Inactivation of RIP3 kinase sensitizes to 15LOX/PEBP1-mediated ferroptotic death

Andrew M Lamade
University of Pittsburgh
April 1, 2022
Redox Biol
https://pubmed.ncbi.nlm.nih.gov/35101798

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/35101798

Research summary

This study investigates the role of RIP3 kinase activity in regulating ferroptotic cell death. Researchers generated RIP3 kinase-inactive Knockin mice (Rip3^K51A/K51A) to assess the impact of RIP3 inactivation on susceptibility to ferroptosis. The findings reveal that inactivation of RIP3 kinase sensitizes mice to ferroptotic death mediated by the 15-lipoxygenase (15LOX)/phosphatidylethanolamine-binding protein 1 (PEBP1) complex, particularly following total body irradiation and brain trauma. The study highlights the interplay between necroptosis and ferroptosis pathways and suggests potential therapeutic targets for conditions involving regulated necrosis.

Key outcome of the study

Inactivation of RIP3 kinase enhances susceptibility to 15LOX/PEBP1-mediated ferroptotic death, indicating a regulatory role of RIP3 in ferroptosis and its potential as a therapeutic target.

Model

RIP3 kinase-inactive Knockin mice (Rip3^K51A/K51A) generated to study the effects of RIP3 inactivation on ferroptotic susceptibility.

TARGET:
Ripk3
RIP3, Receptor-interacting serine/threonine-protein kinase 3

Keywords

Ferroptosis, Necroptosis, Regulated cell death, Oxidative stress, Traumatic brain injury, Radiation injury

Technical specifications

Knockin model, Kinase-inactive mutation, Ferroptosis research, 15LOX/PEBP1 complex, Redox biology

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