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Updated: Feb 12, 2026

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

Necroptosis in development and diseases.

Bing Shan¹, Heling Pan¹, Ayaz Najafov²

¹Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, PuDong District, Shanghai 201203, China.

Genes & Development

|March 30, 2018

Summary

Necroptosis, a regulated cell death pathway involving RIPK1, RIPK3, and MLKL, can occur when apoptosis is blocked. Inhibiting RIPK1 offers a therapeutic strategy for diseases involving both cell death types.

Keywords:

MLKL RIPK1 RIPK3 apoptosis necroptosis

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Area of Science:

Cellular biology
Immunology
Molecular mechanisms of cell death

Background:

Necroptosis is a regulated necrotic cell death pathway.
It is mediated by receptor-interacting protein kinase 1 (RIPK1), RIPK3, and mixed-lineage kinase domain-like pseudokinase (MLKL).
Necroptosis can be activated under conditions where apoptosis is deficient.

Purpose of the Study:

To investigate the role of RIPK1 in regulating necroptosis and apoptosis.
To explore the therapeutic potential of RIPK1 inhibition in disease.

Main Methods:

Analysis of mutant mice deficient in RIPK1, RIPK3, or MLKL.
Investigation of cellular responses under apoptosis-deficient conditions.
Evaluation of RIPK1 inhibition as a therapeutic strategy.

Main Results:

Mutant mice lacking kinase-dead RIPK1, RIPK3, or MLKL exhibit normal development and homeostasis.
Necroptosis and apoptosis are activated in response to mutations causing embryonic abortion.
These cell death pathways are implicated in human inflammatory and neurodegenerative diseases.

Conclusions:

Modulating RIPK1 activity through ubiquitination and phosphorylation is crucial for controlling necroptosis and apoptosis.
RIPK1 inhibition is a promising therapeutic approach for diseases benefiting from the blockade of both necroptosis and apoptosis.