Cross-talk in cell death signaling

Journal of Experimental Medicine

Volumn 192, Issue 8, 2000, Pages

  Roy, Sophie ^a   Nicholson, Donald W ^a  

^a MERCK FROSST CENTRE FOR THERAPEUTIC RESEARCH   (Canada)

Author keywords

[No Author keywords available]

Indexed keywords

CASPASE; CASPASE 3; CASPASE 7; CASPASE 8; CASPASE 9; CYTOCHROME C OXIDASE; FAS ANTIGEN; MITOGEN ACTIVATED PROTEIN KINASE; PROTEIN BCL 2; TUMOR NECROSIS FACTOR ALPHA;

APOPTOSIS; CATALYSIS; CELL DEATH; ENZYME ACTIVATION; GENE OVEREXPRESSION; LIGAND BINDING; LIVER CELL; METABOLISM; MITOCHONDRION; NOTE; PRIORITY JOURNAL; SIGNAL TRANSDUCTION;

EID: 0034676089     PISSN: 00221007     EISSN: None     Source Type: Journal    
DOI: 10.1084/jem.192.8.f21     Document Type: Note

References (15)

1. Biochemical pathways of caspase activation during apoptosis
2. Apoptotic pathways: Paper wraps stone blunts scissors
3. Fas preassociation required for apoptosis signaling and dominant inhibition by pathogenic mutations
4. A domain in TNF receptors that mediates ligand-independent receptor assembly and signaling
5. Two CD95 (APO-1/Fas) signaling pathways
6. Differential modulation of apoptosis sensitivity in CD95 type I and type II cells
7. Bid, a Bc12 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors
8. Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis
9. Bcl-2 protects from lethal hepatic apoptosis induced by an anti-Fas antibody in mice
10. A bcl-2 transgene expressed in hepatocytes protects mice from fulminant liver destruction but not from rapid death induced by anti-Fas antibody injection
11. Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis
12. Activation of Fas by FasL induces apoptosis by a mechanism that cannot be blocked by Bcl-2 or Bcl-x(L)
13. Differences between CD95 type I and II cells detected with the CD95 ligand
14. Bcl-2 does not inhibit cell death induced by the physiological Fas ligand: Implications for the existence of type I and type II cells
15. Fas ligand, Bcl-2, granulocyte colony-stimulating factor, and p38 mitogen-activated protein kinase: Regulators of distinct cell death and survival pathways in granulocytes