The Fas Signaling Pathway: More Than a Paradigm

  title={The Fas Signaling Pathway: More Than a Paradigm},
  author={Harald Wajant},
  pages={1635 - 1636}
Apoptosis and related forms of cell death have central importance in development, homeostasis, tumor surveillance, and the function of the immune system. Apoptosis is initiated by two principal pathways. The intrinsic pathway emerges from mitochondria, whereas the extrinsic pathway is activated by the ligation of death receptors. This Viewpoint introduces the basic mechanisms of the extrinsic pathway, using the example of the prototypical death receptor Fas and its role in apoptosis, but it… 
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Non‐apoptotic functions of apoptosis‐regulatory proteins
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This review highlights the basics concept of apoptosis and its regulation by Bcl-2 family of protein and discusses the interplay of various apoptotic mediators and caspases to decide the fate of the cell.
Major apoptotic mechanisms and genes involved in apoptosis
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FLICE-Inhibitory Proteins: Regulators of Death Receptor-Mediated Apoptosis
Apoptosis, or programmed cell death, is critical for tissue homeostasis in multicellular organisms and plays an important role in many physiological processes, especially in development and in the immune system.
CD95's deadly mission in the immune system
The role of CD95 (Apo-1/Fas)-mediated signalling in T-cell and B-cell development and during the course of an immune response and the understanding of the pathogenesis of diseases such as cancer, autoimmunity and AIDS is improved.
The multifaceted role of Fas signaling in immune cell homeostasis and autoimmunity
It is now recognized that Fas (also known as CD95 or Apo-1) has distinct functions in the life and death of different cell types in the immune system and can also facilitate organ-specific immunopathology.
Fas ligand, death gene
The FasL gene, which is often transcriptionally inactive, becomes activated in many forms of transcription/translation dependent apoptosis, and is discussed here as a candidate death gene.
Fas triggers an alternative, caspase-8–independent cell death pathway using the kinase RIP as effector molecule
F Fas kills activated primary T cells efficiently in the absence of active caspases, which results in necrotic morphological changes and late mitochondrial damage but no cytochrome c release.
Fas receptor signaling inhibits glycogen synthase kinase 3 beta and induces cardiac hypertrophy following pressure overload.
Findings indicate that Fas receptor signaling inhibits GSK3 beta activity in cardiomyocytes and is required for compensation of pressure overload in vivo.