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Journal articles on the topic 'RIPK3-MLKL-necroptotic pathway'

Author: Grafiati

Published: 14 March 2023

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1

Ji, Y., L. A. Ward, and C. J. Hawkins. "Reconstitution of Human Necrosome Interactions in Saccharomyces cerevisiae." Biomolecules 11, no. 2 (2021): 153. http://dx.doi.org/10.3390/biom11020153.

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The necrosome is a large-molecular-weight complex in which the terminal effector of the necroptotic pathway, Mixed Lineage Kinase Domain-Like protein (MLKL), is activated to induce necroptotic cell death. The precise mechanism of MLKL activation by the upstream kinase, Receptor Interacting Serine/Threonine Protein Kinase 3 (RIPK3) and the role of Receptor Interacting Serine/Threonine Protein Kinase 1 (RIPK1) in mediating MLKL activation remain incompletely understood. Here, we reconstituted human necrosome interactions in yeast by inducible expression of these necrosome effectors. Functional i

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Yang, Fang-Hao, Xiao-Lei Dong, Guo-Xiang Liu, et al. "The protective effect of C-phycocyanin in male mouse reproductive system." Food & Function 13, no. 5 (2022): 2631–46. http://dx.doi.org/10.1039/d1fo03741b.

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Petrie, Emma J., Richard W. Birkinshaw, Akiko Koide, et al. "Identification of MLKL membrane translocation as a checkpoint in necroptotic cell death using Monobodies." Proceedings of the National Academy of Sciences 117, no. 15 (2020): 8468–75. http://dx.doi.org/10.1073/pnas.1919960117.

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The necroptosis cell death pathway has been implicated in host defense and in the pathology of inflammatory diseases. While phosphorylation of the necroptotic effector pseudokinase Mixed Lineage Kinase Domain-Like (MLKL) by the upstream protein kinase RIPK3 is a hallmark of pathway activation, the precise checkpoints in necroptosis signaling are still unclear. Here we have developed monobodies, synthetic binding proteins, that bind the N-terminal four-helix bundle (4HB) “killer” domain and neighboring first brace helix of human MLKL with nanomolar affinity. When expressed as genetically encode

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Murphy, James M., and James E. Vince. "Post-translational control of RIPK3 and MLKL mediated necroptotic cell death." F1000Research 4 (November 19, 2015): 1297. http://dx.doi.org/10.12688/f1000research.7046.1.

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Several programmed lytic and necrotic-like cell death mechanisms have now been uncovered, including the recently described receptor interacting protein kinase-3 (RIPK3)-mixed lineage kinase domain-like (MLKL)-dependent necroptosis pathway. Genetic experiments have shown that programmed necrosis, including necroptosis, can play a pivotal role in regulating host-resistance against microbial infections. Alternatively, excess or unwarranted necroptosis may be pathological in autoimmune and autoinflammatory diseases. This review highlights the recent advances in our understanding of the post-transl

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Tian, Qing, Bo Qin, Yufan Gu, et al. "ROS-Mediated Necroptosis Is Involved in Iron Overload-Induced Osteoblastic Cell Death." Oxidative Medicine and Cellular Longevity 2020 (October 16, 2020): 1–22. http://dx.doi.org/10.1155/2020/1295382.

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Excess iron has been reported to lead to osteoblastic cell damage, which is a crucial pathogenesis of iron overload-related osteoporosis. However, the cytotoxic mechanisms have not been fully documented. In the present study, we focused on whether necroptosis contributes to iron overload-induced osteoblastic cell death and related underlying mechanisms. Here, we showed that the cytotoxicity of iron overload in osteoblastic cells was mainly due to necrosis, as evidenced by the Hoechst 33258/PI staining, Annexin-V/PI staining, and transmission electronic microscopy. Furthermore, we revealed that

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Samson, André L., Sarah E. Garnish, Joanne M. Hildebrand, and James M. Murphy. "Location, location, location: A compartmentalized view of TNF-induced necroptotic signaling." Science Signaling 14, no. 668 (2021): eabc6178. http://dx.doi.org/10.1126/scisignal.abc6178.

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Necroptosis is a lytic, proinflammatory cell death pathway, which has been implicated in host defense and, when dysregulated, the pathology of many human diseases. The central mediators of this pathway are the receptor-interacting serine/threonine protein kinases RIPK1 and RIPK3 and the terminal executioner, the pseudokinase mixed lineage kinase domain–like (MLKL). Here, we review the chronology of signaling along the RIPK1-RIPK3-MLKL axis and highlight how the subcellular compartmentalization of signaling events controls the initiation and execution of necroptosis. We propose that a network o

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Speir, Mary, Joanne A. O'Donnell, Alyce A. Chen, Akshay A. D'Cruz, and Ben A. Croker. "Ptpn6 Inhibits IL-1 Release from Neutrophils By Regulation of Caspase-8- and Ripk3/Mlkl-Dependent Forms of Cell Death." Blood 132, Supplement 1 (2018): 274. http://dx.doi.org/10.1182/blood-2018-99-120197.

