Catalytic activity of the caspase-8-FLIPL complex inhibits RIPK3-dependent necrosis
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Summary
It is found that caspase-8 prevents RIPK3-dependent necrosis without inducing apoptosis by functioning in a proteolytically active complex with FLICE-like inhibitory protein long (FLIPL, also known as CFLAR), and this complex is required for the protective function.
- Type
- article
- Published
- 2011-03-02
- Cited by
- 1,273
- References
- 33
- OpenAlex
- https://openalex.org/W1975593978
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:4346403
Keywords
Necrosis, Catalysis, Chemistry, Caspase, Apoptosis
References
- Granzyme B Is Inhibited by the Cowpox Virus Serpin Cytokine Response Modifier A(*)
- c‐FLIPL is a dual function regulator for caspase‐8 activation and CD95‐mediated apoptosis
- CrmA expression in T lymphocytes of transgenic mice inhibits CD95 (Fas/APO‐1)‐transduced apoptosis, but does not cause lymphadenopathy or autoimmune disease.
- Fas triggers an alternative, caspase-8–independent cell death pathway using the kinase RIP as effector molecule
- The multifaceted role of Fas signaling in immune cell homeostasis and autoimmunity
- Requirement for caspase-8 in NF-kappaB activation by antigen receptor.
- Two CD95 (APO‐1/Fas) signaling pathways
- Phosphorylation-Driven Assembly of RIP1-RIP3 Complex Regulates Programmed Necrosis and Virus-Induced Inflammation
- Target Protease Specificity of the Viral Serpin CrmA
- Inducible Dimerization and Inducible Cleavage Reveal a Requirement for Both Processes in Caspase-8 Activation*
- Activation of Procaspases by FK506 Binding Protein-Mediated Oligomerization
- Requirement for Casper (c-FLIP) in regulation of death receptor-induced apoptosis and embryonic development.
- Reconstitution of the death-inducing signaling complex reveals a substrate switch that determines CD95-mediated death or survival.
- FLIPL induces caspase-8 activity in the absence of interdomain caspase-8 cleavage and alters substrate specificity
- Role of proteolysis in caspase-8 activation and stabilization.
- Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha.
- Caspase-8 Is Involved in Neovascularization-Promoting Progenitor Cell Functions
- Activation of caspases-8 and -10 by FLIP(L).
- RIP3, an Energy Metabolism Regulator That Switches TNF-Induced Cell Death from Apoptosis to Necrosis
- Lethal effect of the anti-Fas antibody in mice
Cited by
- RIPK3 Regulates Microvascular Endothelial Cell Necroptosis and Cardiac Allograft Rejection
- Guidance for life, cell death, and colorectal neoplasia by netrin dependence receptors.
- TLR activation regulates damage‐associated molecular pattern isoforms released during pyroptosis
- RIP3, a kinase promoting necroptotic cell death, mediates adverse remodelling after myocardial infarction.
- Necroptosis in health and diseases.
- Absence of RIPK3 predicts necroptosis resistance in malignant melanoma
- Necroptosis in tumorigenesis, activation of anti-tumor immunity, and cancer therapy
- The pseudokinase MLKL and the kinase RIPK3 have distinct roles in autoimmune disease caused by loss of death receptor induced apoptosis
- Regulating the balance between necroptosis, apoptosis and inflammation by inhibitors of apoptosis proteins
- Pyroptosis versus necroptosis: similarities, differences, and crosstalk
- In vivo analysis of the role of FADD in the regulation of intestinal epithelial homeostasis
- Cell Death Regulates Injury and Inflammation During Renal Allograft Transplantation
- Proliferative versus Apoptotic Functions of Caspase-8 Hetero or Homo: The Caspase-8 Dimer Controls Cell Fate
- The microenvironment and treatment resistance in chronic lymphocytic leukemia
- General in vitro caspase assay procedures.
- Characterization of the ripoptosome and its components: implications for anti-inflammatory and cancer therapy.
- The serine threonine kinase RIP3: lost and found
- Characterization of Anti-Fungal Inflammasome Responses and the Role of Caspase-8 in Innate Immune Signaling: A Dissertation
- Caspase-8 and RIP Kinases Regulate Bacteria- Induced Innate Immune Responses and Cell Death: A Dissertation
- Elucidating the Molecular Mechanism of CYLD- Mediated Necrosis: A Dissertation
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