The Pseudokinase MLKL and the Kinase RIPK3 Have Distinct Roles in Autoimmune Disease Caused by Loss of Death-Receptor-Induced Apoptosis

• Published in: Immunity (Cambridge, Mass.) Vol. 45; no. 3; pp. 513 - 526
• Main Authors: Alvarez-Diaz, Silvia, Dillon, Christopher P., Lalaoui, Najoua, Tanzer, Maria C., Rodriguez, Diego A., Lin, Ann, Lebois, Marion, Hakem, Razq, Josefsson, Emma C., O’Reilly, Lorraine A., Silke, John, Alexander, Warren S., Green, Douglas R., Strasser, Andreas
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 20.09.2016; Elsevier Limited
• Subjects: Animals; Apoptosis; Apoptosis - physiology; Autoimmune diseases; Autoimmune Diseases - metabolism; Caspase 8 - metabolism; Cell Death - physiology; Cloning; Evacuations & rescues; Fas-Associated Death Domain Protein - metabolism; Gangrene; Immunoglobulins; Kinases; Ligands; Lymphocytes; Medical research; Mice; Mice, Inbred C57BL; Necrosis - metabolism; Protein Kinases - metabolism; Receptor-Interacting Protein Serine-Threonine Kinases - metabolism; Statistical analysis; Tumor necrosis factor-TNF

The kinases RIPK1 and RIPK3 and the pseudo-kinase MLKL have been identified as key regulators of the necroptotic cell death pathway, although a role for MLKL within the whole animal has not yet been established. Here, we have shown that MLKL deficiency rescued the embryonic lethality caused by loss...