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RIP3 or RIPK3

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https://www.readbyqxmd.com/read/28205631/immature-mice-are-more-susceptible-than-adult-mice-to-acetaminophen-induced-acute-liver-injury
#1
Yan Lu, Cheng Zhang, Yuan-Hua Chen, Hua Wang, Zhi-Hui Zhang, Xi Chen, De-Xiang Xu
Acetaminophen (APAP) overdose induces acute liver injury. The aim of the present study was to analyze the difference of susceptibility between immature and adult mice to APAP-induced acute liver injury. Weanling immature and adult mice were injected with APAP (300 mg/kg). As expected, immature mice were more susceptible than adult mice to APAP-induced acute liver injury. APAP-evoked hepatic c-Jun N-terminal kinase phosphorylation was stronger in immature mice than in adult mice. Hepatic receptor-interacting protein (RIP)1 was obviously activated at APAP-exposed immature and adult mice...
February 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28199887/killing-colon-cancer-cells-through-pcd-pathways-by-a-novel-hyaluronic-acid-modified-shell-core-nanoparticle-loaded-with-rip3-in-combination-with-chloroquine
#2
Xueyan Hou, Chengli Yang, Lijing Zhang, Tingting Hu, Dan Sun, Hua Cao, Fan Yang, Gang Guo, Changyang Gong, Xiaoning Zhang, Aiping Tong, Rui Li, Yu Zheng
Due to extensive apoptosis defects and multidrug resistance, there is great interest regarding non-apoptotic programmed cell death (PCD) pathways, such as lysosomal-mediated programmed cell death (LM-PCD), necroptosis and autophagy. Because there is an intricate effector network among these PCD pathways, it is expected that they may act synergistically in cancer therapy. In this study, chloroquine (CQ) was found to significantly upregulate receptor-interacting protein kinase 3 (RIP3) expression, and RIP3 were involved in CQ-related autophagy...
January 2, 2017: Biomaterials
https://www.readbyqxmd.com/read/28197335/caspase-8-not-so-silently-deadly
#3
REVIEW
Rebecca Feltham, James E Vince, Kate E Lawlor
Apoptosis is a caspase-dependent programmed form of cell death, which is commonly believed to be an immunologically silent process, required for mammalian development and maintenance of cellular homoeostasis. In contrast, lytic forms of cell death, such as RIPK3- and MLKL-driven necroptosis, and caspase-1/11-dependent pyroptosis, are postulated to be inflammatory via the release of damage associated molecular patterns (DAMPs). Recently, the function of apoptotic caspase-8 has been extended to the negative regulation of necroptosis, the cleavage of inflammatory interleukin-1β (IL-1β) to its mature bioactive form, either directly or via the NLRP3 inflammasome, and the regulation of cytokine transcriptional responses...
January 2017: Clinical & Translational Immunology
https://www.readbyqxmd.com/read/28186202/inhibition-of-receptor-interacting-protein-kinase-1-with-necrostatin-1s-ameliorates-disease-progression-in-elastase-induced-mouse-abdominal-aortic-aneurysm-model
#4
Qiwei Wang, Ting Zhou, Zhenjie Liu, Jun Ren, Noel Phan, Kartik Gupta, Danielle M Stewart, Stephanie Morgan, Carmel Assa, K Craig Kent, Bo Liu
Abdominal aortic aneurysm (AAA) is a common aortic disease with a progressive nature. There is no approved pharmacological treatment to effectively slow aneurysm growth or prevent rupture. Necroptosis is a form of programmed necrosis that is regulated by receptor-interacting protein kinases (RIPs). We have recently demonstrated that the lack of RIP3 in mice prevented aneurysm formation. The goal of the current study is to test whether perturbing necroptosis affects progression of existing aneurysm using the RIP1 inhibitors Necrostatin-1 (Nec-1) and an optimized form of Nec-1, 7-Cl-O-Nec-1 (Nec-1s)...
