation inhibits caspase-3 activation in both cell types, p53 inactivation does not affect caspase-3 activation and neuronal loss in Grid2Lc/+ mice. The up-regulation of pro-caspase-3 in Grid2Lc/+ Purkinje cells is Bax and p53 independent. These results suggest that Grid2Lc/+ granule cell death is dependent on Bax and caspase-3 activation, whereas several pathways can mediate Grid2Lc/+ Purkinje cell death. |
