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- Özge Canli
- Institute for Tumor Biology and Experimental Therapy, Georg-Speyer-Haus, Frankfurt, Germany;
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- Yasemin B. Alankuş
- Institute of Clinical Chemistry, Klinikum rechts der Isar, Technical University Munich, Munich, Germany;
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- Sasker Grootjans
- Department of Molecular Biomedical Research, VIB, VIB-Ghent University, Ghent (Zwijnaarde), Belgium;
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- Naidu Vegi
- Institute of Experimental Cancer Research, Comprehensive Cancer Center and University Hospital Ulm, Ulm, Germany;
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- Lothar Hültner
- Institute of Clinical Molecular Biology and Tumor Genetics, Helmholtz Zentrum München, Munich, Germany; and
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- Philipp S. Hoppe
- Department of Biosystems Science and Engineering, Swiss Federal Institute of Technology in Zurich, Basel, Switzerland
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- Timm Schroeder
- Department of Biosystems Science and Engineering, Swiss Federal Institute of Technology in Zurich, Basel, Switzerland
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- Peter Vandenabeele
- Department of Molecular Biomedical Research, VIB, VIB-Ghent University, Ghent (Zwijnaarde), Belgium;
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- Georg W. Bornkamm
- Institute of Clinical Molecular Biology and Tumor Genetics, Helmholtz Zentrum München, Munich, Germany; and
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- Florian R. Greten
- Institute for Tumor Biology and Experimental Therapy, Georg-Speyer-Haus, Frankfurt, Germany;
この論文をさがす
説明
<jats:title>Key Points</jats:title><jats:p>Gpx4 is essential for preventing anemia in mice via inhibiting RIP3-dependent necroptosis in erythroid precursor cells. ROS accumulation and lipid peroxidation in erythroid precursor cells trigger receptor-independent activation of necroptosis.</jats:p>
収録刊行物
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- Blood
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Blood 127 (1), 139-148, 2016-01-07
American Society of Hematology