Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 98, Issue 26, Pages 14985-14990Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.261581498
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Funding
- NCI NIH HHS [R01 CA050239, CA50239, R37 CA050239] Funding Source: Medline
- NHLBI NIH HHS [T32 HL007088, T32 HL07088] Funding Source: Medline
- NIDDK NIH HHS [R01 DK049786, DK49786] Funding Source: Medline
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Granzyme B (GzmB) is a serine protease that is used by activated cytoltoxic T lymphocytes to induce target cell apoptosis. Although GzmB directly cleaves the Bcl2 family member BID on target cell entry, Bid-deficient (and Bax, Bak doubly deficient) cells are susceptible to GzmB-induced death, even though they fail to release cytochrome c from mitochondria. GzmB still induces mitochondrial depolarization in Bax, Bak double knockout cells without cytochrome c release or opening of the permeability transition pore. Because GzmB cannot directly cause depolarization of isolated mitochondria, novel intracellular factor(s) may be required for GzmB to depolarize mitochondria in situ. GzmB therefore utilizes two distinct mitochondrial pathways to amplify the proapoptotic signal that it delivers to target cells.
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