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RIP3 or RIPK3

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https://www.readbyqxmd.com/read/27920775/human-papillomavirus-downregulates-the-expression-of-ifitm1-and-ripk3-to-escape-from-ifn%C3%AE-and-tnf%C3%AE-mediated-antiproliferative-effects-and-necroptosis
#1
Wenbo Ma, Bart Tummers, Edith M G van Esch, Renske Goedemans, Cornelis J M Melief, Craig Meyers, Judith M Boer, Sjoerd H van der Burg
The clearance of a high-risk human papillomavirus (hrHPV) infection takes time and requires the local presence of a strong type 1 cytokine T cell response, suggesting that hrHPV has evolved mechanisms to resist this immune attack. Using an unique system for non, newly, and persistent hrHPV infection, we show that hrHPV infection renders keratinocytes (KCs) resistant to the antiproliferative- and necroptosis-inducing effects of IFNγ and TNFα. HrHPV-impaired necroptosis was associated with the upregulation of several methyltransferases, including EZH2, and the downregulation of RIPK3 expression...
2016: Frontiers in Immunology
https://www.readbyqxmd.com/read/27917412/zbp1-dai-is-an-innate-sensor-of-influenza-virus-triggering-the-nlrp3-inflammasome-and-programmed-cell-death-pathways
#2
Teneema Kuriakose, Si Ming Man, R K Subbarao Malireddi, Rajendra Karki, Sannula Kesavardhana, David E Place, Geoffrey Neale, Peter Vogel, Thirumala-Devi Kanneganti
The interferon-inducible protein Z-DNA binding protein 1 (ZBP1, also known as DNA-dependent activator of IFN-regulatory factors (DAI) and DLM-1) was identified as a dsDNA sensor, which instigates innate immune responses. However, this classification has been disputed and whether ZBP1 functions as a pathogen sensor during an infection has remained unknown. Herein, we demonstrated ZBP1-mediated sensing of the influenza A virus (IAV) proteins NP and PB1, triggering cell death and inflammatory responses via the RIPK1-RIPK3-Caspase-8 axis...
August 5, 2016: Science Immunology
https://www.readbyqxmd.com/read/27913189/construction-and-analysis-of-a-human-testis-sperm-enriched-interaction-network-unraveling-the-ppp1cc2-interactome
#3
Joana Vieira Silva, Sooyeon Yoon, Pieter-Jan De Bock, Alexander V Goltsev, Kris Gevaert, José Fernando F Mendes, Margarida Fardilha
BACKGROUND: Phosphoprotein phosphatase 1 catalytic subunit gamma 2 (PPP1CC2), a PPP1CC tissue-specific alternative splice restricted to testicular germ cells and spermatozoa, is essential for spermatogenesis and spermatozoa motility. The key to understand PPP1CC2 regulation lies on the characterization of its interacting partners. METHODS: We construct a testis/sperm-enriched protein interaction network and analyzed the topological properties and biological context of the network...
November 29, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27901113/programmed-necrosis-a-new-mechanism-of-steroidogenic-luteal-cell-death-and-elimination-during-luteolysis-in-cows
#4
Takuo Hojo, Marta J Siemieniuch, Karolina Lukasik, Katarzyna K Piotrowska-Tomala, Agnieszka W Jonczyk, Kiyoshi Okuda, Dariusz J Skarzynski
Programmed necrosis (necroptosis) is an alternative form of programmed cell death that is regulated by receptor-interacting protein kinase (RIPK) 1 and 3-dependent, but is a caspase (CASP)-independent pathway. In the present study, to determine if necroptosis participates in bovine structural luteolysis, we investigated RIPK1 and RIPK3 expression throughout the estrous cycle, during prostaglandin F2α (PGF)-induced luteolysis in the bovine corpus luteum (CL), and in cultured luteal steroidogenic cells (LSCs) after treatment with selected luteolytic factors...
November 30, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27900566/autophagy-regulates-death-of-retinal-pigment-epithelium-cells-in-age-related-macular-degeneration
#5
REVIEW
Kai Kaarniranta, Paulina Tokarz, Ali Koskela, Jussi Paterno, Janusz Blasiak
Age-related macular degeneration (AMD) is an eye disease underlined by the degradation of retinal pigment epithelium (RPE) cells, photoreceptors, and choriocapillares, but the exact mechanism of cell death in AMD is not completely clear. This mechanism is important for prevention of and therapeutic intervention in AMD, which is a hardly curable disease. Present reports suggest that both apoptosis and pyroptosis (cell death dependent on caspase-1) as well as necroptosis (regulated necrosis dependent on the proteins RIPK3 and MLKL, caspase-independent) can be involved in the AMD-related death of RPE cells...
