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Cell Res. 2014 Feb;24(2):139-40. doi: 10.1038/cr.2014.8. Epub 2014 Jan 14.

MLKL regulates necrotic plasma membrane permeabilization.

Author information

1
1] Gustave Roussy, Villejuif, France [2] Université Paris Descartes/Paris V, Sorbonne Paris Cité, Paris, France [3] Equipe 11 labellisée Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France.
2
1] Equipe 11 labellisée Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France [2] INSERM, U848, Villejuif, France [3] Metabolomics and Cell Biology Platforms, Gustave Roussy, Villejuif, France.
3
1] Université Paris Descartes/Paris V, Sorbonne Paris Cité, Paris, France [2] Equipe 11 labellisée Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France [3] INSERM, U848, Villejuif, France [4] Metabolomics and Cell Biology Platforms, Gustave Roussy, Villejuif, France [5] Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, Paris, France.

Abstract

Recent data from two independent laboratories have shed new light on the molecular mechanisms by which mixed lineage kinase domain-like (MLKL) promotes a peculiar form of regulated necrosis known as necroptosis. Upon phosphorylation by receptor-interacting protein kinase 3 (RIPK3), MLKL appears indeed to form oligomers that localize to the plasma membrane and compromise its ability to preserve ionic homeostasis.

PMID:
24418759
PMCID:
PMC3915909
DOI:
10.1038/cr.2014.8
[Indexed for MEDLINE]
Free PMC Article

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