Bcl-2 Family Members as Sentinels of Cellular Integrity and Role of Mitochondrial Intermembrane Space Proteins in Apoptotic Cell Death

2003 ◽  
Vol 111 (1-2) ◽  
pp. 7-27 ◽  
Author(s):  
Nele Festjens ◽  
Marjan van Gurp ◽  
Geert van Loo ◽  
Xavier Saelens ◽  
Peter Vandenabeele
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Family Members ◽  
Apoptotic Cell Death ◽  
Intermembrane Space ◽  
Mitochondrial Intermembrane Space ◽  
Cellular Integrity

scholarly journals Role of Bcl-2 family members in apoptotic cell death

1999 ◽  
Vol 56 (4) ◽  
pp. 1192
Author(s):  
Craig B. Thompson ◽  
Matthew Vander Heiden ◽  
Brian S. Chang ◽  
Andrew J. Minn ◽  
Michael Sattler ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Family Members ◽  
Apoptotic Cell Death

Arsenic Trioxide-Induced Cell Death Occurs Partially Independent of the Pro-Apoptotic Bcl-2-Family Members Bax and Bak.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4585-4585
Author(s):  
Christian Scholz ◽  
Antje Richter ◽  
Anja Richter ◽  
Bernd Dörken ◽  
Peter T. Daniel
Keyword(s):  
Cell Death ◽  
Arsenic Trioxide ◽  
Cell Lines ◽  
Apoptotic Cell ◽  
Family Members ◽  
Death Receptor ◽  
Hematologic Malignancies ◽  
Mitochondrial Pathway ◽  
Cell Death Pathways

Abstract Arsenic trioxide (As2O3, arsenite) efficiently kills cells from various hematologic malignancies and has successfully been employed for the treatment of acute promyelocytic leukaemia, myelodysplastic syndrome, and multiple myeloma. Investigating the mechanisms of arsenic trioxide-induced cell death, we recently demonstrated that arsenite-mediated cell demise has a partially necrotic phenotype, occurs independently of the extrinsic death receptor pathway of apoptosis, and is not hampered by the absence of functioning caspases. On the contrary, cell death proceeded entirely via an intrinsic, mitochondrial pathway and was efficiently blocked by the anti-apoptotic Bcl-2 family members Bcl-2 or Bcl-xL. Here, we address the role of the pro-apoptotic multi-domain Bcl-2 family members Bax and Bak. By employing different cell lines deficient for Bax and/or Bak, we demonstrate that Bax- or Bak-deficiency as well as the combined absence only partially blocks arsenite-induced cell death. While the detection of an additive effect of the combined Bax-/Bak-deficiency argues for a non redundant function of Bax and Bak, the persistence of a substantial percentage of arsenite-mediated cell demise in different double deficient cell lines nevertheless suggests a mode of arsenic trioxide-mediated cell death independent from these central inducers of apoptotic cell demise. The presented data add to the notion that arsenic trioxide kills tumor cells independent of the apoptotic machinery, and warrants further investigation on the efficacy of this compound in malignancies with deficiencies of the apoptotic cell death pathways.

Role of Apoptotic Cell Death in Sepsis

2003 ◽  
Vol 35 (9) ◽  
pp. 585-592 ◽  
Author(s):  
Richard S. Hotchkiss ◽  
Kevin W. Tinsley ◽  
Irene E. Karl
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death

scholarly journals The role of apoptotic cell death in cardiovascular disease

2001 ◽  
Vol 170 (2) ◽  
pp. 132-140 ◽  
Author(s):  
R. McLaughlin ◽  
C. J. Kelly ◽  
E. Kay ◽  
D. Bouchier-Hayes
Keyword(s):  
Cardiovascular Disease ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death
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