February 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28179994/matrine-induces-rip3-dependent-necroptosis-in-cholangiocarcinoma-cells
#5
Beibei Xu, Minying Xu, Yuan Tian, Qiang Yu, Yujie Zhao, Xiong Chen, Panying Mi, Hanwei Cao, Bing Zhang, Gang Song, Yan-Yan Zhan, Tianhui Hu
The development of acquired resistance to pro-apoptotic antitumor agents is a major impediment to the cure of cholangiocarcinoma (CCA). Antitumor drugs inducing non-apoptotic cell death are considered as a new approach to overcome such drug resistance. Here, we reported for the first time that matrine-induced necroptosis in CCA cell lines, differing from its classical role to induce apoptosis in many other kinds of cancer cells. CCA cells under matrine treatment exhibited typical necrosis-like but not apoptotic morphologic change...
2017: Cell Death Discovery
https://www.readbyqxmd.com/read/28176780/rip1-autophosphorylation-is-promoted-by-mitochondrial-ros-and-is-essential-for-rip3-recruitment-into-necrosome
#6
Yingying Zhang, Sheng Sean Su, Shubo Zhao, Zhentao Yang, Chuan-Qi Zhong, Xin Chen, Qixu Cai, Zhang-Hua Yang, Deli Huang, Rui Wu, Jiahuai Han
Necroptosis is a type of programmed cell death with great significance in many pathological processes. Tumour necrosis factor-α(TNF), a proinflammatory cytokine, is a prototypic trigger of necroptosis. It is known that mitochondrial reactive oxygen species (ROS) promote necroptosis, and that kinase activity of receptor interacting protein 1 (RIP1) is required for TNF-induced necroptosis. However, how ROS function and what RIP1 phosphorylates to promote necroptosis are largely unknown. Here we show that three crucial cysteines in RIP1 are required for sensing ROS, and ROS subsequently activates RIP1 autophosphorylation on serine residue 161 (S161)...
February 8, 2017: Nature Communications
https://www.readbyqxmd.com/read/28151480/ripk1-ripk3-promotes-vascular-permeability-to-allow-tumor-cell-extravasation-independent-of-its-necroptotic-function
#7
Kay Hänggi, Lazaros Vasilikos, Aida Freire Valls, Rosario Yerbes, Janin Knop, Lisanne M Spilgies, Kristy Rieck, Tvisha Misra, John Bertin, Peter J Gough, Thomas Schmidt, Carmen Ruiz de Almodòvar, W Wei-Lynn Wong
Necroptosis is an inflammatory form of programmed cell death requiring receptor-interacting protein kinase 1, 3 (RIPK1, RIPK3) and mixed lineage kinase domain-like protein (MLKL). The kinase of RIPK3 phosphorylates MLKL causing MLKL to form a pore-like structure, allowing intracellular contents to release and cell death to occur. Alternatively, RIPK1 and RIPK3 have been shown to regulate cytokine production directly influencing inflammatory immune infiltrates. Recent data suggest that necroptosis may contribute to the malignant transformation of tumor cells in vivo and we asked whether necroptosis may have a role in the tumor microenvironment altering the ability of the tumor to grow or metastasize...
February 2, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28151467/augmented-trophoblast-cell-death-in-preeclampsia-can-proceed-via-ceramide-mediated-necroptosis
#8
Liane Jennifer Bailey, Sruthi Alahari, Andrea Tagliaferro, Martin Post, Isabella Caniggia
Preeclampsia, a serious hypertensive disorder of pregnancy, is characterized by elevated ceramide (CER) content that is responsible for heightened trophoblast cell death rates via apoptosis and autophagy. Whether trophoblast cells undergo necroptosis, a newly characterized form of regulated necrosis, and the potential role of CER in this process remain to be established. Herein, we report that exposure of both JEG3 cells and primary isolated cytotrophoblasts to C16:0 CER in conjunction with a caspase-8 inhibitor (Q-VD-OPh) promoted necroptotic cell death, as evidenced by increased expression and association of receptor-interacting protein kinases RIP1 and RIP3, as well as phosphorylation of mixed lineage kinase domain-like (MLKL) protein...
