TY - JOUR
T1 - Mitochondrial cell death effectors
AU - Brenner, Dirk
AU - Mak, Tak W.
N1 - Funding Information:
The authors would like to thank Dr. Heiko Blaser and Mailin Brenner for critical reading of this manuscript and Mary Saunders for scientific editing. The authors’ work is funded by the Alexander von Humboldt Foundation, the Terry Fox Cancer Foundation and the Canadian Institutes of Health Research.
PY - 2009/12
Y1 - 2009/12
N2 - Programmed cell death (apoptosis) is crucial for embryogenesis and tissue homeostasis. Deregulated apoptosis leads to immunodeficiency, autoimmune disorders or cancer. The two main routes to apoptosis are the extrinsic and intrinsic (mitochondrial) pathways. Both involve caspase activation that leads to the cleavage of multiple intracellular substrates [1,9]. This review highlights recent advances in our understanding of the intrinsic pathway. We describe how BCL-2-family members preserve or disrupt mitochondrial integrity, the contribution of BH3-only proteins to this process, and the importance of cytotoxic factors released by the mitochondria. The growing evidence that the intrinsic pathway is crucial for tumourigenesis makes this an intriguing field. In particular, the finding that BCL-2 homologues are inhibited by BH3-only proteins may have future therapeutic applications.
AB - Programmed cell death (apoptosis) is crucial for embryogenesis and tissue homeostasis. Deregulated apoptosis leads to immunodeficiency, autoimmune disorders or cancer. The two main routes to apoptosis are the extrinsic and intrinsic (mitochondrial) pathways. Both involve caspase activation that leads to the cleavage of multiple intracellular substrates [1,9]. This review highlights recent advances in our understanding of the intrinsic pathway. We describe how BCL-2-family members preserve or disrupt mitochondrial integrity, the contribution of BH3-only proteins to this process, and the importance of cytotoxic factors released by the mitochondria. The growing evidence that the intrinsic pathway is crucial for tumourigenesis makes this an intriguing field. In particular, the finding that BCL-2 homologues are inhibited by BH3-only proteins may have future therapeutic applications.
UR - http://www.scopus.com/inward/record.url?scp=70549107710&partnerID=8YFLogxK
U2 - 10.1016/j.ceb.2009.09.004
DO - 10.1016/j.ceb.2009.09.004
M3 - Review article
C2 - 19822411
AN - SCOPUS:70549107710
SN - 0955-0674
VL - 21
SP - 871
EP - 877
JO - Current Opinion in Cell Biology
JF - Current Opinion in Cell Biology
IS - 6
ER -