Proteolytic Activation and Inactivation of the Serine Protease Activity of Plasma Hyaluronan Binding Protein.

2001 ◽  
Vol 24 (5) ◽  
pp. 448-452 ◽  
Author(s):  
Nam-Ho CHOI-MIURA ◽  
Katsuhiko TAKAHASHI ◽  
Madoka YODA ◽  
Kiyomi SAITO ◽  
Toshio MAZDA ◽  
...  
2001 ◽  
Vol 24 (3) ◽  
pp. 221-225 ◽  
Author(s):  
Nam-Ho CHOI-MIURA ◽  
Kiyomi SAITO ◽  
Katsuhiko TAKAHASHI ◽  
Madoka YODA ◽  
Motowo TOMITA

1999 ◽  
Vol 46 (1) ◽  
pp. 76-81 ◽  
Author(s):  
Martin W Elmlinger ◽  
Regine Grund ◽  
Michael Buck ◽  
Hartmut A Wollmann ◽  
Norman Feist ◽  
...  

Blood ◽  
2004 ◽  
Vol 103 (6) ◽  
pp. 2299-2307 ◽  
Author(s):  
Masayuki Okada ◽  
Souichi Adachi ◽  
Tsuyoshi Imai ◽  
Ken-ichiro Watanabe ◽  
Shin-ya Toyokuni ◽  
...  

Abstract Caspase-independent programmed cell death can exhibit either an apoptosis-like or a necrosis-like morphology. The ABL kinase inhibitor, imatinib mesylate, has been reported to induce apoptosis of BCR-ABL–positive cells in a caspase-dependent fashion. We investigated whether caspases alone were the mediators of imatinib mesylate–induced cell death. In contrast to previous reports, we found that a broad caspase inhibitor, zVAD-fmk, failed to prevent the death of imatinib mesylate–treated BCR-ABL–positive human leukemic cells. Moreover, zVAD-fmk–preincubated, imatinib mesylate–treated cells exhibited a necrosis-like morphology characterized by cellular pyknosis, cytoplasmic vacuolization, and the absence of nuclear signs of apoptosis. These cells manifested a loss of the mitochondrial transmembrane potential, indicating the mitochondrial involvement in this caspase-independent necrosis. We excluded the participation of several mitochondrial factors possibly involved in caspase-independent cell death such as apoptosis-inducing factor, endonuclease G, and reactive oxygen species. However, we observed the mitochondrial release of the serine protease Omi/HtrA2 into the cytosol of the cells treated with imatinib mesylate or zVAD-fmk plus imatinib mesylate. Furthermore, serine protease inhibitors prevented the caspase-independent necrosis. Taken together, our results suggest that imatinib mesylate induces a caspase-independent, necrosis-like programmed cell death mediated by the serine protease activity of Omi/HtrA2.


2011 ◽  
Vol 47 (3) ◽  
pp. 345-353 ◽  
Author(s):  
P. Mäntylä ◽  
E. Buduneli ◽  
G. Emingil ◽  
T. Tervahartiala ◽  
P. J. Pussinen ◽  
...  

2001 ◽  
Vol 285 (4) ◽  
pp. 863-872 ◽  
Author(s):  
Marie-Thérèse Château ◽  
Véronique Robert-Hebmann ◽  
Christian Devaux ◽  
Jean-Bernard Lazaro ◽  
Bruno Canard ◽  
...  

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