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RIPK3

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https://www.readbyqxmd.com/read/29449668/rhinovirus-3c-protease-suppresses-apoptosis-and-triggers-caspase-independent-cell-death
#1
Mark Lötzerich, Pascal S Roulin, Karin Boucke, Robert Witte, Oleg Georgiev, Urs F Greber
Apoptosis and programmed necrosis (necroptosis) determine cell fate, and antagonize infection. Execution of these complementary death pathways involves the formation of receptor-interacting protein kinase 1 (RIPK1) containing complexes. RIPK1 binds to adaptor proteins, such as TRIF (Toll-IL-1 receptor-domain-containing-adaptor-inducing interferon-beta factor), FADD (Fas-associated-protein with death domain), NEMO (NF-κB regulatory subunit IKKγ), SQSTM1 (sequestosome 1/p62), or RIPK3 (receptor-interacting protein kinase 3), which are involved in RNA sensing, NF-κB signaling, autophagosome formation, apoptosis, and necroptosis...
February 15, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29449584/crispr-whole-genome-screening-identifies-new-necroptosis-regulators-and-ripk1-alternative-splicing
#2
Marinella G Callow, Colin Watanabe, Katherine E Wickliffe, Russell Bainer, Sarah Kummerfield, Julie Weng, Trinna Cuellar, Vasantharajan Janakiraman, Honglin Chen, Ben Chih, Yuxin Liang, Benjamin Haley, Kim Newton, Michael R Costa
The necroptotic cell death pathway is a key component of human pathogen defense that can become aberrantly derepressed during tissue homeostasis to contribute to multiple types of tissue damage and disease. While formation of the necrosome kinase signaling complex containing RIPK1, RIPK3, and MLKL has been extensively characterized, additional mechanisms of its regulation and effector functions likely remain to be discovered. We screened 19,883 mouse protein-coding genes by CRISPR/Cas9-mediated gene knockout for resistance to cytokine-induced necroptosis and identified 112 regulators and mediators of necroptosis, including 59 new candidate pathway components with minimal or no effect on cell growth in the absence of necroptosis induction...
February 15, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29445128/the-brace-helices-of-mlkl-mediate-interdomain-communication-and-oligomerisation-to-regulate-cell-death-by-necroptosis
#3
Katherine A Davies, Maria C Tanzer, Michael D W Griffin, Yee Foong Mok, Samuel N Young, Rui Qin, Emma J Petrie, Peter E Czabotar, John Silke, James M Murphy
The programmed cell death pathway, necroptosis, relies on the pseudokinase, Mixed Lineage Kinase domain-Like (MLKL), for cellular execution downstream of death receptor or Toll-like receptor ligation. Receptor-interacting protein kinase-3 (RIPK3)-mediated phosphorylation of MLKL's pseudokinase domain leads to MLKL switching from an inert to activated state, where exposure of the N-terminal four-helix bundle (4HB) 'executioner' domain leads to cell death. The precise molecular details of MLKL activation, including the stoichiometry of oligomer assemblies, mechanisms of membrane translocation and permeabilisation, remain a matter of debate...
February 14, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29444413/involvement-of-alveolar-epithelial-cell-necroptosis-in-ipf-pathogenesis
#4
Ji-Min Lee, Masahiro Yoshida, Mi-So Kim, June-Hyuk Lee, Ae-Rin Baek, An Soo Jang, Do Jin Kim, Shunsuke Minagawa, Su Sie Chin, Choon-Sik Park, Jun Araya, Kazuyoshi Kuwano, Sung Woo Park
RATIONALE: Alveolar epithelial cell (AEC) injury leading to cell death is involved in the process of fibrosis development during idiopathic pulmonary fibrosis (IPF). Among regulated/programmed cell death, the excessive apoptosis of AECs has been widely implicated in IPF pathogenesis. Necroptosis is a type of regulated/programmed necrosis. A multiprotein complex composed of receptor-interacting protein kinase-1 and -3 (RIPK1/3) plays a key regulatory role in initiating necroptosis. Although necroptosis participates in disease pathogeneses through the release of damage-associated molecular patterns (DAMPs), its association with IPF progression remains elusive...
February 14, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29434332/the-p55tnfr-ikk2-ripk3-axis-orchestrates-arthritis-by-regulating-death-and-inflammatory-pathways-in-synovial-fibroblasts
#5
Marietta Armaka, Caroline Ospelt, Manolis Pasparakis, George Kollias
NFκB activation and regulated cell death are important in tissue homeostasis, inflammation and pathogenesis. Here we show the role of the p55TNFR-IKK2l-Ripk3 axis in the regulation of synovial fibroblast homeostasis and pathogenesis in TNF-mediated mouse models of arthritis. Mesenchymal-specific p55TNFR triggering is indispensable for arthritis in acute and chronic TNF-dependent models. IKK2 in joint mesenchymal cells is necessary for the development of cartilage destruction and bone erosion; however, in its absence synovitis still develops...
