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| Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis |
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| Author(s): Li HL, Zhu H, Xu CJ, Yuan JY |
| Source: CELL Volume: 94 Issue: 4 Pages: 491-501 Published: AUG 21 1998 |
| Times Cited: 2,288 References: 43 |
| Abstract: We report here that BID, a BH3 domain-containing proapoptotic Bcl2 family member, is a specific proximal substrate of Casp8 in the Fas apoptotic signaling pathway. While full-length BID is localized in cytosol, truncated BID (tBID) translocates to mitochondria and thus transduces apoptotic signals from cytoplasmic membrane to mitochondria, tBID induces first the clustering of mitochondria around the nuclei and release of cytochrome c independent of caspase activity, and then the loss of mitochondrial membrane potential, cell shrinkage, and nuclear condensation in a caspase-dependent fashion. Coexpression of Bclx(L) inhibits all the apoptotic changes induced by tBID. Our results indicate that BID is a mediator of mitochondrial damage induced by Casp8. |
| Document Type: Article |
| Language: English |
| Reprint Address: Yuan, JY (reprint author), Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA |
Addresses:
1. Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA |
| Publisher: CELL PRESS, 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 USA |
| Subject Category: Biochemistry & Molecular Biology; Cell Biology |
| IDS Number: 113GB |
| ISSN: 0092-8674 |
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| | | | | | | | | Record from Web of Science® | | | | | | | | | |