Hypoxia and acidosis activate cardiac myocyte death through the Bcl-2 family protein BNIP3

Proceedings of the National Academy of Sciences of the United States of America

Volumn 99, Issue 20, 2002, Pages 12825-12830

  Kubasiak, Lori A ^a   Hernandez, Olga M ^a   Bishopric, Nanette H ^a   Webster, Keith A ^a  

^a UNIVERSITY OF MIAMI   (United States)

Author keywords

Antisense; Apoptosis; Heart; Ischemia; Mitochondria

Indexed keywords

ANTISENSE OLIGONUCLEOTIDE; PROTEIN; PROTEIN BCL 2; PROTEIN BNIP3; UNCLASSIFIED DRUG;

ACIDOSIS; ANIMAL CELL; APOPTOSIS; ARTICLE; CELL CULTURE; CELL MEMBRANE PERMEABILITY; CONTROLLED STUDY; ENZYME ACTIVATION; HEART MITOCHONDRION; HEART MUSCLE CELL; HYPOXIA; NEWBORN; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN STABILITY; RAT; WILD TYPE;

ANIMALS; ANOXIA; APOPTOSIS; BLOTTING, NORTHERN; BLOTTING, WESTERN; CELL DEATH; CELL MEMBRANE; CELLS, CULTURED; CULTURE MEDIA, SERUM-FREE; HYDROGEN-ION CONCENTRATION; INTRACELLULAR MEMBRANES; ISCHEMIA; MEMBRANE PROTEINS; MITOCHONDRIA; MUSCLE, SKELETAL; NECROSIS; OLIGONUCLEOTIDES, ANTISENSE; PLASMIDS; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-BCL-2; RATS; RNA, MESSENGER; SUBCELLULAR FRACTIONS; TIME FACTORS; TRANSFECTION; TUMOR SUPPRESSOR PROTEINS;

ANIMALIA;

EID: 0036789917     PISSN: 00278424     EISSN: None     Source Type: Journal    
DOI: 10.1073/pnas.202474099     Document Type: Article

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