Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha.
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Summary
Data indicate RIP3 as the determinant for cellular necrosis in response to TNF-alpha family of death-inducing cytokines.
- Type
- article
- Published
- 2009-06-12
- Cited by
- 1,882
- References
- 38
- Access
- Open access
- OpenAlex
- https://openalex.org/W2052605153
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:2501643
Keywords
Biology, Cell biology, Tumor necrosis factor alpha, Protein kinase A, Receptor
References
- The death domain kinase RIP mediates the TNF-induced NF-kappaB signal.
- Fas triggers an alternative, caspase-8–independent cell death pathway using the kinase RIP as effector molecule
- Tumor necrosis factor can induce both apoptic and necrotic forms of cell lysis.
- Identification of RIP3, a RIP-like kinase that activates apoptosis and NFκB
- RIP3, a Novel Apoptosis-inducing Kinase*
- The CD95(APO-1/Fas) DISC and beyond
- A small molecule Smac mimic potentiates TRAIL- and TNFalpha-mediated cell death.
- Cleavage of the death domain kinase RIP by caspase-8 prompts TNF-induced apoptosis.
- Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors.
- A Role for Tumor Necrosis Factor Receptor-2 and Receptor-interacting Protein in Programmed Necrosis and Antiviral Responses*
- Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition.
- Apoptosis: A Basic Biological Phenomenon with Wide-ranging Implications in Tissue Kinetics
- Cell Death in Pancreatitis
- Caspases: enemies within.
- Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis.
- Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death
- IAP antagonists induce autoubiquitination of c-IAPs, NF-kappaB activation, and TNFalpha-dependent apoptosis.
- IAP antagonists target cIAP1 to induce TNFalpha-dependent apoptosis.
- Identification of a Novel Homotypic Interaction Motif Required for the Phosphorylation of Receptor-interacting Protein (RIP) by RIP3*
- TNF-dependent recruitment of the protein kinase RIP to the TNF receptor-1 signaling complex.
Cited by
- RIPK3 Regulates Microvascular Endothelial Cell Necroptosis and Cardiac Allograft Rejection
- Update in Acute Pancreatitis
- Mitochondrial Control of Cellular Life, Stress, and Death
- The role of SIRT2 in programmed necrosis: implications for stroke and neurodegenerative disorders.
- Rip3 knockdown rescues photoreceptor cell death in blind pde6c zebrafish
- Quantitative phosphoproteomic analysis of RIP3‐dependent protein phosphorylation in the course of TNF‐induced necroptosis
- RIP3, a kinase promoting necroptotic cell death, mediates adverse remodelling after myocardial infarction.
- Necroptosis in health and diseases.
- Structural basis of cell apoptosis and necrosis in TNFR signaling
- FTY720 induces autophagy-related apoptosis and necroptosis in human glioblastoma cells.
- Absence of RIPK3 predicts necroptosis resistance in malignant melanoma
- Live or Let Die: Is There any Cell Death in Podocytes?
- Necroptosis in tumorigenesis, activation of anti-tumor immunity, and cancer therapy
- Cyanidin-3-o-glucoside directly binds to ERα36 and inhibits EGFR-positive triple-negative breast cancer
- Noncanonical cell death program independent of caspase activation cascade and necroptotic modules is elicited by loss of TGFβ-activated kinase 1
- Programmed necrosis in cardiomyocytes: mitochondria, death receptors and beyond
- c-Jun N-terminal kinases differentially regulate TNF- and TLRs-mediated necroptosis through their kinase-dependent and -independent activities
- A RNA Interference Screen Identifies RIP3 as an Essential Inducer of TNF-Induced Programmed Necrosis
- Vemurafenib inhibits necroptosis in normal and pathological conditions as a RIPK1 antagonist
- The Role of Bax and Bak in Necrotic Cell Death
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