Mitochondrial fission is an upstream and required event for bax foci formation in response to nitric oxide in cortical neurons

Cell Death and Differentiation

Volumn 14, Issue 3, 2007, Pages 462-471

  Yuan, H ^a   Gerencser, A A ^a   Liot, G ^a   Lipton, S A ^a   Ellisman, M ^b   Perkins, G A ^b   Bossy Wetzel, E ^a  

^a BURNHAM INSTITUTE   (United States)

^b UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

NITRIC OXIDE; PROTEIN BAX;

ANIMAL CELL; APOPTOSIS; ARTICLE; BINDING SITE; BRAIN CELL; CONTROLLED STUDY; DEGENERATIVE DISEASE; DISORDERS OF MITOCHONDRIAL FUNCTIONS; EMBRYO; NERVE CELL NECROSIS; NITROSATIVE STRESS; NONHUMAN; PRIORITY JOURNAL; PROTEIN FUNCTION; PROTEIN SYNTHESIS INHIBITION; RAT; SPRAGUE DAWLEY RAT;

ADENOSINE TRIPHOSPHATE; ANIMALS; BCL-2-ASSOCIATED X PROTEIN; BCL-X PROTEIN; CELL DEATH; CELLS, CULTURED; CEREBRAL CORTEX; GLYCOLYSIS; MEMBRANE PROTEINS; MITOCHONDRIA; MITOCHONDRIAL PROTEINS; MODELS, BIOLOGICAL; NEURONS; NITRIC OXIDE; PROTEIN TRANSPORT; RATS; RATS, SPRAGUE-DAWLEY; TRANSFECTION;

EID: 33847012075     PISSN: 13509047     EISSN: 14765403     Source Type: Journal    
DOI: 10.1038/sj.cdd.4402046     Document Type: Article

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