February 2, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28139717/deferasirox-induced-iron-depletion-promotes-bclxl-downregulation-and-death-of-proximal-tubular-cells
#9
Diego Martin-Sanchez, Angel Gallegos-Villalobos, Miguel Fontecha-Barriuso, Susana Carrasco, Maria Dolores Sanchez-Niño, Francisco J Lopez-Hernandez, Marta Ruiz-Ortega, Jesus Egido, Alberto Ortiz, Ana Belén Sanz
Iron deficiency has been associated with kidney injury. Deferasirox is an oral iron chelator used to treat blood transfusion-related iron overload. Nephrotoxicity is the most serious and common adverse effect of deferasirox and may present as an acute or chronic kidney disease. However, scarce data are available on the molecular mechanisms of nephrotoxicity. We explored the therapeutic modulation of deferasirox-induced proximal tubular cell death in culture. Deferasirox induced dose-dependent tubular cell death and AnexxinV/7AAD staining showed features of apoptosis and necrosis...
January 31, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28127258/tnf-%C3%AE-sensitizes-chemotherapy-and-radiotherapy-against-breast-cancer-cells
#10
Xiao Wu, Meng-Yao Wu, Min Jiang, Qiaoming Zhi, Xiaojie Bian, Meng-Dan Xu, Fei-Ran Gong, Juan Hou, Min Tao, Liu-Mei Shou, Weiming Duan, Kai Chen, Meng Shen, Wei Li
PURPOSE: Despite new developments in cancer therapy, chemotherapy and radiotherapy remain the cornerstone of breast cancer treatment. Therefore, finding ways to reduce the toxicity and increase sensitivity is particularly important. Tumor necrosis factor alpha (TNF-α) exerts multiple functions in cell proliferation, differentiation and apoptosis. In the present study, we investigated whether TNF-α could enhance the effect of chemotherapy and radiotherapy against breast cancer cells...
2017: Cancer Cell International
https://www.readbyqxmd.com/read/28126382/complex-pathologic-roles-of-ripk1-and-ripk3-moving-beyond-necroptosis
#11
REVIEW
Kelby W Wegner, Danish Saleh, Alexei Degterev
A process of regulated necrosis, termed necroptosis, has been recognized as a major contributor to cell death and inflammation occurring under a wide range of pathologic settings. The core event in necroptosis is the formation of the detergent-insoluble 'necrosome' complex of homologous Ser/Thr kinases, receptor protein interacting kinase 1 (RIPK1) and receptor interacting protein kinase 3 (RIPK3), which promotes phosphorylation of a key prodeath effector, mixed lineage kinase domain-like (MLKL), by RIPK3. Core necroptosis mediators are under multiple controls, which have been a subject of intense investigation...
January 23, 2017: Trends in Pharmacological Sciences
https://www.readbyqxmd.com/read/28125817/participation-of-necroptosis-in-the-host-response-to-acute-bacterial-pneumonia
#12
Danielle Ahn, Alice Prince
Common pulmonary pathogens, such as Streptococcus pneumoniae and Staphylococcus aureus, as well as the host-adapted pathogens responsible for health care-associated pneumonias, such as the carbapenem-resistant Klebsiella pneumoniae and Serratia marcecsens, are able to activate cell death through the RIPK1/RIPK3/MLKL cascade that causes necroptosis. Necroptosis can influence the pathogenesis of pneumonia through several mechanisms. Activation of this pathway can result in the loss of specific types of immune cells, especially macrophages, and, in so doing, contribute to host pathology through the loss of their critical immunoregulatory functions...