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Abstract Neutrophilic dermatoses are a group of inflammatory skin disorders characterized by sterile infiltrates of neutrophils. These syndromes include pyoderma gangrenosum (PG) and Sweet's syndrome (SS), and they are associated with an increased risk of inflammatory bowel disease, rheumatoid arthritis, and hematologic malignancy, particularly monocytic or myelomonocytic leukemia (AML). IL-1 was first proposed in 1987 as a factor in SS, and the presence of "fragmented neutrophil nuclei" was hypothesized to contribute to disease. IL-1 has subsequently been reported at high levels in lesions of

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Huang, Ming, Shuai Zhu, Huihui Huang, et al. "Integrin-Linked Kinase Deficiency in Collecting Duct Principal Cell Promotes Necroptosis of Principal Cell and Contributes to Kidney Inflammation and Fibrosis." Journal of the American Society of Nephrology 30, no. 11 (2019): 2073–90. http://dx.doi.org/10.1681/asn.2018111162.

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BackgroundNecroptosis is a newly discovered cell death pathway that plays a critical role in AKI. The involvement of integrin-linked kinase (ILK) in necroptosis has not been studied.MethodsWe performed experiments in mice with an Ilk deletion in collecting duct (CD) principal cells (PCs), and cultured tubular epithelial cells treated with an ILK inhibitor or ILK siRNA knockdown.ResultsIlk deletion in CD PCs resulted in acute tubular injury and early mortality in mice. Progressive interstitial fibrosis and inflammation associated with the activation of the canonical TGF-β signaling cascade were

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Picon, Carmen, Anusha Jayaraman, Rachel James, et al. "Neuron-specific activation of necroptosis signaling in multiple sclerosis cortical grey matter." Acta Neuropathologica 141, no. 4 (2021): 585–604. http://dx.doi.org/10.1007/s00401-021-02274-7.

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AbstractSustained exposure to pro-inflammatory cytokines in the leptomeninges is thought to play a major role in the pathogenetic mechanisms leading to cortical pathology in multiple sclerosis (MS). Although the molecular mechanisms underlying neurodegeneration in the grey matter remain unclear, several lines of evidence suggest a prominent role for tumour necrosis factor (TNF). Using cortical grey matter tissue blocks from post-mortem brains from 28 secondary progressive MS subjects and ten non-neurological controls, we describe an increase in expression of multiple steps in the TNF/TNF recep

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Chen, Jing, Renate Kos, Johan Garssen, and Frank Redegeld. "Molecular Insights into the Mechanism of Necroptosis: The Necrosome as a Potential Therapeutic Target." Cells 8, no. 12 (2019): 1486. http://dx.doi.org/10.3390/cells8121486.

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Necroptosis, or regulated necrosis, is an important type of programmed cell death in addition to apoptosis. Necroptosis induction leads to cell membrane disruption, inflammation and vascularization. It plays important roles in various pathological processes, including neurodegeneration, inflammatory diseases, multiple cancers, and kidney injury. The molecular regulation of necroptotic pathway has been intensively studied in recent years. Necroptosis can be triggered by multiple stimuli and this pathway is regulated through activation of receptor-interacting protein kinase 1 (RIPK1), RIPK3 and

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Thomas, Chloe N., Adam M. Thompson, Zubair Ahmed, and Richard J. Blanch. "Retinal Ganglion Cells Die by Necroptotic Mechanisms in a Site-Specific Manner in a Rat Blunt Ocular Injury Model." Cells 8, no. 12 (2019): 1517. http://dx.doi.org/10.3390/cells8121517.

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Closed-globe injury can cause visual loss in military and civilian populations, with retinal cell death, including retinal ganglion cell (RGC) degeneration, leading to irreversible blindness. RGC and optic nerve (ON) degeneration after eye or head injury is termed traumatic optic neuropathy (TON). There are currently no treatments for RGC loss, therefore novel therapeutics to prevent RGC death or promote axonal regeneration are a priority. We investigated necroptotic signaling mechanisms in a rat blunt ocular injury model. After bilateral blunt trauma, protein expression and retinal localizati

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Garnish, Sarah E., and Joanne M. Hildebrand. "Rare catastrophes and evolutionary legacies: human germline gene variants in MLKL and the necroptosis signalling pathway." Biochemical Society Transactions 50, no. 1 (2022): 529–39. http://dx.doi.org/10.1042/bst20210517.

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Programmed cell death has long been characterised as a key player in the development of human disease. Necroptosis is a lytic form of programmed cell death that is universally mediated by the effector protein mixed lineage kinase domain-like (MLKL), a pseudokinase. MLKL's activating kinase, receptor interacting protein kinase 3 (RIPK3), is itself activated within context specific scaffolds of receptor interacting protein kinase 1 (RIPK1), Z-DNA Binding Protein-1 (ZBP1) or TIR domain-containing adaptor inducing interferon-β (TRIF). These core necroptosis modulating proteins have been comprehens

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Cacciola, Nunzio Antonio, Angela Salzano, Nunzia D’Onofrio, et al. "Buffalo Milk Whey Activates Necroptosis and Apoptosis in a Xenograft Model of Colorectal Cancer." International Journal of Molecular Sciences 23, no. 15 (2022): 8464. http://dx.doi.org/10.3390/ijms23158464.

