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The Killer Pseudokinase Mixed Lineage Kinase Domain-Like Protein (MLKL).

Authors
  • Murphy, James M1, 2
  • 1 Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia. , (Australia)
  • 2 Department of Medical Biology, University of Melbourne, Parkville, Victoria 3052, Australia. , (Australia)
Type
Published Article
Journal
Cold Spring Harbor Perspectives in Biology
Publisher
Cold Spring Harbor Laboratory
Publication Date
Aug 03, 2020
Volume
12
Issue
8
Identifiers
DOI: 10.1101/cshperspect.a036376
PMID: 31712266
Source
Medline
Language
English
License
Unknown

Abstract

Whereas the apoptosis cell death pathway typically enables cells to undergo death in an immunologically silent manner, cell death by necroptosis induces cell lysis and release of cellular constituents known to elicit an immune response. Consequently, the origins of necroptosis likely originated in host defense against pathogens, although recently it has emerged that dysregulation of the pathway underlies many human pathologies. The past decade has seen a rapid advance in our understanding of the molecular mechanisms underlying necroptotic cell death, including the implication of the pseudokinase, mixed lineage kinase domain-like protein (MLKL), as the terminal effector in the pathway. Here, I review our current understanding of how MLKL is activated by the upstream receptor interacting protein kinase (RIPK)3, the proposed mechanism(s) by which MLKL kills cells, and recently described layers of regulation that tune MLKL's killing activity. Copyright © 2020 Cold Spring Harbor Laboratory Press; all rights reserved.

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