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Glutathione peroxidase 4 prevents necroptosis in mouse erythroid precursors by Özge Canli, Yasemin B. Alankuş, Sasker Grootjans, Naidu Vegi, Lothar Hültner, Philipp S. Hoppe, Timm Schroeder, Peter Vandenabeele, Georg W. Bornkamm, and Florian R. Greten Blood Volume 127(1):139-148 January 7, 2016 ©2016 by American Society of Hematology Loss of Gpx4 in hematopoietic cells induces anemia that is compensated by increased erythropoiesis. Özge Canli et al. Blood 2016;127:139-148 ©2016 by American Society of Hematology Increased lipid peroxidation and oxidative stress in Gpx4Δ erythroid cells does not impair their life span in the periphery. Özge Canli et al. Blood 2016;127:139-148 ©2016 by American Society of Hematology Increased erythropoiesis in Gpx4Δ mice depends on vitamin E. (A) Schematic overview of treatment: bone marrow from Gpx4F/F or Mx1-Cre/Gpx4F/F mice was transplanted (BMT) into wild-type recipients; mice were kept on a vitamin E–depleted diet (VitEΔ) after th... Özge Canli et al. Blood 2016;127:139-148 ©2016 by American Society of Hematology RIP3-dependent necroptosis, but not ferroptosis, causes cell death in Gpx4-deficient erythroid progenitor cells. Özge Canli et al. Blood 2016;127:139-148 ©2016 by American Society of Hematology Genetic deletion of Rip3 normalizes red cell parameters and rescues anemia. Özge Canli et al. Blood 2016;127:139-148 ©2016 by American Society of Hematology Necroptosis in Gpx4Δ mice is triggered independently of TNFR or CD95 engagement and PARP activation. Özge Canli et al. Blood 2016;127:139-148 ©2016 by American Society of Hematology Caspase 8 is inactivated in Gpx4-deficient cells. Özge Canli et al. Blood 2016;127:139-148 ©2016 by American Society of Hematology