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Recent pharmacological research on milk whey, a byproduct of the dairy industry, has identified several therapeutic properties that could be exploited in modern medicine. In the present study, we investigated the anticancer effects of whey from Mediterranean buffalo (Bubalus bubalis) milk. The antitumour effect of delactosed milk whey (DMW) was evaluated using the HCT116 xenograft mouse model of colorectal cancer (CRC). There were no discernible differences in tumour growth between treated and untreated groups. Nevertheless, haematoxylin and eosin staining of the xenograft tissues showed clear

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Ward, George A., Simone Jueliger, Martin Sims, et al. "Combining the IAP Antagonist Tolinapant with a DNA Hypomethylating Agent Enhances Immunogenic Cell Death in Preclinical Models of T-Cell Lymphoma." Blood 138, Supplement 1 (2021): 3986. http://dx.doi.org/10.1182/blood-2021-152176.

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Abstract Introduction: Tolinapant is a potent, non-peptidomimetic antagonist of cIAP1, cIAP2 and XIAP. In ongoing Phase 2 trial (NCT02503423), tolinapant has shown activity against highly pre-treated peripheral and cutaneous T-cell lymphoma (Samaniego et al., Hematological Oncology, 2019). Hypomethylating agents (HMAs) have also shown clinical responses in some subsets of PTCL (Lemonnier et al., Blood, 2019). Both HMAs and IAP antagonists show immunomodulatory anti-cancer potential in pre-clinical studies. A Phase 1 clinical study investigating the combination of tolinapant and ASTX727 (oral d

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Lyu, Ah-Ra, Tae-Hwan Kim, Sun-Ae Shin, et al. "Hearing Impairment in a Mouse Model of Diabetes Is Associated with Mitochondrial Dysfunction, Synaptopathy, and Activation of the Intrinsic Apoptosis Pathway." International Journal of Molecular Sciences 22, no. 16 (2021): 8807. http://dx.doi.org/10.3390/ijms22168807.

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Although previous studies continuously report an increased risk of hearing loss in diabetes patients, the impact of the disease on the inner ear remains unexplored. Herein, we examine the pathophysiology of diabetes-associated hearing impairment and cochlear synaptopathy in a mouse model of diabetes. Male B6.BKS(D)-Leprdb/J (db/db, diabetes) and heterozygote (db/+, control) mice were assigned into each experimental group (control vs. diabetes) based on the genotype and tested for hearing sensitivity every week from 6 weeks of age. Each cochlea was collected for histological and biological assa

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Huang, Huihui, William W. Jin, Ming Huang, et al. "Gentamicin-Induced Acute Kidney Injury in an Animal Model Involves Programmed Necrosis of the Collecting Duct." Journal of the American Society of Nephrology 31, no. 9 (2020): 2097–115. http://dx.doi.org/10.1681/asn.2019020204.

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BackgroundGentamicin is a potent aminoglycoside antibiotic that targets gram-negative bacteria, but nephrotoxicity limits its clinical application. The cause of gentamicin-induced AKI has been attributed mainly to apoptosis of the proximal tubule cells. However, blocking apoptosis only partially attenuates gentamicin-induced AKI in animals.MethodsMice treated with gentamicin for 7 days developed AKI, and programmed cell death pathways were examined using pharmacologic inhibitors and in RIPK3-deficient mice. Effects in porcine and murine kidney cell lines were also examined.ResultsGentamicin ca

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Santos, Leonardo Duarte, Krist Helen Antunes, Stéfanie Primon Muraro, et al. "TNF-mediated alveolar macrophage necroptosis drives disease pathogenesis during respiratory syncytial virus infection." European Respiratory Journal 57, no. 6 (2020): 2003764. http://dx.doi.org/10.1183/13993003.03764-2020.

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Respiratory syncytial virus (RSV) is the major cause of acute bronchiolitis in infants under 2 years old. Necroptosis has been implicated in the outcomes of respiratory virus infections. We report that RSV infection triggers necroptosis in primary mouse macrophages and human monocytes in a RIPK1-, RIPK3- and MLKL-dependent manner. Moreover, necroptosis pathways are harmful to RSV clearance from alveolar macrophages. Additionally, Ripk3−/− mice were protected from RSV-induced weight loss and presented with reduced viral loads in the lungs.Alveolar macrophage depletion also protected mice from w

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D'Cruz, Akshay A., Meghan Bliss-Moreau, Maria Ericcson, and Ben A. Croker. "Mlkl Pores Release Neutrophil Extracellular Traps in Necroptotic Neutrophils." Blood 126, no. 23 (2015): 2200. http://dx.doi.org/10.1182/blood.v126.23.2200.2200.

