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J. Cell Biol. 150 (4): 887-894

Copyright © 2000 by the Rockefeller University Press.

© The Rockefeller University Press, /2000/8/887/ $5.00
The Journal of Cell Biology, Volume 150, Number 4, August 21, 2000 887-894
Report Cross-talk between Two Cysteine Protease Families: Activation of Caspase-12 by Calpain in Apoptosis Toshiyuki Nakagawaa and Junying Yuana a Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115 Junying Yuan, Department of Cell Biology, Harvard Medical School, 240 Longwood Ave., Boston, MA 02115. Tel:(617) 432-4170 Fax:(617) 432-4177 E-mail:jyuan{at}hms.harvard.edu.

Calpains and caspases are two cysteine protease families that play important roles in regulating pathological cell death. Here, we report that m-calpain may be responsible for cleaving procaspase-12, a caspase localized in the ER, to generate active caspase-12. In addition, calpain may be responsible for cleaving the loop region in Bcl-xL and, therefore, turning an antiapoptotic molecule into a proapoptotic molecule. We propose that disturbance to intracellular calcium storage as a result of ischemic injury or amyloid ß peptide cytotoxicity may induce apoptosis through calpain- mediated caspase-12 activation and Bcl-xL inactivation. These data suggest a novel apoptotic pathway involving calcium-mediated calpain activation and cross-talks between calpain and caspase families.

calcium, Alzheimer's disease, Bcl-xL, endoplasmic reticulum, ER stress

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Methamphetamine induces neuronal apoptosis via cross-talks between endoplasmic reticulum and mitochondria-dependent death cascades.
S. JAYANTHI, X. DENG, P.-A. H. NOAILLES, B. LADENHEIM, and J. L. CADET (2004)
FASEB J 18, 238-251
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Paracetamol-Induced Renal Tubular Injury: A Role for ER Stress.
C. Lorz, P. Justo, A. Sanz, D. Subira, J. Egido, and A. Ortiz (2004)
J. Am. Soc. Nephrol. 15, 380-389
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R115777 induces Ras-independent apoptosis of myeloma cells via multiple intrinsic pathways.
D. M. Beaupre, E. Cepero, E. A. Obeng, L. H. Boise, and M. G. Lichtenheld (2004)
Mol. Cancer Ther. 3, 179-186
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Molecular Components of a Cell Death Pathway Activated by Endoplasmic Reticulum Stress.
R. V. Rao, K. S. Poksay, S. Castro-Obregon, B. Schilling, R. H. Row, G. del Rio, B. W. Gibson, H. M. Ellerby, and D. E. Bredesen (2004)
J. Biol. Chem. 279, 177-187
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Impact of Endoplasmic Reticulum Stress Pathway on Pancreatic {beta}-Cells and Diabetes Mellitus.
E. Araki, S. Oyadomari, and M. Mori (2003)
Experimental Biology and Medicine 228, 1213-1217
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The Combination of Calmodulin Antagonists and Interferon-{gamma} Induces Apoptosis through Caspase-Dependent and -Independent Pathways in Cholangiocarcinoma Cells.
E.-Y. Ahn, G. Pan, J. H. Oh, E. M. Tytler, and J. M. McDonald (2003)
Am. J. Pathol. 163, 2053-2063
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