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.
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.
RIP3 kinase-inactive Knockin mice (Rip3^K51A/K51A) generated to study the effects of RIP3 inactivation on ferroptotic susceptibility.
Ferroptosis, Necroptosis, Regulated cell death, Oxidative stress, Traumatic brain injury, Radiation injury
Knockin model, Kinase-inactive mutation, Ferroptosis research, 15LOX/PEBP1 complex, Redox biology
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
