| First Author | Waterhouse NJ | Year | 2005 |
| Journal | J Biol Chem | Volume | 280 |
| Issue | 6 | Pages | 4476-82 |
| PubMed ID | 15574417 | Mgi Jnum | J:96908 |
| Mgi Id | MGI:3573841 | Doi | 10.1074/jbc.M410985200 |
| Citation | Waterhouse NJ, et al. (2005) A central role for Bid in granzyme B-induced apoptosis. J Biol Chem 280(6):4476-82 |
| abstractText | Granzyme B, a protease released from cytotoxic lymphocytes, has been proposed to induce target cell death by cleaving and activating the pro-apoptotic Bcl-2 family member Bid. It has also been proposed that granzyme B can induce target cell death by activating caspases directly, by cleaving caspase substrates, and/or by cleaving several non-caspase substrates. The relative importance of Bid in granzyme B-induced cell death has therefore remained unclear. Here we report that cells isolated from various tissues of Bid-deficient mice were resistant to granzyme B-induced cell death. Consistent with the proposed role of Bid in regulating mitochondrial outer membrane permeabilization, cytochrome c remained in the mitochondria of Bid-deficient cells treated with granzyme B. Unlike wild type cells, Bid-deficient cells survived and were then able to proliferate normally, demonstrating the critical role for Bid in mediating granzyme B-induced apoptosis. |
