| First Author | Urase K | Year | 1999 |
| Journal | Brain Res Dev Brain Res | Volume | 116 |
| Issue | 1 | Pages | 69-78 |
| PubMed ID | 10446348 | Mgi Jnum | J:56748 |
| Mgi Id | MGI:1342378 | Doi | 10.1016/s0165-3806(99)00076-0 |
| Citation | Urase K, et al. (1999) Bcl-xL is a negative regulator of caspase-3 activation in immature neurons during development. Brain Res Dev Brain Res 116(1):69-78 |
| abstractText | Caspases and Bcl-xL, the mammalian homologues of the Caenorhabditis elegans (C. elegans) ced-3 and ced-9 genes, respectively, regulate apoptosis of various cells. Caspase-3 is processed into an active form (p20 or p17 and p12) during apoptosis. We investigated the relation between caspase-3 and Bcl-xL during development by examining activation of caspase-3 and apoptotic cells in Bcl-x-deficient (bcl-x(-/-)) mice at embryonic (E) day 11.5. We used a double-staining technique with a cleavage site-directed antibody against caspase-3 (anti-p20/17) and terminal-deoxytransferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL). Bcl-xL-deficiency increased both numbers of p20/17-positive and -negative apoptotic cells in dorsal root ganglia (DRG); the numbers of p20/17-positive apoptotic cells in the caudal parts of the ventral hindbrain and ventral spinal cord; and the numbers of p20/17-negative apoptotic cells in the dorsal midbrain, dorsal hindbrain, and dorsal spinal cord. Thus, Bcl-xL blocks the caspase-3-dependent apoptotic pathway in the restricted regions of the nervous system during development. Furthermore, these observations suggest that Bcl-xL protects against activation of the caspase-3-independent apoptotic pathway. Other caspases or apoptotic mechanisms may also be activated in the nervous systems of bcl-x(-/-) mice. Copyright 1999 Elsevier Science B.V. |