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Abstract Neutrophil extracellular traps (NETs) are networks of extracellular nuclear DNA and microbicidal proteins released from neutrophils in response to tissue damage and infection. Despite evidence of pathogenic roles for NETs in systemic lupus erythematosus, rheumatoid arthritis, diabetes, artherosclerosis and Alzheimer's disease, the major biochemical pathways controlling their formation remains poorly understood. Apoptosis does not contribute to NET formation but the role of regulated non-apoptotic cell death pathways such as necroptosis is not known. We have investigated the role of po

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Belizário, José, Luiz Vieira-Cordeiro, and Sylvia Enns. "Necroptotic Cell Death Signaling and Execution Pathway: Lessons from Knockout Mice." Mediators of Inflammation 2015 (2015): 1–15. http://dx.doi.org/10.1155/2015/128076.

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Under stress conditions, cells in living tissue die by apoptosis or necrosis depending on the activation of the key molecules within a dying cell that either transduce cell survival or death signals that actively destroy the sentenced cell. Multiple extracellular (pH, heat, oxidants, and detergents) or intracellular (DNA damage and Ca2+overload) stress conditions trigger various types of the nuclear, endoplasmic reticulum (ER), cytoplasmatic, and mitochondrion-centered signaling events that allow cells to preserve the DNA integrity, protein folding, energetic, ionic and redox homeostasis, thus

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Daley-Bauer, Lisa P., Linda Roback, Lynsey N. Crosby, et al. "Mouse cytomegalovirus M36 and M45 death suppressors cooperate to prevent inflammation resulting from antiviral programmed cell death pathways." Proceedings of the National Academy of Sciences 114, no. 13 (2017): E2786—E2795. http://dx.doi.org/10.1073/pnas.1616829114.

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The complex interplay between caspase-8 and receptor-interacting protein (RIP) kinase RIP 3 (RIPK3) driving extrinsic apoptosis and necroptosis is not fully understood. Murine cytomegalovirus triggers both apoptosis and necroptosis in infected cells; however, encoded inhibitors of caspase-8 activity (M36) and RIP3 signaling (M45) suppress these antiviral responses. Here, we report that this virus activates caspase-8 in macrophages to trigger apoptosis that gives rise to secondary necroptosis. Infection with double-mutant ΔM36/M45mutRHIM virus reveals a signaling pattern in which caspase-8 acti

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Lai, Ming-Zong, Yung-Hsuan Wu, Ting-Fang Chou, et al. "Regulation of necroptosis by targeting tumor suppressor death-associated protein kinase 1." Journal of Immunology 204, no. 1_Supplement (2020): 144.11. http://dx.doi.org/10.4049/jimmunol.204.supp.144.11.

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Abstract Death-associated protein kinase 1 (DAPK1, DAPk, DAPK) is known for its involvement in apoptosis and autophagy-associated cell death. Here, we identified an unexpected function of DAPK1 in suppressing necroptosis. DAPK1-deficiency renders macrophages and dendritic cells susceptible to necroptotic induction by different stimuli. We also observed an inhibitory role for DAPK1 in necroptosis in HT-29 cells, since knockdown or knockout of DAPK1 in such cells increased their sensitivity to necroptosis. Increased necroptosis was associated with enhanced formation of the RIPK1-RIPK3-MLKL compl

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Bedient, Lori, Swechha Mainali Pokharel, Kim Roxana Chiok Casimiro, and Santanu Bose. "Lytic cell death mechanisms in human respiratory syncytial virus-infected macrophages." Journal of Immunology 204, no. 1_Supplement (2020): 93.16. http://dx.doi.org/10.4049/jimmunol.204.supp.93.16.

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Abstract Human respiratory syncytial virus (hRSV) is the most common cause of viral pneumonia in infants and children worldwide and creates significant airway disease in immunocompromised people and the elderly. Inflammation induced by hRSV infection is responsible for its hallmark manifestations of bronchiolitis and pneumonia. The cellular debris created secondary to lytic cell death of infected cells is a potent initiator of this inflammation. Macrophages are known to play a pivotal role in the early innate immune and inflammatory response to viral pathogens. While previous studies have inve

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Kim, Do-Yeon, Yea-Hyun Leem, Jin-Sun Park, et al. "RIPK1 Regulates Microglial Activation in Lipopolysaccharide-Induced Neuroinflammation and MPTP-Induced Parkinson’s Disease Mouse Models." Cells 12, no. 3 (2023): 417. http://dx.doi.org/10.3390/cells12030417.

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Increasing evidence suggests a pivotal role of receptor-interacting protein kinase 1 (RIPK1), an initiator of necroptosis, in neuroinflammation. However, the precise role of RIPK1 in microglial activation remains unclear. In the present study, we explored the role of RIPK1 in lipopolysaccharide (LPS)-induced neuroinflammation and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD model mice by using RIPK1-specific inhibitors necrostatin-1 (Nec-1) and necrostatin-1 stable (Nec-1s). Nec-1/Nec-1s or RIPK1 siRNA inhibited the production of proinflammatory molecules and the phosphorylat

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Garnish, Sarah E., Yanxiang Meng, Akiko Koide, et al. "Conformational interconversion of MLKL and disengagement from RIPK3 precede cell death by necroptosis." Nature Communications 12, no. 1 (2021). http://dx.doi.org/10.1038/s41467-021-22400-z.

