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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
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