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Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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Related Experiment Video

Updated: Mar 9, 2026

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
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Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

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The Inflammatory Signal Adaptor RIPK3: Functions Beyond Necroptosis.

K Moriwaki1, F K-M Chan1

  • 1Department of Pathology, Immunology and Microbiology Program, University of Massachusetts Medical School, Worcester, MA, United States.

International Review of Cell and Molecular Biology
|January 11, 2017
PubMed
Summary
This summary is machine-generated.

Receptor interacting protein kinase 3 (RIPK3) drives inflammation through necroptosis and other functions. Understanding these roles is key to developing therapies for inflammatory diseases.

Keywords:
MLKLNF-κBRIPK1RIPK3TNFapoptosiscaspase 8inflammasomeinflammationnecroptosis

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Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Receptor interacting protein kinase 3 (RIPK3) is crucial for necroptosis, a regulated necrosis pathway.
  • Necroptosis triggers inflammation due to the release of intracellular contents.
  • RIPK3 deficiency reduces inflammation in various disease models, implicating necroptosis in pathogenesis.

Purpose of the Study:

  • To review the necroptotic and nonnecroptotic functions of RIPK3.
  • To discuss the contribution of these functions to RIPK3-mediated inflammation.
  • To highlight RIPK3's multifaceted roles in inflammatory diseases.

Main Methods:

  • Literature review of studies on RIPK3 function and inflammation.
  • Analysis of experimental evidence linking RIPK3 to necroptosis, NF-κB, inflammasomes, and apoptosis.
  • Synthesis of findings on RIPK3's impact on inflammatory disease models.

Main Results:

  • RIPK3 activates MLKL, leading to necroptosis and inflammation.
  • RIPK3 also regulates NF-κB, inflammasome activation, and kinase-independent apoptosis.
  • Nonnecroptotic RIPK3 functions significantly contribute to disease pathogenesis and inflammation.

Conclusions:

  • RIPK3 orchestrates inflammation through both necroptotic and nonnecroptotic pathways.
  • Targeting RIPK3 may offer therapeutic strategies for inflammatory conditions.
  • Further research into RIPK3's diverse functions is warranted.