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AbstractPhosphorylation of the MLKL pseudokinase by the RIPK3 kinase leads to MLKL oligomerization, translocation to, and permeabilization of, the plasma membrane to induce necroptotic cell death. The precise choreography of MLKL activation remains incompletely understood. Here, we report Monobodies, synthetic binding proteins, that bind the pseudokinase domain of MLKL within human cells and their crystal structures in complex with the human MLKL pseudokinase domain. While Monobody-32 constitutively binds the MLKL hinge region, Monobody-27 binds MLKL via an epitope that overlaps the RIPK3 bind

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Meng, Yanxiang, Katherine A. Davies, Cheree Fitzgibbon, et al. "Human RIPK3 maintains MLKL in an inactive conformation prior to cell death by necroptosis." Nature Communications 12, no. 1 (2021). http://dx.doi.org/10.1038/s41467-021-27032-x.

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AbstractThe ancestral origins of the lytic cell death mode, necroptosis, lie in host defense. However, the dysregulation of necroptosis in inflammatory diseases has led to widespread interest in targeting the pathway therapeutically. This mode of cell death is executed by the terminal effector, the MLKL pseudokinase, which is licensed to kill following phosphorylation by its upstream regulator, RIPK3 kinase. The precise molecular details underlying MLKL activation are still emerging and, intriguingly, appear to mechanistically-diverge between species. Here, we report the structure of the human

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Moujalled, Diane, Pradnya Gangatirkar, Maria Kauppi, et al. "The necroptotic cell death pathway operates in megakaryocytes, but not in platelet synthesis." Cell Death & Disease 12, no. 1 (2021). http://dx.doi.org/10.1038/s41419-021-03418-z.

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AbstractNecroptosis is a pro-inflammatory cell death program executed by the terminal effector, mixed lineage kinase domain-like (MLKL). Previous studies suggested a role for the necroptotic machinery in platelets, where loss of MLKL or its upstream regulator, RIPK3 kinase, impacted thrombosis and haemostasis. However, it remains unknown whether necroptosis operates within megakaryocytes, the progenitors of platelets, and whether necroptotic cell death might contribute to or diminish platelet production. Here, we demonstrate that megakaryocytes possess a functional necroptosis signalling casca

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Preston, Simon P., Cody C. Allison, Jan Schaefer, et al. "A necroptosis-independent function of RIPK3 promotes immune dysfunction and prevents control of chronic LCMV infection." Cell Death & Disease 14, no. 2 (2023). http://dx.doi.org/10.1038/s41419-023-05635-0.

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AbstractNecroptosis is a lytic and inflammatory form of cell death that is highly constrained to mitigate detrimental collateral tissue damage and impaired immunity. These constraints make it difficult to define the relevance of necroptosis in diseases such as chronic and persistent viral infections and within individual organ systems. The role of necroptotic signalling is further complicated because proteins essential to this pathway, such as receptor interacting protein kinase 3 (RIPK3) and mixed lineage kinase domain-like (MLKL), have been implicated in roles outside of necroptotic signalli

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Chen, Jing, Shiyu Wang, Bart Blokhuis, Rob Ruijtenbeek, Johan Garssen, and Frank Redegeld. "Cell Death Triggers Induce MLKL Cleavage in Multiple Myeloma Cells, Which may Promote Cell Death." Frontiers in Oncology 12 (July 28, 2022). http://dx.doi.org/10.3389/fonc.2022.907036.

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Necroptosis is a type of caspase-independent programmed cell death that has been implicated in cancer development. Activation of the canonical necroptotic pathway is often characterized with successive signaling events as the phosphorylation of mixed lineage kinase domain-like (MLKL) by receptor-interacting protein kinase-3 (RIPK3), followed by MLKL oligomerization and plasma membrane rupture. Here, we demonstrate that omega-3 polyunsaturated fatty acids DHA/EPA and the proteasome inhibitor bortezomib induce necroptosis in human multiple myeloma (MM) cells in a RIPK3 independent manner. In add

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Tovey Crutchfield, Emma C., Sarah E. Garnish, Jessica Day, et al. "MLKL deficiency protects against low-grade, sterile inflammation in aged mice." Cell Death & Differentiation, February 8, 2023. http://dx.doi.org/10.1038/s41418-023-01121-4.

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AbstractMLKL and RIPK3 are the core signaling proteins of the inflammatory cell death pathway, necroptosis, which is a known mediator and modifier of human disease. Necroptosis has been implicated in the progression of disease in almost every physiological system and recent reports suggest a role for necroptosis in aging. Here, we present the first comprehensive analysis of age-related histopathological and immunological phenotypes in a cohort of Mlkl–/– and Ripk3–/– mice on a congenic C57BL/6 J genetic background. We show that genetic deletion of Mlkl in female mice interrupts immune system a

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Li, Dianrong, Jie Chen, Jia Guo та ін. "A phosphorylation of RIPK3 kinase initiates an intracellular apoptotic pathway that promotes prostaglandin2α-induced corpus luteum regression". eLife 10 (24 травня 2021). http://dx.doi.org/10.7554/elife.67409.

