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https://www.readbyqxmd.com/read/28626232/the-rip3-rip1-nf-%C3%AE%C2%BAb-signaling-axis-is-dispensable-for-necroptotic-cells-to-elicit-cross-priming-of-cd8-t-cells
#1
Junming Ren, Xian Jia, Yihao Zhao, Wenke Shi, Jiongcong Lu, Yingying Zhang, Jianfeng Wu, Bo Liang, Rui Wu, Guo Fu, Jiahuai Han
No abstract text is available yet for this article.
June 19, 2017: Cellular & Molecular Immunology
https://www.readbyqxmd.com/read/28592284/biogenic-selenium-nanoparticles-induce-ros-mediated-necroptosis-in-pc-3-cancer-cells-through-tnf-activation
#2
Praveen Sonkusre, Swaranjit Singh Cameotra
BACKGROUND: Selenium is well documented to inhibit cancer at higher doses; however, the mechanism behind this inhibition varies widely depending on the cell type and selenium species. Previously, we have demonstrated that Bacillus licheniformis JS2 derived biogenic selenium nanoparticles (SeNPs) induce non-apoptotic cell death in prostate adenocarcinoma cell line, PC-3, at a minimal concentration of 2 µg Se/ml, without causing toxicity to the primary cells. However, the mechanism behind its anticancer activity was elusive...
June 7, 2017: Journal of Nanobiotechnology
https://www.readbyqxmd.com/read/28579326/rip1-rip3-drp1-pathway-regulates-nlrp3-inflammasome-activation-following-subarachnoid-hemorrhage
#3
Keren Zhou, Ligen Shi, Zhen Wang, Jingyi Zhou, Anatol Manaenko, Cesar Reis, Sheng Chen, Jianmin Zhang
The NLRP3 inflammasome functions as a crucial component of the inflammatory response in early brain injury (EBI) after subarachnoid hemorrhage (SAH). However, the mechanisms underlying the activation of NLRP3 inflammasome has not been well elucidated. In this study, we hypothesized the RIP1-RIP3-DRP1 pathway was involved in the activation of the NLRP3 inflammasome following SAH. SAH was induced by endovascular perforation in rats. Necrostatin-1 (Nec-1) or mitochondrial division inhibitor (Mdivi-1) was administered 1h after SAH by intraperitoneal injection...
June 2, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28574501/rip1-kinase-activity-dependent-roles-in-embryonic-development-of-fadd-deficient-mice
#4
Yongbo Liu, Cunxian Fan, Yifan Zhang, Xianjun Yu, Xiaoxia Wu, Xixi Zhang, Qun Zhao, Haiwei Zhang, Qun Xie, Ming Li, Xiaoming Li, Qiurong Ding, Hao Ying, Dali Li, Haibing Zhang
RIP1 is an essential regulator of TNF-induced signaling complexes mediating NF-κB activation, apoptosis and necroptosis. Loss of Rip1 rescues the embryonic lethality of Fadd or Caspase-8-deficient mice, even though the double knockout mice die shortly after birth like Rip1-deficient mice. Recent studies demonstrated that mice expressing RIP1 kinase-dead mutants developed normally and resisted necroptotic stimuli in vitro and in vivo. However, the impact of RIP1 kinase activity on Fadd(-/-) embryonic development remains unknown...
June 2, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28572508/cardioprotective-role-of-traf2-by-suppressing-apoptosis-and-necroptosis
#5
Xiaoyun Guo, Haifeng Yin, Lei Li, Yi Chen, Jing Li, Jessica Doan, Rachel N Steinmetz, Qinghang Liu
Background -Programed cell death, including apoptosis, mitochondria-mediated necrosis, and necroptosis, is critically involved in ischemic cardiac injury, pathological cardiac remodeling, and heart failure progression. Whereas apoptosis and mitochondria-mediated necrosis signaling is well established, the regulatory mechanisms of necroptosis and its significance in the pathogenesis of heart failure remain elusive. Methods -We examined the role of Traf2 (TNF receptor-associated factor 2) in regulating myocardial necroptosis and remodeling using genetic mouse models...
