Glutathione depletion enforces the mitochondrial permeability transition and causes cell death in Bcl-2 overexpressing HL60 cells.

The FASEB journal : official publication of the Federation of American Societies for Experimental Biology

Volumn 16, Issue 10, 2002, Pages 1263-1265

  Armstrong, Jeffrey S ^a   Jones, Dean P ^a  

^a EMORY UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BUTHIONINE SULFOXIMINE; CARRIER PROTEIN; ENZYME INHIBITOR; GLUTATHIONE; ION CHANNEL; MALEIC ACID DERIVATIVE; MALEIC ACID DIETHYL ESTER; MITOCHONDRIAL PERMEABILITY TRANSITION PORE; PROTEIN BCL 2; REACTIVE OXYGEN METABOLITE;

APOPTOSIS; ARTICLE; CELL STRAIN HL 60; DRUG EFFECT; ELECTRON TRANSPORT; GENETIC TRANSFECTION; GENETICS; HUMAN; METABOLISM; MITOCHONDRION; OXIDATION REDUCTION REACTION; PHYSIOLOGY;

APOPTOSIS; BUTHIONINE SULFOXIMINE; ELECTRON TRANSPORT; ENZYME INHIBITORS; GLUTATHIONE; HL-60 CELLS; HUMANS; ION CHANNELS; MALEATES; MITOCHONDRIA; MITOCHONDRIAL MEMBRANE TRANSPORT PROTEINS; OXIDATION-REDUCTION; PROTO-ONCOGENE PROTEINS C-BCL-2; REACTIVE OXYGEN SPECIES; TRANSFECTION;

EID: 0036673665     PISSN: None     EISSN: 15306860     Source Type: Journal    
DOI: 10.1096/fj.02-0097fje     Document Type: Article

References (0)