Fas preassociation required for apoptosis signaling and dominant inhibition by pathogenic mutations

Science

Volumn 288, Issue 5475, 2000, Pages 2354-2357

  Siegel, Richard M ^a   Frederiksen, John K ^a   Zacharias, David A ^b   Chan, Francis Ka Ming ^a   Johnson, Michele ^a   Lynch, David ^c   Tsien, Roger Y ^b   Lenardo, Michael J ^a  

^a NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES   (United States)

^b San Diego   (United States)

^c AMGEN INC   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

FAS ANTIGEN; GREEN FLUORESCENT PROTEIN; LYMPHOCYTE ANTIGEN RECEPTOR;

ANIMAL CELL; APOPTOSIS; ARTICLE; COMPLEX FORMATION; GENE MUTATION; HUMAN; HUMAN CELL; LIGAND BINDING; LYMPHOPROLIFERATIVE DISEASE; NONHUMAN; OLIGOMERIZATION; PRIORITY JOURNAL; PROTEIN DOMAIN; PROTEIN PROTEIN INTERACTION; SIGNAL TRANSDUCTION;

ANIMALS; ANTIGENS, CD95; APOPTOSIS; AUTOIMMUNE DISEASES; CELL LINE; CELL MEMBRANE; CROSS-LINKING REAGENTS; FAS LIGAND PROTEIN; HUMANS; LIGANDS; LYMPHOCYTES; LYMPHOPROLIFERATIVE DISORDERS; MACROMOLECULAR SUBSTANCES; MEMBRANE GLYCOPROTEINS; MICE; MUTATION; POINT MUTATION; RECOMBINANT FUSION PROTEINS; SIGNAL TRANSDUCTION; SUCCINIMIDES; TUMOR CELLS, CULTURED;

EID: 0034733584     PISSN: 00368075     EISSN: None     Source Type: Journal    
DOI: 10.1126/science.288.5475.2354     Document Type: Article

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36. We thank D. Martin, L. Zheng, and D. Smith for plasm id construction; K. Holmes, R. Swofford, and D. Stephany for excellent technical assistance; M. Peter and B. Herman for valuable reagents; T. Waldmann, R. Germain, H. Metzger, J. O'Shea, C. Jackson, and F. Hornung for critical reading of the manuscript and helpful comments; and S. Starnes for editorial assistance. S. Straus, J. Puck, C. Jackson, and J. Dale of the NIH ALPS working group provided clinical material and encouragement that were essential for this work. Supported by a Cancer Research Institute/Miriam and Benedict Wolf fellowship (F.K.-M.C), NIH grant NS27177 (R.Y.T.), and a fellowship in the HHMI/NIH scholar program (M.J.).