June 1, 2017: Circulation
https://www.readbyqxmd.com/read/28564603/2-hg-inhibits-necroptosis-by-stimulating-dnmt1-dependent-hypermethylation-of-the-rip3-promoter
#6
Zhentao Yang, Bin Jiang, Yan Wang, Hengxiao Ni, Jia Zhang, Jinmei Xia, Minggang Shi, Li-Man Hung, Jingsong Ruan, Tak Wah Mak, Qinxi Li, Jiahuai Han
2-hydroxyglutarate-(2-HG)-mediated inhibition of TET2 activity influences DNA hypermethylation in cells harboring mutations of isocitrate dehydrogenases 1 and 2 (IDH1/2). Here, we show that 2-HG also regulates DNA methylation mediated by DNA methyltransferase 1 (DNMT1). DNMT1-dependent hypermethylation of the RIP3 promoter occurred in both IDH1 R132Q knockin mutant mouse embryonic fibroblast (MEFs) and 2-HG-treated wild-type (WT) MEFs. We found that 2-HG bound to DNMT1 and stimulated its association with the RIP3 promoter, inducing hypermethylation that reduces RIP3 protein and consequently impaired RIP3-dependent necroptosis...
May 30, 2017: Cell Reports
https://www.readbyqxmd.com/read/28560421/a-novel-damage-mechanism-contribution-of-the-interaction-between-necroptosis-and-ros-to-high-glucose-induced-injury-and-inflammation-in-h9c2-cardiac-cells
#7
Weijie Liang, Meiji Chen, Dongdan Zheng, Jieyi He, Mingcai Song, Liqiu Mo, Jianqiang Feng, Jun Lan
Recently, a novel mechanism known as 'programmed necrosis' or necroptosis has been shown to be another important mechanism of cell death in the heart. In this study, we investigated the role of necroptosis in high glucose (HG)-induced injury and inflammation, as well as the underlying mechanisms. In particular, we focused on the interaction between necroptosis and reactive oxygen species (ROS) in H9c2 cardiac cells. Our results demonstrated that the exposure of H9c2 cardiac cells to 35 mM glucose (HG) markedly enhanced the expression level of receptor-interacting protein 3 (RIP3), a kinase which promotes necroptosis...
May 29, 2017: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/28558962/galangin-ameliorates-cisplatin-induced-nephrotoxicity-by-attenuating-oxidative-stress-inflammation-and-cell-death-in-mice-through-inhibition-of-erk-and-nf-kappab-signaling
#8
Yu-Ching Huang, Ming-Shiun Tsai, Pei-Chi Hsieh, Jheng-Hong Shih, Tsu-Shing Wang, Yi-Chun Wang, Ting-Hui Lin, Sue-Hong Wang
Cisplatin is a chemotherapeutic agent widely used in the treatment of various cancers. However, cisplatin can induce nephrotoxicity and neurotoxicity, limiting its dosage and usage. Galangin, a natural flavonol, has been found to exhibit anti-oxidant and anti-inflammatory effects in vivo. Here, we investigated the effects of galangin on cisplatin-induced acute kidney injury (AKI) and its molecular mechanisms in mice. Galangin administration reduced the cisplatin-induced oxidative stress by decreasing renal MDA and 3-NT formations...
May 27, 2017: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/28501693/necrostatin-1-protects-hippocampal-neurons-against-ischemia-reperfusion-injury-via-the-rip3-daxx-signaling-pathway-in-rats
#9
Rongli Yang, Kun Hu, Jieyun Chen, Shiguang Zhu, Lei Li, Hailong Lu, Pingjing Li, Ruiguo Dong
Global cerebral ischemia/reperfusion (I/R) induces selective neuronal injury in CA1 region of hippocampus, leading to severe impairment in behavior, learning and memory functions. However, the molecular mechanism underlying the processes was not elucidated clearly. RIP3 is a key molecular switch connecting apoptosis, necrosis and necroptosis. DAXX, as a novel substrate of RIP3, plays a vital role in ischemia-induced neuronal death. The aim of this study is to investigate the role and mechanism of RIP3/DAXX signaling pathway on neurons in CA1 region of the rat hippocampus after cerebral I/R...
May 10, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28485476/necroptosis-resumes-apoptosis-in-hippocampus-but-not-in-frontal-cortex
#10
Sara Nikseresht, Fariba Khodagholi, Leila Dargahi, Abolhassan Ahmadiani
Cell death subsequent to concurrent with neuroinflammation results in some damages like neuron loss and spatial memory impairment. In this study we demonstrate the temporal pattern of neuroinflammation, necroptotic and apoptotic cell deaths in hippocampus and frontal cortex following intracerebroventricular administration of lipopolysaccharide (LPS). We evaluated receptor interacting protein kinase 1 (RIP1), RIP3 and two related metabolic enzymes including glutamate-ammonia ligase (GLUL) and glutamate dehydrogenase (GLUD) as necroptosis factors...
