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Recently, the development of olefin metathesis polymerization advanced the field of polymer synthesis. Simply put, the reorganization of substituents on their double bonds between two olefins in the presence of a catalyst is known as the olefin metathesis reaction. The use of metathesis reaction for polymer synthesis is called olefin metathesis polymerization.
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Chain-growth or addition polymerization is successive addition reactions of monomers with a polymer chain. In radical chain-growth polymerization, the reaction proceeds via a free-radical intermediate. The free radical is formed from radical initiators, which spontaneously generate free radicals by homolytic fission. Organic peroxides (such as dibenzoyl peroxide, as shown in Figure 1) or azo compounds are popular radical initiators. A low concentration ratio of radical initiator to monomer is...
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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
Summary
This summary is machine-generated.

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.

Keywords:
Amyloid-like polymerMLKLNecroptosisThioredoxin

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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.