Differential effects of Bcl-2 on cell death triggered under ATP-depleting conditions

Experimental Cell Research

Volumn 262, Issue 1, 2001, Pages 8-16

  Single, Barbara ^a   Leist, Marcel ^a   Nicotera, Pierluigi ^a  

^a UNIVERSITY OF KONSTANZ   (Germany)

Author keywords

Apoptosis; ATP; Bcl 2; Cytochrome c; Mitochondria; Necrosis; NO

Indexed keywords

ADENOSINE TRIPHOSPHATE; CYTOCHROME C; GLUCOSE; PROTEIN BCL 2; ROTENONE; S NITROSOGLUTATHIONE; STAUROSPORINE;

APOPTOSIS; ARTICLE; CELL DEATH; CONCENTRATION RESPONSE; CONTROLLED STUDY; ENERGY; ENZYME RELEASE; GLYCOLYSIS; HUMAN; HUMAN CELL; LEUKEMIA CELL LINE; MODULATION; PRIORITY JOURNAL; PROTEIN ANALYSIS;

EID: 0034775662     PISSN: 00144827     EISSN: None     Source Type: Journal    
DOI: 10.1006/excr.2000.5059     Document Type: Article

References (49)

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3. Nitric oxide inhibits execution of apoptosis at two distinct ATP-dependent steps upstream and downstream of mitochondrial cytochrome c release
4. bcl-2 transgene inhibits T cell death and perturbs thymic self-censorship
5. Overexpression of BCL-2 in transgenic mice protects neurons from naturally occurring cell death and experimental ischemia
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7. A bcl-2 transgene expressed in hepatocytes protects mice from fulminant liver destruction but not from rapid death induced by anti-Fas antibody injection
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15. Bcl-2 and Fas/APO-1 regulate distinct pathways to lymphocyte apoptosis
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32. Apoptosis in the absence of poly-(ADP-ribose) polymerase
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45. Apoptosis, in human monocytic THP 1 cells, results in the release of cytochrome c from mitochondria prior to their ultracondensation, formation of outer membrane discontinuities and reduction in inner membrane potential
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48. Mitochondria are excitable organelles capable of generating and conveying electrical and calcium signals
49. The mitochondrial permeability transition