February 12, 2018: Nature Communications
https://www.readbyqxmd.com/read/29434255/ripk1-dependent-cell-death-a-novel-target-of-the-aurora-kinase-inhibitor-tozasertib-vx-680
#6
Sofie Martens, Vera Goossens, Lars Devisscher, Sam Hofmans, Polien Claeys, Marnik Vuylsteke, Nozomi Takahashi, Koen Augustyns, Peter Vandenabeele
The Aurora kinase family (Aurora A, B and C) are crucial regulators of several mitotic events, including cytokinesis. Increased expression of these kinases is associated with tumorigenesis and several compounds targeting Aurora kinase are under evaluation in clinical trials (a.o. AT9283, AZD1152, Danusertib, MLN8054). Here, we demonstrate that the pan-Aurora kinase inhibitor Tozasertib (VX-680 and MK-0457) not only causes cytokinesis defects through Aurora kinase inhibition, but is also a potent inhibitor of necroptosis, a cell death process regulated and executed by the RIPK1, RIPK3 and MLKL signalling axis...
February 12, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29426003/programmed-necrosis-in-heart-disease-molecular-mechanisms-and-clinical-implications
#7
Hong Zhu, Aijun Sun
Programmed cell death plays an essential role in myocardial homeostasis and pathology. Three distinct forms of programmed cell death have been identified, namely apoptosis, necrosis, and autophagic cell death. Necrosis, previously known as an unregulated form of cell death, has been recognized as a highly regulated process now and attracted great attention over the past decade. Programmed necrosis mainly refers to necroptosis, pyroptosis, ferroptosis, and mitochondrial permeability transition (MPT)-dependent necrosis...
February 6, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29415885/ripk3-promotes-kidney-fibrosis-via-akt-dependent-atp-citrate-lyase
#8
Mitsuru Imamura, Jong-Seok Moon, Kuei-Pin Chung, Kiichi Nakahira, Thangamani Muthukumar, Roman Shingarev, Stefan W Ryter, Augustine Mk Choi, Mary E Choi
Renal fibrosis is a common pathogenic response to injury in chronic kidney disease (CKD). The receptor-interacting protein kinase-3 (RIPK3), a regulator of necroptosis, has been implicated in disease pathogenesis. In mice subjected to unilateral ureteral obstruction-induced (UUO-induced) or adenine diet-induced (AD-induced) renal fibrosis, models of progressive kidney fibrosis, we demonstrate increased kidney expression of RIPK3. Mice genetically deficient in RIPK3 displayed decreased kidney fibrosis and improved kidney function relative to WT mice when challenged with UUO or AD...
February 8, 2018: JCI Insight
https://www.readbyqxmd.com/read/29413844/ripk3-regulates-cardiac-microvascular-reperfusion-injury-the-role-of-ip3r-dependent-calcium-overload-xo-mediated-oxidative-stress-and-f-action-filopodia-based-cellular-migration
#9
Hao Zhou, Jin Wang, Pingjun Zhu, Shunying Hu, Jun Ren
Ripk3-mediated cellular apoptosis is a major contributor to the pathogenesis of myocardial ischemia reperfusion (IR) injury. However, the mechanisms by which Ripk3 influences microvascular homeostasis and endothelial apoptosis are not completely understood. In this study, loss of Ripk3 inhibited endothelial apoptosis, alleviated luminal swelling, maintained microvasculature patency, reduced the expression of adhesion molecules and limited the myocardial inflammatory response. In vitro, Ripk3 deficiency protected endothelial cells from apoptosis and migratory arrest induced by HR injury...
January 27, 2018: Cellular Signalling
https://www.readbyqxmd.com/read/29407229/combined-analysis-of-dna-methylation-and-gene-expression-profiles-of-osteosarcoma-identified-several-prognosis-signatures
#10
Wen Tian, Yongsheng Li, Jinghua Zhang, Jijun Li, Jinghua Gao
Osteosarcoma (OS) is a common primary malignancy in children and adolescents with relative high survival rate after chemotherapy. While, the toxicity of chemotherapy and personalized different response to chemotherapy makes it difficult for the selection of therapeutics and improvement of diagnosis. In this study, we conducted a combined analysis of two types of microarray datasets (gene expression and DNA methylation) from the Gene Expression Omnibus (GEO). Differential methylation sites (DMS) were identified by the IMA package and differential expression genes (DEGs) were screened out via the limma package...
