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Relevant bibliographies by topics / RIPK3-MLKL-necroptotic pathway

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Academic literature on the topic 'RIPK3-MLKL-necroptotic pathway'

Author: Grafiati

Published: 14 March 2023

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

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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3

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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4

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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5

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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6

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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8

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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9

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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10

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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