January 27, 2017: Journal of Innate Immunity
https://www.readbyqxmd.com/read/28115086/necroptosis-mediates-the-antineoplastic-effects-of-the-soluble-fraction-of-polysaccharide-from-red-wine-in-walker-256-tumor-bearing-rats
#13
Maria Carolina Stipp, Iglesias de Lacerda Bezerra, Claudia Rita Corso, Francislaine A Dos Reis Livero, Luiz Alexandre Lomba, Adriana Rute Cordeiro Caillot, Aleksander Roberto Zampronio, José Ederaldo Queiroz-Telles, Giseli Klassen, Edneia A S Ramos, Guilherme Lanzi Sassaki, Alexandra Acco
Polysaccharides are substances that modify the biological response to several stressors. The present study investigated the antitumor activity of the soluble fraction of polysaccharides (SFP), extracted from cabernet franc red wine, in Walker-256 tumor-bearing rats. The monosaccharide composition had a complex mixture, suggesting the presence of arabinoglactans, mannans, and pectins. Treatment with SFP (30 and 60mg/kg, oral) for 14days significantly reduced the tumor weight and volume compared with controls...
March 15, 2017: Carbohydrate Polymers
https://www.readbyqxmd.com/read/28108311/rip1-and-rip3-contribute-to-shikonin-induced-dna-double-strand-breaks-in-glioma-cells-via-increase-of-intracellular-reactive-oxygen-species
#14
Zijian Zhou, Bin Lu, Chen Wang, Zongqi Wang, Tianfei Luo, Meihua Piao, Fankai Meng, Guangfan Chi, Yinan Luo, Pengfei Ge
Shikonin has been reported to induce glioma cell death via necroptosis, a type of programmed necrosis primarily mediated by RIP1 and RIP3. Although RIP1 and RIP3 are found to regulate some features of necrosis such as energy depletion and cellular membrane disruption, it remains unclear whether RIP1 and RIP3 could modulate DNA double strand breaks (DSBs), which is a crucial event leading to chromatinolysis. In this study, we used glioma cell lines and mice model of xenograft glioma to investigate the roles of RIP1 and RIP3 in shikonin-induced DNA DSBs...
April 1, 2017: Cancer Letters
https://www.readbyqxmd.com/read/28106882/combination-of-iap-antagonist-and-ifn%C3%AE-activates-novel-caspase-10-and-ripk1-dependent-cell-death-pathways
#15
Maria C Tanzer, Nufail Khan, James A Rickard, Nima Etemadi, Najoua Lalaoui, Sukhdeep Kaur Spall, Joanne M Hildebrand, David Segal, Maria Miasari, Diep Chau, WendyWei-Lynn Wong, Mark McKinlay, Srinivas K Chunduru, Christopher A Benetatos, Stephen M Condon, James E Vince, Marco J Herold, John Silke
Peptido-mimetic inhibitor of apoptosis protein (IAP) antagonists (Smac mimetics (SMs)) can kill tumour cells by depleting endogenous IAPs and thereby inducing tumour necrosis factor (TNF) production. We found that interferon-γ (IFNγ) synergises with SMs to kill cancer cells independently of TNF- and other cell death receptor signalling pathways. Surprisingly, CRISPR/Cas9 HT29 cells doubly deficient for caspase-8 and the necroptotic pathway mediators RIPK3 or MLKL were still sensitive to IFNγ/SM-induced killing...
January 20, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28099966/involvement-of-xbp1s-in-blue-light-induced-a2e-containing-retinal-pigment-epithelium-cell-death
#16
Bing Lu, Pengfei Zhang, Minwen Zhou, Wenqiu Wang, Qing Gu, Jingyang Feng, Xueting Luo, Xiangjun Sun, Fenghua Wang, Xiaodong Sun
PURPOSE: Retinal pigment epithelium (RPE) cell dysfunction is essential to the development of retinal degenerative disease. This study was designed to investigate how spliced X-box-binding protein 1 (XBP1s) regulates different modes of RPE cell death in vitro. METHODS: Human ARPE19 cells were incubated with 25 μM N-retinylidene-N-retinylethanolamine (A2E) and irradiated with blue light. Expressions of glucose-regulated protein 78 (GRP78) and XBP1s were detected by real-time quantitative PCR and Western blot...
