Two CD95 (APO‐1/Fas) signaling pathways

No abstract is available for this paper.

• Publication year

  1998

• Venue

  EMBO Journal

• Publication date

  1998-03-16

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1093/emboj/17.6.1675PMID 9501089PMCID PMC1170515
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• The death receptors.

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  1997cited by this paper
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• Loss of Function of Cytochrome c in Jurkat Cells Undergoing Fas-mediated Apoptosis*

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• CD95 (APO-1/Fas) induces activation of SAP kinases downstream of ICE-like proteases.

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• Bcl-2 expression prevents activation of the ICE protease cascade.

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• Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice

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• The Caenorhabditis elegans cell-death protein CED-3 is a cysteine protease with substrate specificities similar to those of the human CPP32 protease.

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• Bcl-2 Prevents CD95 (Fas/APO-1)-induced Degradation of Lamin B and Poly(ADP-ribose) Polymerase and Restores the NF-κB Signaling Pathway*

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• Apoptosis signaling pathways in normal T cells: differential activity of Bcl-2 and IL-1beta-converting enzyme family protease inhibitors on glucocorticoid- and Fas-mediated cytotoxicity.

  1996cited by this paper
• CPP32/Apopain Is a Key Interleukin 1 Converting Enzyme-like Protease Involved in Fas-mediated Apoptosis (*)

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  1995cited by this paper
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• A Novel Protein That Interacts with the Death Domain of Fas/APO1 Contains a Sequence Motif Related to the Death Domain (*)

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