A central role for Bid in granzyme B-induced apoptosis
| Autor: | Michelle E Wowk, Kylie A. Browne, Christopher J.P. Clarke, Phillip I. Bird, Vivien R. Sutton, Karin A Sedelies, Jane Oliaro, Joseph A. Trapani, Ricky W. Johnstone, Nigel J. Waterhouse, Ralph K. Lindemann, Andrea Newbold |
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| Rok vydání: | 2004 |
| Předmět: |
Chromium
Programmed cell death Lymphoma B-Cell Time Factors Apoptosis Bone Marrow Cells Biochemistry Granzymes Membrane Potentials Mice medicine Cytotoxic T cell Animals Lymphocytes neoplasms Molecular Biology B cell Caspase Cells Cultured Cell Proliferation biology Cell Death Dose-Response Relationship Drug Chemistry Cell growth Serine Endopeptidases Cytochromes c Cell Biology Dendrites Dendritic Cells Intracellular Membranes Fibroblasts Cell biology Mitochondria Granzyme B Mice Inbred C57BL medicine.anatomical_structure Granzyme biology.protein Carrier Proteins BH3 Interacting Domain Death Agonist Protein |
| Zdroj: | The Journal of biological chemistry. 280(6) |
| ISSN: | 0021-9258 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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