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Receptor-interacting serine/threonine-protein kinase 3 (RIPK3) normally signals to necroptosis by phosphorylating MLKL. We report here that when the cellular RIPK3 chaperone Hsp90/CDC37 level is low, RIPK3 also signals to apoptosis. The apoptotic function of RIPK3 requires phosphorylation of the serine 165/threonine 166 sites on its kinase activation loop, resulting in inactivation of RIPK3 kinase activity while gaining the ability to recruit RIPK1, FADD, and caspase-8 to form a cytosolic caspase-activating complex, thereby triggering apoptosis. We found that PGF2α induces RIPK3 expression in

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Zhang, Wenbin, Weiliang Fan, Jia Guo, and Xiaodong Wang. "Osmotic stress activates RIPK3/MLKL-mediated necroptosis by increasing cytosolic pH through a plasma membrane Na ⁺ /H ⁺ exchanger." Science Signaling 15, no. 734 (2022). http://dx.doi.org/10.1126/scisignal.abn5881.

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Necroptosis is a form of cell death triggered by stimuli such as the tumor necrosis factor family of cytokines, which induce necrotic cell death through the RIPK1-RIPK3-MLKL pathway. We report here that necroptosis is also activated by extracellular osmotic stresses. Unlike the previously identified inducers of necroptosis, osmotic stress stimulated necroptosis through the direct activation of the kinase activity of RIPK3 by an increase in cytosolic pH mediated by the Na + /H + exchanger SLC9A1. Knockout, knockdown, or chemical inhibition of SLC9A1 blocked necroptosis induced by osmotic stress

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Águeda-Pinto, Ana, Luís Q. Alves, Fabiana Neves, et al. "Convergent Loss of the Necroptosis Pathway in Disparate Mammalian Lineages Shapes Viruses Countermeasures." Frontiers in Immunology 12 (September 1, 2021). http://dx.doi.org/10.3389/fimmu.2021.747737.

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Programmed cell death is a vital process in the life cycle of organisms. Necroptosis, an evolutionary form of programmed necrosis, contributes to the innate immune response by killing pathogen-infected cells. This virus-host interaction pathway is organized around two components: the receptor-interacting protein kinase 3 (RIPK3), which recruits and phosphorylates the mixed lineage kinase-like protein (MLKL), inducing cellular plasma membrane rupture and cell death. Critically, the presence of necroptotic inhibitors in viral genomes validates necroptosis as an important host defense mechanism.

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Jacobsen, Annette V., Catia L. Pierotti, Kym N. Lowes, et al. "The Lck inhibitor, AMG-47a, blocks necroptosis and implicates RIPK1 in signalling downstream of MLKL." Cell Death & Disease 13, no. 4 (2022). http://dx.doi.org/10.1038/s41419-022-04740-w.

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AbstractNecroptosis is a form of caspase-independent programmed cell death that arises from disruption of cell membranes by the mixed lineage kinase domain-like (MLKL) pseudokinase after its activation by the upstream kinases, receptor interacting protein kinase (RIPK)-1 and RIPK3, within a complex known as the necrosome. Dysregulated necroptosis has been implicated in numerous inflammatory pathologies. As such, new small molecule necroptosis inhibitors are of great interest, particularly ones that operate downstream of MLKL activation, where the pathway is less well defined. To better underst

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Wang, Xiaoliang, Damjan Avsec, Aleš Obreza, Shida Yousefi, Irena Mlinarič-Raščan, and Hans-Uwe Simon. "A Putative Serine Protease is Required to Initiate the RIPK3-MLKL—Mediated Necroptotic Death Pathway in Neutrophils." Frontiers in Pharmacology 11 (January 21, 2021). http://dx.doi.org/10.3389/fphar.2020.614928.

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Adhesion receptors, such as CD44, have been shown to activate receptor interacting protein kinase-3 (RIPK3)—mixed lineage kinase-like (MLKL) signaling, leading to a non-apoptotic cell death in human granulocyte/macrophage colony-stimulating factor (GM-CSF) – primed neutrophils. The signaling events of this necroptotic pathway, however, remain to be investigated. In the present study, we report the design, synthesis, and characterization of a series of novel serine protease inhibitors. Two of these inhibitors, compounds 1 and 3, were able to block CD44-triggered necroptosis in GM-CSF-primed neu

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Yu, Ziyu, Nan Jiang, Wenru Su, and Yehong Zhuo. "Necroptosis: A Novel Pathway in Neuroinflammation." Frontiers in Pharmacology 12 (July 12, 2021). http://dx.doi.org/10.3389/fphar.2021.701564.