January 30, 2018: Gene
https://www.readbyqxmd.com/read/29400632/ulinastatin-supplementation-during-human-amniotic-membrane-preservation-to-improve-its-viability
#11
Kyoung Woo Kim, Jung Huh, Soo Jin Lee, Sung Po Kim, Eung Bae Kim, Jae Chan Kim
PURPOSE: The amniotic membrane (AM) is the transparent innermost layer of the placenta and it facilitates rapid wound healing in a diversity of ocular surface disorders. However, extended periods of cryopreservation before use induce significant impairment of cell viability due to oxidative stresses and inflammatory responses. We investigated the effect of supplementing ulinastatin (ULI), a known serine protease inhibitor, and relevant mechanisms of action in AM preservation solution through the hypothermic continuum on inflammatory and apoptotic signals and viability of AM tissue...
February 5, 2018: Current Eye Research
https://www.readbyqxmd.com/read/29391237/sulforaphane-attenuates-microglia-mediated-neuronal-necroptosis-through-down-regulation-of-mapk-nf-%C3%AE%C2%BAb-signaling-pathways-in-lps-activated-bv-2-microglia
#12
Sisi Qin, Canhong Yang, Weihua Huang, Shuhua Du, Hantao Mai, Jijie Xiao, Tianming Lü
Sulforaphane (SFN), a natural dietary isothiocyanate in cruciferous vegetables such as broccoli and cabbage, has very strong anti-inflammatory activity. Activation of microglia leads to overexpression of a series of pro-inflammatory mediators, which play a vital role in neuronal damage. SFN may have neuroprotective effects in different neurodegenerative diseases related to inflammation. However, the mechanisms underlying SFN's protection of neurons against microglia-mediated neuronal damage are not fully understood...
January 29, 2018: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
https://www.readbyqxmd.com/read/29371616/necroptosis-and-neutrophil-associated-disorders
#13
REVIEW
Xiaoliang Wang, Shida Yousefi, Hans-Uwe Simon
Necroptosis is a form of regulated necrosis and is dependent on a signaling pathway involving receptor interacting protein kinase-3 (RIPK3) and mixed lineage kinase domain-like protein (MLKL). Necroptosis is considered to have important functions in inflammation and, based on studies with animal disease models, is believed likely to be involved in the pathogenesis of many human inflammatory diseases. In neutrophils, necroptosis has recently been reported to be triggered by tumor necrosis factor (TNF) stimulation, ligation of adhesion receptors, exposure to monosodium urate (MSU) crystals, or phagocytosis of Staphylococcus aureus (S...
January 25, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29352166/epstein-barr-virus-encoded-latent-membrane-protein-1-suppresses-necroptosis-through-targeting-ripk1-3-ubiquitination
#14
Xiaolan Liu, Yueshuo Li, Songling Peng, Xinfang Yu, Wei Li, Feng Shi, Xiangjian Luo, Min Tang, Zheqiong Tan, A M Bode, Ya Cao
Necroptosis is an alternative programmed cell death pathway that is unleashed in the absence of apoptosis and mediated by signaling complexes containing receptor-interating protein kinase 1 (RIPK1) and RIPK3. This form of cell death has recently been implicated in host defense system to eliminate pathogen-infected cells. However, only a few viral species such as herpes simplex virus (HSV) and cytomegalovirus (CMV) have evolved mechanisms inhibiting necroptosis to overcome host antiviral defense, which is important for successful pathogenesis...
January 19, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29337619/the-role-of-necroptosis-apoptosis-and-inflammation-in-fowl-cholera-associated-liver-injury-in-a-chicken-model
#15
Qiyu Tang, Weitian Li, Na Dai, Yiming Gao, Yu Han, Guofu Cheng, Changqin Gu
Fowl cholera resulting from infection with Pasteurella multocida causes huge economic losses in the poultry industry. Necrotic hepatitis is reported to be a significant lesion associated with fowl cholera in chickens. Clarifying the underlying molecular mechanism of hepatic injury caused by P. multocida infection is needed to develop new strategies to control fowl cholera. Pasteurella multocida Q (the standard reference strain) and P. multocida 1G1 (a clinical strain) were used to infect healthy laying hens...