May 9, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28476895/regression-of-apoptosis-resistant-colorectal-tumors-by-induction-of-necroptosis-in-mice
#11
Gui-Wei He, Claudia Günther, Veronika Thonn, Yu-Qiang Yu, Eva Martini, Barbara Buchen, Markus F Neurath, Michael Stürzl, Christoph Becker
Cancer cells often acquire capabilities to evade cell death induced by current chemotherapeutic treatment approaches. Caspase-8, a central initiator of death receptor-mediated apoptosis, for example, is frequently inactivated in human cancers via multiple mechanisms such as mutation. Here, we show an approach to overcome cell death resistance in caspase-8-deficient colorectal cancer (CRC) by induction of necroptosis. In both a hereditary and a xenograft mouse model of caspase-8-deficient CRC, second mitochondria-derived activator of caspase (SMAC) mimetic treatment induced massive cell death and led to regression of tumors...
June 5, 2017: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/28475174/diverse-ubiquitin-linkages-regulate-rip-kinases-mediated-inflammatory-and-cell-death-signaling
#12
REVIEW
Axel Witt, Domagoj Vucic
Members of the RIP kinase family are key regulators of inflammation and cell death signaling implicated in maintaining immune responses and proper tissue homeostasis. Increasing evidence points to post-translational modifications of RIP1, RIP2 and RIP3 as being critical for regulating their function. Ubiquitination and the E3 ligases, such as inhibitors of apoptosis (IAP) proteins and LUBAC, that direct substrate selectivity as well as the deubiquitinating enzymes, such as A20 and OTULIN, that reverse these modifications dictate the outcome of RIP kinase signaling...
May 5, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28472590/evidence-of-necroptosis-in-hearts-subjected-to-various-forms-of-ischemic-insults
#13
Adriana Adameova, Jaroslav Hrdlicka, Adrian Szobi, Veronika Farkasova, Katarina Kopaskova, Martina Murarikova, Jan Neckar, Frantisek Kolar, Tatiana Ravingerova, Naranjan S Dhalla
Long-lasting ischemia can result in cell loss; however, repeated episodes of brief ischemia increase the resistance of the heart against deleterious effects of subsequent prolonged ischemic insult and promote cell survival. Traditionally, it is believed that the supply of blood to the ischemic heart is associated with release of cytokines, activation of inflammatory response, and induction of necrotic cell death. In the past few years, this paradigm of passive necrosis as an uncontrolled cell death has been re-examined and the existence of a strictly regulated form of necrotic cell death, necroptosis, has been documented...
May 4, 2017: Canadian Journal of Physiology and Pharmacology
https://www.readbyqxmd.com/read/28456683/patchouli-alcohol-ameliorates-dextran-sodium-sulfate-induced-experimental-colitis-and-suppresses-tryptophan-catabolism
#14
Chang Qu, Zhong-Wen Yuan, Xiu-Ting Yu, Yan-Feng Huang, Guang-Hua Yang, Jian-Nan Chen, Xiao-Ping Lai, Zi-Ren Su, Hui-Fang Zeng, Ying Xie, Xiao-Jun Zhang
Despite the increased morbidity of ulcerative colitis (UC) in recent years, available treatments remain unsatisfactory. Pogostemon cablin has been widely applied to treat a variety of gastrointestinal disorders in clinic for centuries, in which patchouli alcohol (PA, C15H26O) has been identified as the major active component. This study attempted to determine the bioactivity of PA on dextran sulfate sodium (DSS)-induced mice colitis and clarify the mechanism of action. Acute colitis was induced in mice by 3% DSS for 7 days...
April 27, 2017: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
https://www.readbyqxmd.com/read/28454582/analysis-of-necroptotic-proteins-in-failing-human-hearts
#15
Adrián Szobi, Eva Gonçalvesová, Zoltán Varga, Przemyslaw Leszek, Mariusz Kuśmierczyk, Michal Hulman, Ján Kyselovič, Péter Ferdinandy, Adriana Adameová
BACKGROUND: Cell loss and subsequent deterioration of contractile function are hallmarks of chronic heart failure (HF). While apoptosis has been investigated as a participant in the progression of HF, it is unlikely that it accounts for the total amount of non-functional tissue. In addition, there is evidence for the presence of necrotic cardiomyocytes in HF. Therefore, the objective of this study was to investigate the necroptotic proteins regulating necroptosis, a form of programmed necrosis, and thereby assess its potential role in human end-stage HF...
