RIPK1 Regulates RIPK3-MLKL-Driven Systemic Inflammation and Emergency Hematopoiesis
Top Cited Papers
- 1 May 2014
- journal article
- Published by Elsevier BV in Cell
- Vol. 157 (5), 1175-1188
- https://doi.org/10.1016/j.cell.2014.04.019
Abstract
No abstract availableKeywords
This publication has 46 references indexed in Scilit:
- TNF can activate RIPK3 and cause programmed necrosis in the absence of RIPK1Cell Death & Disease, 2013
- Survival Function of the FADD-CASPASE-8-cFLIPL ComplexCell Reports, 2012
- Mixed lineage kinase domain-like is a key receptor interacting protein 3 downstream component of TNF-induced necrosisProceedings of the National Academy of Sciences of the United States of America, 2012
- Mixed Lineage Kinase Domain-like Protein Mediates Necrosis Signaling Downstream of RIP3 KinaseCell, 2012
- IL-33 is processed into mature bioactive forms by neutrophil elastase and cathepsin GProceedings of the National Academy of Sciences of the United States of America, 2012
- cIAPs Block Ripoptosome Formation, a RIP1/Caspase-8 Containing Intracellular Cell Death Complex Differentially Regulated by cFLIP IsoformsMolecular Cell, 2011
- RIP3 mediates the embryonic lethality of caspase-8-deficient miceNature, 2011
- Catalytic activity of the caspase-8–FLIPL complex inhibits RIPK3-dependent necrosisNature, 2011
- Differential release of chromatin-bound IL-1α discriminates between necrotic and apoptotic cell death by the ability to induce sterile inflammationProceedings of the National Academy of Sciences of the United States of America, 2010
- Activation of IKK by TNFα Requires Site-Specific Ubiquitination of RIP1 and Polyubiquitin Binding by NEMOMolecular Cell, 2006