January 19, 2017: Ophthalmic Research
https://www.readbyqxmd.com/read/28096356/active-mlkl-triggers-the-nlrp3-inflammasome-in-a-cell-intrinsic-manner
#17
Stephanie A Conos, Kaiwen W Chen, Dominic De Nardo, Hideki Hara, Lachlan Whitehead, Gabriel Núñez, Seth L Masters, James M Murphy, Kate Schroder, David L Vaux, Kate E Lawlor, Lisa M Lindqvist, James E Vince
Necroptosis is a physiological cell suicide mechanism initiated by receptor-interacting protein kinase-3 (RIPK3) phosphorylation of mixed-lineage kinase domain-like protein (MLKL), which results in disruption of the plasma membrane. Necroptotic cell lysis, and resultant release of proinflammatory mediators, is thought to cause inflammation in necroptotic disease models. However, we previously showed that MLKL signaling can also promote inflammation by activating the nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome to recruit the adaptor protein apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC) and trigger caspase-1 processing of the proinflammatory cytokine IL-1β...
February 7, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28088644/tert-butyl-hydroperoxide-t-bhp-induced-apoptosis-and-necroptosis-in-endothelial-cells-roles-of-nox4-and-mitochondrion
#18
Wenwen Zhao, Haitao Feng, Wen Sun, Kang Liu, Jin-Jian Lu, Xiuping Chen
Oxidative stress causes endothelial death while underlying mechanisms remain elusive. Herein, the pro-death effect of tert-butyl hydroperoxide (t-BHP) was investigated with low concentration (50μM) of t-BHP (t-BHPL) and high concentration (500μM) of t-BHP (t-BHPH). Both t-BHPL and t-BHPH induced endothelial cell death was determined. T-BHPL induced caspase-dependent apoptosis and reactive oxygen species (ROS) generation, which was inhibited by N-acetyl-L-cysteine (NAC). Furthermore, NADPH oxidase inhibitor diphenyleneiodonium (DPI), NOX4 siRNA, and NOX4 inhibitor GKT137831 reduced t-BHPL-induced ROS generation while mitochondrial respiratory chain inhibitors rotenone (Rot), 2-thenoyltrifluoroacetone (TTFA), and antimycin A (AA) failed to do so...
January 5, 2017: Redox Biology
https://www.readbyqxmd.com/read/28087739/tnf-signaling-through-rip1-kinase-enhances-sn38-induced-death-in-colon-adenocarcinoma
#19
Lucia Cabal-Hierro, Peter J O'Dwyer
: Elucidation of tumor necrosis factor (TNF)-directed mechanisms for cell death induction and maintenance of tumor growth has revealed a role for receptor-interacting protein kinases 1 and 3 (RIPK1/RIP1 and RIPK3/RIP3), components of the necrosome complex, as determinants of cell fate. Here the participation of TNF signaling was analyzed with regard to the cytotoxic action of different DNA damaging agents in a panel of colon cancer cells. While most of these cell lines were insensitive to TNF, combination with these drugs increased sensitivity by inducing cell death and DNA damage, especially in the case of the topoisomerase inhibitor SN38...
January 13, 2017: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/28077640/viral-rna-at-two-stages-of-reovirus-infection-is-required-for-the-induction-of-necroptosis
#20
Angela K Berger, Bradley E Hiller, Deepti Thete, Anthony J Snyder, Encarnacion Perez, Jason W Upton, Pranav Danthi
: Necroptosis, a regulated form of necrotic cell death requires the activation of the RIP3 kinase. Here, we identify that infection of host cells with reovirus can result in necroptosis. We find that necroptosis requires sensing of the genomic RNA within incoming virus particles via cytoplasmic RNA sensors to produce type I IFN. While these events that occur prior to de novo synthesis of viral RNA are required for induction of necroptosis, they are not sufficient. Induction of necroptosis also requires late stages of reovirus infection...
January 11, 2017: Journal of Virology
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