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Neuroinflammation is a complex inflammatory process in the nervous system that is expected to play a significant role in neurological diseases. Necroptosis is a kind of necrosis that triggers innate immune responses by rupturing dead cells and releasing intracellular components; it can be caused by Toll-like receptor (TLR)-3 and TLR-4 agonists, tumor necrosis factor (TNF), certain microbial infections, and T cell receptors. Necroptosis signaling is modulated by receptor-interacting protein kinase (RIPK) 1 when the activity of caspase-8 becomes compromised. Activated death receptors (DRs) cause

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Kluck, George E. G., Alexander S. Qian, Emmanuel H. Sakarya, Henry Quach, Yak D. Deng, and Bernardo L. Trigatti. "Apolipoprotein A1 Protects Against Necrotic Core Development in Atherosclerotic Plaques: PDZK1-Dependent HDL (High-Density Lipoprotein) Suppression of Necroptosis in Macrophages." Arteriosclerosis, Thrombosis, and Vascular Biology, November 10, 2022. http://dx.doi.org/10.1161/atvbaha.122.318062.

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BACKGROUND: Atherosclerosis is a chronic disease affecting artery wall and a major contributor to cardiovascular diseases. Large necrotic cores increase risk of plaque rupture leading to thrombus formation. Necrotic cores are rich in debris from dead macrophages. Programmed necrosis (necroptosis) contributes to necrotic core formation. HDL (high-density lipoprotein) exerts direct atheroprotective effects on different cells within atherosclerotic plaques. Some of these depend on the SR-B1 (scavenger receptor class B type 1) and the adapter protein PDZK1 (postsynaptic density protein/Drosophila

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Xiao, Peng, Changhua Wang, Jie Li, et al. "COP9 Signalosome Suppresses RIPK1-RIPK3–Mediated Cardiomyocyte Necroptosis in Mice." Circulation: Heart Failure 13, no. 8 (2020). http://dx.doi.org/10.1161/circheartfailure.120.006996.

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Background: Mechanisms governing the induction of heart failure by the impairment of autophagy and the ubiquitin-proteasome system and the molecular pathways to cardiomyocyte necrosis remain incompletely understood. COPS8 is an essential subunit of the COP9 (COnstitutive Photomorphogenesis 9) signalosome, a key regulator of ubiquitination. Mice with cardiomyocyte-restricted knockout of Cops8 (Cops8-cko) show autophagic and ubiquitin-proteasome system malfunction and massive cardiomyocyte necrosis followed by acute heart failure and premature death, providing an excellent animal model to addres

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Jayaraman, Anusha, Thein Than Htike, Rachel James, Carmen Picon, and Richard Reynolds. "TNF-mediated neuroinflammation is linked to neuronal necroptosis in Alzheimer's disease hippocampus." Acta Neuropathologica Communications 9, no. 1 (2021). http://dx.doi.org/10.1186/s40478-021-01264-w.

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AbstractThe pathogenetic mechanisms underlying neuronal death and dysfunction in Alzheimer’s disease (AD) remain unclear. However, chronic neuroinflammation has been implicated in stimulating or exacerbating neuronal damage. The tumor necrosis factor (TNF) superfamily of cytokines are involved in many systemic chronic inflammatory and degenerative conditions and are amongst the key mediators of neuroinflammation. TNF binds to the TNFR1 and TNFR2 receptors to activate diverse cellular responses that can be either neuroprotective or neurodegenerative. In particular, TNF can induce programmed nec

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Altman, Aaron M., Michael J. Miller, Jamil Mahmud, Nicholas A. Smith, and Gary C. Chan. "Human Cytomegalovirus-Induced Autophagy Prevents Necroptosis of Infected Monocytes." Journal of Virology 94, no. 22 (2020). http://dx.doi.org/10.1128/jvi.01022-20.

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ABSTRACT Key to the viral dissemination strategy of human cytomegalovirus (HCMV) is the induction of monocyte survival, where monocytes are normally short-lived cells. Autophagy is a cellular process that preserves cellular homeostasis and promotes cellular survival during times of stress. We found that HCMV rapidly induced autophagy within infected monocytes. The early induction of autophagy during HCMV infection was distinctly required for the survival of HCMV-infected monocytes, as repression of autophagosome formation led to cellular death of infected cells but had no effect on the viabili

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Karunakaran, Denuja, My-Anh Nguyen, Michele Geoffrion та ін. "RIPK1 Expression Associates with Inflammation in Early Atherosclerosis in Humans and Can be Therapeutically Silenced to Reduce NF-κB Activation and Atherogenesis in Mice". Circulation, 23 листопада 2020. http://dx.doi.org/10.1161/circulationaha.118.038379.

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Background: Chronic activation of the innate immune system drives inflammation and contributes directly to atherosclerosis. Previously, we showed that macrophages in the atherogenic plaque undergo RIPK3-MLKL-dependent programmed necroptosis in response to sterile ligands such as oxidized LDL and damage-associated patterns (DAMPs) and necroptosis is active in advanced atherosclerotic plaques. Upstream of the RIPK3-MLKL necroptotic machinery lies RIPK1, which acts as a master switch that controls whether the cell undergoes NFκB-dependent inflammation, caspase-dependent apoptosis or necroptosis i

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Fan, Guo-Chang, Dongze Qin, Xiaohong Wang, Liwang Yang, Wei Huang, and Yigang Wang. "Abstract 325: miR-223 Negatively Regulate Ischemia/Reperfusion-induced Cardiac Necroptosis." Circulation Research 117, suppl_1 (2015). http://dx.doi.org/10.1161/res.117.suppl_1.325.

