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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
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RIPK1- and RIPK3-induced cell death mode is determined by target availability.

W D Cook1, D M Moujalled2, T J Ralph1

  • 1La Trobe Institute for Molecular Science, La Trobe University, Kingsbury Drive, Bundoora, Victoria 3086, Australia.

Cell Death and Differentiation
|June 7, 2014
PubMed
Summary

Receptor-interacting protein kinases (RIPK1 and RIPK3) trigger cell death. Their activation mode, independent of death ligands, depends on downstream protein availability, not a simple switch.

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Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Immunology

Background:

  • Receptor-interacting protein kinase 1 (RIPK1) and RIPK3 are key regulators of programmed cell death.
  • Understanding RIPK-triggered cell death independent of death receptor signaling is crucial for disease research.

Purpose of the Study:

  • To investigate the signaling requirements for RIPK1 and RIPK3-induced cell death in the absence of death receptor ligands.
  • To elucidate the mechanisms by which RIPK1 and RIPK3 activate distinct cell death pathways.

Main Methods:

  • Engineered inducible versions of RIPK1 and RIPK3 activated by dimerization with coumermycin.
  • Studied cell death mechanisms in the absence of TNF or other death ligands.
  • Assessed the roles of FADD, caspase 8, and MLKL in RIPK-mediated cell death.

Main Results:

  • RIPK1 dimerization induced cell death via caspase- or RIPK3-dependent pathways.
  • RIPK3 dimerization triggered MLKL-dependent death and also FADD, caspase 8, and RIPK1-mediated death.
  • RIPK3 kinase activity was essential for MLKL-dependent but not caspase 8-dependent death.

Conclusions:

  • The mode of RIPK-induced cell death is determined by the availability of downstream signaling molecules like FADD, caspase 8, and MLKL.
  • RIPK-mediated cell death does not operate via a simple switch but is modulated by the levels of signaling and effector proteins.