December 2017: Avian Diseases
https://www.readbyqxmd.com/read/29337003/mouse-lung-fibroblasts-are-highly-susceptible-to-necroptosis-in-a-reactive-oxygen-species-dependent-manner
#16
Muadh Hussain, Vanessa Zimmermann, Sjoerd J L van Wijk, Simone Fulda
Mouse embryonic fibroblasts (MEFs) have extensively been used to study necroptosis, a recently identified form of programmed cell death. However, very little is yet known about the role of necroptosis and its regulation by reactive oxygen species (ROS) in cell types naturally exposed to high oxygen levels such as mouse lung fibroblasts (MLFs). Here, we discover that MLFs are highly susceptible to undergo necroptosis in a ROS-dependent manner upon exposure to a prototypic death receptor-mediated necroptotic stimulus, i...
January 11, 2018: Biochemical Pharmacology
https://www.readbyqxmd.com/read/29248440/jtc801-induces-ph-dependent-death-specifically-in-cancer-cells-and-slows-growth-of-tumors-in-mice
#17
Xinxin Song, Shan Zhu, Yangchun Xie, Jiao Liu, Lingyi Sun, Dexing Zeng, Pengcheng Wang, Xiaochao Ma, Guido Kroemer, David L Bartlett, Timothy R Billiar, Michael Lotze, Herbert Zeh, Rui Kang, Daolin Tang
BACKGROUND & AIMS: Maintenance of acid-base homeostasis is required for normal physiology, metabolism, and development. It is not clear how cell death is activated in response to changes in pH. We performed a screen to identify agents that induce cell death in a pH-dependent manner (we call this alkaliptosis) in pancreatic ductal adenocarcinoma cancer (PDAC) cells and tested their effects in mice. METHODS: We screened a library of 254 compounds that interact with G protein-coupled receptors (GPCRs) to identify those with cytotoxic activity against a human PDAC cell line (PANC1)...
December 14, 2017: Gastroenterology
https://www.readbyqxmd.com/read/29248164/deficiency-of-receptor-interacting-protein-kinase-3-ripk3-attenuates-inflammation-and-organ-injury-in-neonatal-sepsis
#18
Laura W Hansen, Asha Jacob, Weng Lang Yang, Alexandra C Bolognese, Jose Prince, Jeffrey M Nicastro, Gene F Coppa, Ping Wang
INTRODUCTION: Sepsis is the third leading cause of morbidity and mortality in neonates. Sepsis in neonates is characterized as the systemic inflammation owing to infection within the first 28days after birth. The molecular mechanism causing the exaggerated inflammation phenotype in neonates has not been completely elucidated. Receptor interacting protein kinase 3 (RIPK3) is a protein identified as a mediator in programmed necrosis or necroptosis. We hypothesize that RIPK3 could be responsible for the inflammatory response in neonates and that deficiency in the RIPK3 protein attenuates inflammation and organ injury in neonatal sepsis...
November 23, 2017: Journal of Pediatric Surgery
https://www.readbyqxmd.com/read/29247776/necrostatin-1-improves-long-term-functional-recovery-through-protecting-oligodendrocyte-precursor-cells-after-transient-focal-cerebral-ischemia-in-mice
#19
Yingzhu Chen, Lingling Zhang, Hailong Yu, Kangping Song, Jinling Shi, Linlin Chen, Jian Cheng
Ischemic stroke often results in severe injury to white matter structures including the axons, oligodendroglia, and other glial cells. Immature stages of oligodendroglia, such as oligodendrocyte precursor cells (OPCs) and premature oligodendroglia, are more vulnerable to ischemia than mature oligodendroglia. Extensive studies have been performed on the necroptosis of neurons following cerebral ischemia. The present study aimed to investigate the effect of necrostatin-1 (Nec-1), a necroptosis inhibitor, on the survival of OPCs and long-term functional recovery following transient cerebral ischemia...
December 13, 2017: Neuroscience
https://www.readbyqxmd.com/read/29238045/ripk3-promotes-adenovirus-type-5-activity
#20
Melanie Weigert, Alex Binks, Suzanne Dowson, Elaine Y L Leung, Dmitris Athineos, Xinzi Yu, Margaret Mullin, Josephine B Walton, Clare Orange, Darren Ennis, Karen Blyth, Stephen W G Tait, Iain A McNeish
Oncolytic adenoviral mutants infect human malignant cells and replicate selectively within them. This induces direct cytotoxicity that can also trigger profound innate and adaptive immune responses. However, the mechanism by which adenoviruses produce cell death remains uncertain. We previously suggested that type 5 adenoviruses, including the E1A CR2 deletion mutant dl922-947, might induce a novel form of programmed death resembling necroptosis. Here we have investigated the roles of core necrosis proteins RIPK1, RIPK3 and MLKL in the cytotoxicity of dl922-947 and other adenovirus serotypes...
December 13, 2017: Cell Death & Disease
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