RIPK3 deficiency blocks R-2-hydroxyglutarate–induced necroptosis in IDH-mutated AML cells
Mutant isocitrate dehydrogenases (IDHs) produce R-2-hydroxyglutarate (R-2HG), which inhibits the growth of most acute myeloid leukemia (AML) cells.
Shuanghong Zhu +18 more
semanticscholar +1 more source
Bacillus cereus Induces Necroptosis in Microglia via the RIPK1/3‐MLKL Pathway
Bacillus cereus induces necroptosis in murine/human microglia via the RIPK1/3‐MLKL pathway, triggering inflammatory cytokine release—uncovering a new pathogenic mechanism for its severe ocular infection. ABSTRACT Bacillus cereus endophthalmitis is a rapidly progressing intraocular infection that often results in poor visual outcomes due to extensive ...
Jing Yang +7 more
wiley +1 more source
RIPK3 mediates pathogenesis of experimental ventilator-induced lung injury [PDF]
In patients requiring ventilator support, mechanical ventilation (MV) may induce acute lung injury (ventilator-induced lung injury [VILI]). VILI is associated with substantial morbidity and mortality in mechanically ventilated patients with and without acute respiratory distress syndrome. At the cellular level, VILI induces necrotic cell death. However,
Ilias I. Siempos +13 more
openaire +2 more sources
Necrostatin-1 Analogues: Critical Issues on the Specificity, Activity and In Vivo Use in Experimental Disease Models [PDF]
Necrostatin-1 (Nec-1) is widely used in disease models to examine the contribution of receptor-interacting protein kinase (RIPK) 1 in cell death and inflammation.
Callewaert, N +15 more
core +2 more sources
Objectives To investigate the mechanism by which intestinal epithelial cell (IEC) death induces arthritis. Methods IEC death was assessed by staining for necroptosis and apoptosis markers and fluorescence in situ hybridisation at different time points ...
P. Lyu +13 more
semanticscholar +1 more source
Liquid–Liquid Phase Separation in Viral Infection and Immunology
LLPS organizes viral replication and antiviral immunity. Viruses hijack LLPS to form replication factories and evade immune sensors, while hosts assemble LLPS‐driven signaling hubs (e.g., MAVS, RIG‐I, and SGs) to amplify interferon responses. Targeting these condensate interfaces offers novel therapeutic strategies against infectious diseases ...
Jiuzhi Xu +5 more
wiley +1 more source
Necroptosis induced by RIPK3 requires MLKL but not Drp1 [PDF]
Necroptosis is a mechanism by which cells can kill themselves that does not require caspase activity or the presence of the pro-apoptotic Bcl-2 family members Bax or Bak. It has been reported that RIPK3 (receptor interacting protein kinase 3) activates MLKL (mixed lineage kinase domain-like) to cause cell death that requires dynamin-related protein 1 ...
Moujalled, DM +3 more
openaire +3 more sources
Reformulating Pro-Oxidant Microglia in Neurodegeneration [PDF]
In neurodegenerative diseases, microglia-mediated neuroinflammation and oxidative stress are central events. Recent genome-wide transcriptomic analyses of microglial cells under different disease conditions have uncovered a new subpopulation named ...
Alonso Bellido, Isabel María +13 more
core +2 more sources
RIPK3 cleavage is dispensable for necroptosis inhibition but restricts NLRP3 inflammasome activation
Caspase-8 activity is required to inhibit necroptosis during embryogenesis in mice. In vitro studies have suggested that caspase-8 directly cleaves RIPK1, CYLD and the key necroptotic effector kinase RIPK3 to repress necroptosis.
H. Tran +8 more
semanticscholar +1 more source
Cerebral Infarction: Epidemiology, Classification, Mechanisms, Diagnosis, and Management
Within minutes after ischemia onset, deprivation of oxygen and glucose leads to rapid ATP depletion, resulting in failure of Na+/K+‐ATPase activity and membrane depolarization. This ionic imbalance promotes uncontrolled synaptic release of glutamate and excessive activation of postsynaptic NMDA and AMPA receptors.
Meibiao Zhang +4 more
wiley +1 more source