April 28, 2017: Journal of Translational Medicine
https://www.readbyqxmd.com/read/28423682/rip3-deficiency-ameliorates-inflammatory-response-in-mice-infected-with-influenza-h7n9-virus-infection
#16
Yu-Lin Xu, Hai-Lin Tang, Hao-Ran Peng, Ping Zhao, Zhong-Tian Qi, Wen Wang
Influenza H7N9 virus infection causes an acute, highly contagious respiratory illness that triggers cell death of infected cells and airway epithelial destruction. RIP3 is a key regulator of cell death responses to a growing number of viral and microbial agents. This study aimed to investigate the role of RIP3 in inflammation of influenza H7N9 virus infection. Here, RIP3 knock out (RIP3-/-) mice and littermate wild type mice were infected intranasally with influenza H7N9 virus (A/Fujian/S03/2015) to determine the contribution of RIP3 to the inflammatory response of influenza H7N9 virus infection...
April 25, 2017: Oncotarget
https://www.readbyqxmd.com/read/28415572/inhibition-of-iron-overload-induced-apoptosis-and-necrosis-of-bone-marrow-mesenchymal-stem-cells-by-melatonin
#17
Fan Yang, Yuan Li, Gege Yan, Tianyi Liu, Chao Feng, Rui Gong, Ye Yuan, Fengzhi Ding, Lai Zhang, Elina Idiiatullina, Valentin Pavlov, Zhenbo Han, Wenya Ma, Qi Huang, Ying Yu, Zhengyi Bao, Xiuxiu Wang, Bingjie Hua, Zhimin Du, Benzhi Cai, Lei Yang
Iron overload induces severe damage to several vital organs such as the liver, heart and bone, and thus contributes to the dysfunction of these organs. The aim of this study is to investigate whether iron overload causes the apoptosis and necrosis of bone marrow mesenchymal stem cells (BMSCs) and melatonin may prevent its toxicity. Perls' Prussion blue staining showed that exposure to increased concentrations of ferric ammonium citrate (FAC) induced a gradual increase of intracellular iron level in BMSCs. Trypan blue staining demonstrated that FAC decreased the viability of BMSCs in a concentration-dependent manner...
May 9, 2017: Oncotarget
https://www.readbyqxmd.com/read/28414098/cytosolic-calcium-mediates-rip1-rip3-complex-dependent-necroptosis-through-jnk-activation-and-mitochondrial-ros-production-in-human-colon-cancer-cells
#18
Wen Sun, Xiaxia Wu, Hongwei Gao, Jie Yu, Wenwen Zhao, Jin-Jian Lu, Jinhua Wang, Guanhua Du, Xiuping Chen
Necroptosis is a form of programmed necrosis mediated by signaling complexes with receptor-interacting protein 1 (RIP1) and RIP3 kinases as the main mediators. However, the underlying execution pathways of this phenomenon have yet to be elucidated in detail. In this study, a RIP1/RIP3 complex was formed in 2-methoxy-6-acetyl-7-methyljuglone (MAM)-treated HCT116 and HT29 colon cancer cells. With this formation, mitochondrial reactive oxygen species (ROS) levels increased, mitochondrial depolarization occurred, and ATP concentrations decreased...
April 14, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28396243/mechanical-force-mediated-pathological-cartilage-thinning-is-regulated-by-necroptosis-and-apoptosis
#19
C Zhang, S Lin, T Li, Y Jiang, Z Huang, J Wen, W Cheng, H Li
OBJECTIVE: This study aimed to identify the mechanisms underlying mandibular chondrocyte cell death and cartilage thinning in response to mechanical force. MATERIAL AND METHODS: An in vivo model (compressive mechanical force) and an in vitro model (TNF-α+cycloheximide) were used to induce mandibular chondrocyte necroptosis. Hematoxylin and eosin staining and transmission electron microscopy were used to assess histological and subcellular changes in mandibular chondrocyte...
April 7, 2017: Osteoarthritis and Cartilage
https://www.readbyqxmd.com/read/28387756/pore-forming-toxin-mediated-ion-dysregulation-leads-to-death-receptor-independent-necroptosis-of-lung-epithelial-cells-during-bacterial-pneumonia
#20
Norberto González-Juarbe, Kelley Margaret Bradley, Anukul Taranath Shenoy, Ryan Paul Gilley, Luis Felipe Reyes, Cecilia Anahí Hinojosa, Marcos Ignacio Restrepo, Peter Herman Dube, Molly Ann Bergman, Carlos Javier Orihuela
We report that pore-forming toxins (PFTs) induce respiratory epithelial cell necroptosis independently of death receptor signaling during bacterial pneumonia. Instead, necroptosis was activated as a result of ion dysregulation arising from membrane permeabilization. PFT-induced necroptosis required RIP1, RIP3 and MLKL, and could be induced in the absence or inhibition of TNFR1, TNFR2 and TLR4 signaling. We detected activated MLKL in the lungs from mice and nonhuman primates experiencing Serratia marcescens and Streptococcus pneumoniae pneumonia, respectively...
May 2017: Cell Death and Differentiation
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