西亚试剂：Receptor Interacting Protein Kinase-3 Determines Cellular N

Receptor Interacting Protein Kinase-3 Determines Cellular Necrotic Response to TNF-α

Sudan He1,2,Lai Wang3,Lin Miao2,Tao Wang2,Fenghe Du3,Liping Zhao2andXiaodong Wang3,,

1 Graduate Program, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100730, China
2 National Institute of Biological Sciences, No. 7 Science Park Road, Zhongguancun Life Science Park, Beijing 102206, China
3 Howard Hughes Medical Institute, Department of Biochemistry, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA

Smac mimetics induce apoptosis synergistically with TNF- by triggering the formation of a caspase-8-activating complex containing receptor interacting protein kinase-1 (RIPK1). Caspase inhibitors block this form of apoptosis in many types of cells. However, in several other cell lines, caspase inhibitors switch the apoptotic response to necrosis. A genome wide siRNA screen revealed another member of the RIP kinase family, RIP3, to be required for necrosis. The expression of RIP3 in different cell lines correlates with their responsiveness to necrosis induction. The kinase activity of RIP3 is essential for necrosis execution. Upon induction of necrosis, RIP3 is recruited to RIPK1 to form a necrosis-inducing complex. Embryonic fibroblasts from RIP3 knockout mice are resistant to necrosis and RIP3 knockout animals are devoid of inflammation inflicted tissue damage in an acute pancreatitis model. These data indicate RIP3 as the determinant for cellular necrosis in response to TNF- family of death-inducing cytokines.

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