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MLKL Requires the Inositol Phosphate Code to Execute Necroptosis.

Abstract：

:Necroptosis is an important form of lytic cell death triggered by injury and infection, but whether mixed lineage kinase domain-like (MLKL) is sufficient to execute this pathway is unknown. In a genetic selection for human cell mutants defective for MLKL-dependent necroptosis, we identified mutations in IPMK and ITPK1, which encode inositol phosphate (IP) kinases that regulate the IP code of soluble molecules. We show that IP kinases are essential for necroptosis triggered by death receptor activation, herpesvirus infection, or a pro-necrotic MLKL mutant. In IP kinase mutant cells, MLKL failed to oligomerize and localize to membranes despite proper receptor-interacting protein kinase-3 (RIPK3)-dependent phosphorylation. We demonstrate that necroptosis requires IP-specific kinase activity and that a highly phosphorylated product, but not a lowly phosphorylated precursor, potently displaces the MLKL auto-inhibitory brace region. These observations reveal control of MLKL-mediated necroptosis by a metabolite and identify a key molecular mechanism underlying regulated cell death.

journal_name

Mol Cell

journal_title

Molecular cell

authors

Dovey CM,Diep J,Clarke BP,Hale AT,McNamara DE,Guo H,Brown NW Jr,Cao JY,Grace CR,Gough PJ,Bertin J,Dixon SJ,Fiedler D,Mocarski ES,Kaiser WJ,Moldoveanu T,York JD,Carette JE

doi

10.1016/j.molcel.2018.05.010

subject

Has Abstract

pub_date

2018-06-07 00:00:00

pages

936-948.e7

issue

5

eissn

1097-2765

issn

1097-4164

pii

S1097-2765(18)30360-5

journal_volume

70

pub_type

杂志文章

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