Activation of Fas by FasL induces apoptosis by a mechanism that cannot be blocked by Bcl-2 or Bcl-xL

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

Volumn 96, Issue 26, 1999, Pages 14871-14876

  Huang, David C S ^a   Hahne, Michael ^b,d   Schroeter, Michael ^b   Frei, Karl ^c   Fontana, Adriano ^c   Villunger, Andreas ^a   Newton, Kim ^a   Tschopp, Juerg ^b   Strasser, Andreas ^a  

^a ROYAL MELBOURNE HOSPITAL   (Australia)

^b UNIVERSITY OF LAUSANNE   (Switzerland)

^c UNIVERSITY HOSPITAL ZURICH   (Switzerland)

^d CENTRO NACIONAL DE BIOTECNOLOGÍA   (Spain)

Author keywords

APO 1; CD95; Signal transduction

Indexed keywords

CASPASE; FAS ANTIGEN; PROTEIN BCL 2; PROTEIN BCL X;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; APOPTOSIS; ARTICLE; CONTROLLED STUDY; LIVER CELL; LYMPHOCYTE; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN AGGREGATION; SIGNAL TRANSDUCTION; TRANSGENIC MOUSE;

ADAPTOR PROTEINS, SIGNAL TRANSDUCING; ANIMALS; ANTIGENS, CD95; APOPTOSIS; BCL-X PROTEIN; BIOLOGICAL TRANSPORT; CARRIER PROTEINS; CASPASE 8; CASPASE 9; CASPASES; CELL MEMBRANE; FAS LIGAND PROTEIN; FAS-ASSOCIATED DEATH DOMAIN PROTEIN; IMMUNOLOGIC CAPPING; LIVER; LYMPHOCYTES; MEMBRANE GLYCOPROTEINS; MICE; MICE, TRANSGENIC; PROTEIN PRECURSORS; PROTO-ONCOGENE PROTEINS C-BCL-2; SIGNAL TRANSDUCTION;

ANIMALIA; MUS MUSCULUS;

EID: 0033592984     PISSN: 00278424     EISSN: None     Source Type: Journal    
DOI: 10.1073/pnas.96.26.14871     Document Type: Article

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