Bax regulates primary necrosis through mitochondrial dynamics

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

Volumn 109, Issue 17, 2012, Pages 6566-6571

  Whelan, Russell S ^a   Konstantinidis, Klitos ^a   Wei, An Chi ^b   Chen, Yun ^c   Reyna, Denis E ^a   Jha, Saurabh ^a   Yang, Ying ^a   Calvert, John W ^d   Lindsten, Tullia ^e   Thompson, Craig B ^e   Crow, Michael T ^b   Gavathiotis, Evripidis ^a   Dorn II, Gerald W ^c   O'Rourke, Brian ^b   Kitsis, Richard N ^a  

^a ALBERT EINSTEIN COLLEGE OF MEDICINE   (United States)

^b JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE   (United States)

^c WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

^d EMORY UNIVERSITY SCHOOL OF MEDICINE   (United States)

^e MEMORIAL SLOAN KETTERING CANCER CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CYCLOPHILIN D; MITOCHONDRIAL PERMEABILITY TRANSITION PORE; MITOFUSIN 2; PROTEIN BAK; PROTEIN BAX;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; APOPTOSIS; ARTICLE; CELL DEATH; CELL PERMEABILIZATION; HEART INFARCTION; HEART INFARCTION SIZE; IN VIVO STUDY; MITOCHONDRION; MOUSE; NONHUMAN; OLIGOMERIZATION; PRIORITY JOURNAL;

ADENOSINE TRIPHOSPHATE; ANIMALS; BCL-2-ASSOCIATED X PROTEIN; MICE; MICE, KNOCKOUT; MITOCHONDRIA; MYOCARDIAL INFARCTION; NECROSIS;

EID: 84860180832     PISSN: 00278424     EISSN: 10916490     Source Type: Journal    
DOI: 10.1073/pnas.1201608109     Document Type: Article

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