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It is well known that myocardial ischemia/reperfusion (I/R) causes myocyte apoptosis and necrosis. For many years, apoptosis was considered to be the only form of gene-regulated cell death, whereas necrosis was thought as a passive accidental cell death. Recent studies, however, clearly indicate that necrosis can be controlled by multiple genes, and RIPK1/3-regulated necrosis, called necroptosis, has gained well attention. We and others previously showed that miR-223, an anti-inflammatory miRNA, was greatly up-regulated in the infarcted heart. To test whether miR-223 regulates I/R-induced card

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Patton, Timothy, Zhe Zhao, Xin Yi Lim, et al. "RIPK3 controls MAIT cell accumulation during development but not during infection." Cell Death & Disease 14, no. 2 (2023). http://dx.doi.org/10.1038/s41419-023-05619-0.

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AbstractCell death mechanisms in T lymphocytes vary according to their developmental stage, cell subset and activation status. The cell death control mechanisms of mucosal-associated invariant T (MAIT) cells, a specialized T cell population, are largely unknown. Here we report that MAIT cells express key necroptotic machinery; receptor-interacting protein kinase 3 (RIPK3) and mixed lineage kinase domain-like (MLKL) protein, in abundance. Despite this, we discovered that the loss of RIPK3, but not necroptotic effector MLKL or apoptotic caspase-8, specifically increased MAIT cell abundance at st

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Rodriguez, Diego A., Giovanni Quarato, Swantje Liedmann, et al. "Caspase-8 and FADD prevent spontaneous ZBP1 expression and necroptosis." Proceedings of the National Academy of Sciences 119, no. 41 (2022). http://dx.doi.org/10.1073/pnas.2207240119.

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The absence of Caspase-8 or its adapter, Fas-associated death domain (FADD), results in activation of receptor interacting protein kinase-3 (RIPK3)- and mixed-lineage kinase-like (MLKL)–dependent necroptosis in vivo. Here, we show that spontaneous activation of RIPK3, phosphorylation of MLKL, and necroptosis in Caspase-8– or FADD-deficient cells was dependent on the nucleic acid sensor, Z-DNA binding protein-1 (ZBP1). We genetically engineered a mouse model by a single insertion of FLAG tag onto the N terminus of endogenous MLKL ( Mlkl FLAG/FLAG ), creating an inactive form of MLKL that permit

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Jonczyk, Agnieszka Walentyna, Katarzyna Karolina Piotrowska-Tomala та Dariusz Jan Skarzynski. "Effects of prostaglandin F2α (PGF2α) on cell-death pathways in the bovine corpus luteum (CL)". BMC Veterinary Research 15, № 1 (2019). http://dx.doi.org/10.1186/s12917-019-2167-3.

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Abstract Background Prostaglandin F2α (PGF2α) may differentially affect viability of luteal cells by inducing either proliferation or cell death (via apoptosis or necroptosis). The diverse effects of PGF2α may depend on its local vs. systemic actions. In our study, we determined changes in expression of genes related to: (i) apoptosis: caspase (CASP) 3, CASP8, BCL2 associated X (BAX), B-cell lymphoma 2 (BCL2) and (ii) necroptosis: receptor-interacting protein kinase (RIPK) 1, RIPK3, cylindromatosis (CYLD), and mixed lineage kinase domain-like (MLKL) in the early and mid-stage corpus luteum (CL

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Puertas-Neyra, Kevin, Nadia Galindo-Cabello, Leticia A. Hernández-Rodríguez, et al. "Programmed Cell Death and Autophagy in an in vitro Model of Spontaneous Neuroretinal Degeneration." Frontiers in Neuroanatomy 16 (February 11, 2022). http://dx.doi.org/10.3389/fnana.2022.812487.

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Retinal neurodegenerative diseases are the leading causes of visual impairment and irreversible blindness worldwide. Although the retinal response to injury remains closely similar between different retinal neurodegenerative diseases, available therapeutic alternatives are only palliative, too expensive, or very specific, such as gene therapy. In that sense, the development of broad-spectrum neuroprotective therapies seems to be an excellent option. In this regard, it is essential to identify molecular targets involved in retinal degeneration, such as cell death mechanisms. Apoptosis has been

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Molnár, Tamás, Anett Mázló, Vera Tslaf, Attila Gábor Szöllősi, Gabriella Emri, and Gábor Koncz. "Current translational potential and underlying molecular mechanisms of necroptosis." Cell Death & Disease 10, no. 11 (2019). http://dx.doi.org/10.1038/s41419-019-2094-z.

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Abstract Cell death has a fundamental impact on the evolution of degenerative disorders, autoimmune processes, inflammatory diseases, tumor formation and immune surveillance. Over the past couple of decades extensive studies have uncovered novel cell death pathways, which are independent of apoptosis. Among these is necroptosis, a tightly regulated, inflammatory form of cell death. Necroptosis contribute to the pathogenesis of many diseases and in this review, we will focus exclusively on necroptosis in humans. Necroptosis is considered a backup mechanism of apoptosis, but the in vivo appearan

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