| First Author | Fujita E | Year | 2001 |
| Journal | Cell Death Differ | Volume | 8 |
| Issue | 4 | Pages | 335-44 |
| PubMed ID | 11550085 | Mgi Jnum | J:115634 |
| Mgi Id | MGI:3692014 | Doi | 10.1038/sj.cdd.4400824 |
| Citation | Fujita E, et al. (2001) Caspase-9 processing by caspase-3 via a feedback amplification loop in vivo. Cell Death Differ 8(4):335-44 |
| abstractText | In contrast to the autoprocessing of caspase-9, little is known about the biological significance of caspase-9 processing by caspase-3 via a feedback loop in vivo. We prepared antisera against mouse caspase-9 cleavage sites so that only the activated form of mouse caspase-9 was recognized. Using these antisera and caspase-9- and caspase-3-deficient mouse embryonic fibroblasts, we demonstrated that mouse caspase-9 is initially autoprocessed at D(353) and D(368) at low levels during staurosporine-induced apoptosis, whereupon the D(368) and D(168) sites are preferentially processed over D(353) by activated caspase-3 as part of a feedback amplification loop. Ac-DEVD-MCA (caspase-3-like) and Ac-LEHD-MCA (caspase-9-like) cleavage activities clearly showed that caspase-9 autoprocessing was necessary for the activation of caspase-3, whereas full activation of caspase-3 and caspase-9 was achieved only through the feedback amplification loop. This feedback amplification loop also played a predominant role during programmed cell death of dorsal root ganglia neurons at mouse embryonic day 11.5. |
