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Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
08:55

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

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Necroptosis: MLKL Polymerization

Andrea Johnston1, Zhigao Wang1

  • 1Department of Molecular Biology, UT Southwestern, 6000 Harry Hines Blvd., NA8.202, Dallas, Texas 75390, USA.

Journal of Nature and Science
|October 9, 2018
PubMed

Insights

Necroptosis is a regulated cell death pathway crucial when caspases fail. Key proteins RIPK1/3 and MLKL form amyloid structures, leading to cell membrane rupture and immunogenic cell death.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Immunology

Background:

  • Necroptosis is a regulated necrosis pathway.
  • It is caspase-independent and immunogenic.
  • It is triggered by cell death receptor stimulation.

Purpose of the Study:

  • To elucidate the core necroptosis pathway.
  • To understand the roles of RIPK1, RIPK3, and MLKL.
  • To identify mechanisms of MLKL-mediated membrane disruption.

Main Methods:

  • Analysis of the necroptosis signaling cascade.
  • Investigation of receptor interacting protein kinase (RIPK) 1 and 3 interactions.
  • Study of mixed lineage kinase domain-like pseudokinase (MLKL) function.

Main Results:

  • Receptor interacting protein kinase (RIPK) 1 and 3 interact via RHIM domains, forming the necrosome.
  • RIPK3 phosphorylates mixed lineage kinase domain-like pseudokinase (MLKL).
  • MLKL polymerizes into amyloid structures, causing cell membrane disruption.

Conclusions:

  • The core necroptosis pathway involves RIPK1/3 and MLKL.
  • MLKL forms amyloid structures that disrupt cell membranes.
  • Details of MLKL membrane translocation and disruption require further research.
Keywords:
Amyloid-like polymerMLKLNecroptosisThioredoxin

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