November 29, 2016: Cell Biology and Toxicology
https://www.readbyqxmd.com/read/27886851/the-role-of-necroptosis-in-pulmonary-diseases
#6
REVIEW
Kenji Mizumura, Shuichiro Maruoka, Yasuhiro Gon, Augustine M K Choi, Shu Hashimoto
By regulating the cell number and eliminating harmful cells, programmed cell death plays a critical role in development, homeostasis, and disease. While apoptosis is a recognized form of programmed cell death, necrosis was considered a type of uncontrolled cell death induced by extreme physical or chemical stress. However, recent studies have revealed the existence of a genetically programmed and regulated form of necrosis, termed necroptosis. Necroptosis is defined as necrotic cell death that is dependent on receptor-interacting protein kinase 3 (RIPK3)...
November 2016: Respiratory Investigation
https://www.readbyqxmd.com/read/27869161/therapeutic-targeting-of-necroptosis-by-smac-mimetic-bypasses-apoptosis-resistance-in-acute-myeloid-leukemia-cells
#7
C Safferthal, K Rohde, S Fulda
Resistance to apoptosis, for example due to overexpression of Inhibitor of Apoptosis (IAP) proteins, is associated with poor prognosis in acute myeloid leukemia (AML). Here, we identify that Smac mimetics such as BV6, which antagonizes IAP proteins, elicit necroptosis in AML cells, in which apoptosis is inhibited pharmacologically by caspase inhibitors or genetically by caspase-8 knockdown. Importantly, BV6 triggers necroptosis also in apoptosis-resistant patient-derived AML blasts, underlining the clinical relevance of our findings...
November 21, 2016: Oncogene
https://www.readbyqxmd.com/read/27856241/palmitate-induces-rip1-rip3-dependent-necrosis-via-mlkl-mediated-pore-formation-in-the-plasma-membrane-of-raw-264-7%C3%A2-cells
#8
Seong Keun Kim, Mihee Yun, Gimoon Seo, Ji-Young Lee, Seong-Beom Lee
We previously reported that palmitate induces receptor-interacting protein (RIP)1-dependent necrosis in RAW 264.7 macrophage cells. In response to death receptor stimuli, RIP1 is reported to activate RIP3, which causes the phosphorylation and translocation of mixed-lineage kinase domain-like (MLKL) protein to the plasma membrane, subsequent pore formation in the plasma membrane, and necrotic cell death. In the current study, we investigated the role of MLKL in palmitate-induced, RIP1/RIP3-dependent necrotic cell death in RAW 264...
November 14, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27850980/1344-plasma-rip3-a-regulator-of-necroptosis-is-associated-with-mortality-organ-dysfunction-in-sepsis
#9
John Reilly, Michael Shashaty, Brian Anderson, Jessica Palakshappa, Meghan Hotz, Jason Christie, Nuala Meyer, Nilam Mangalmurti
No abstract text is available yet for this article.
December 2016: Critical Care Medicine
https://www.readbyqxmd.com/read/27834956/a-bak-dependent-mitochondrial-amplification-step-contributes-to-smac-mimetic-glucocorticoid-induced-necroptosis
#10
Katharina Rohde, Lara Kleinesudeik, Stefanie Roesler, Oliver Löwe, Juliana Heidler, Katrin Schröder, Ilka Wittig, Stefan Dröse, Simone Fulda
Necroptosis is a form of programmed cell death that critically depends on RIP3 and MLKL. However, the contribution of mitochondria to necroptosis is still poorly understood. In the present study, we discovered that mitochondrial perturbations play a critical role in Smac mimetic/Dexamethasone (Dexa)-induced necroptosis independently of death receptor ligands. We demonstrate that the Smac mimetic BV6 and Dexa cooperate to trigger necroptotic cell death in acute lymphoblastic leukemia (ALL) cells that are deficient in caspase activation due to absent caspase-8 expression or pharmacological inhibition by the caspase inhibitor zVAD...
November 11, 2016: Cell Death and Differentiation
https://www.readbyqxmd.com/read/27832137/atp-competitive-mlkl-binders-have-no-functional-impact-on-necroptosis
#11
Bin Ma, Doug Marcotte, Murugan Paramasivam, Klaus Michelsen, Ti Wang, Andrea Bertolotti-Ciarlet, John Howard Jones, Ben Moree, Margaret Butko, Joshua Salafsky, Xin Sun, Timothy McKee, Laura F Silvian
MLKL is a pore forming pseudokinase involved in the final stage of necroptosis, a form of programmed cell death. Its phosphorylation by RIPK3 is necessary for triggering necroptosis but not for triggering apoptosis, which makes it a unique target for pharmacological inhibition to block necroptotic cell death. This mechanism has been described as playing a role in disease progression in neurodegenerative and inflammatory diseases. A type II kinase inhibitor (cpd 1) has been described that reportedly binds to the MLKL pseudokinase domain and prevents necroptosis...
2016: PloS One
https://www.readbyqxmd.com/read/27819682/ripk1-inhibits-zbp1-driven-necroptosis-during-development
#12
Kim Newton, Katherine E Wickliffe, Allie Maltzman, Debra L Dugger, Andreas Strasser, Victoria C Pham, Jennie R Lill, Merone Roose-Girma, Søren Warming, Margaret Solon, Hai Ngu, Joshua D Webster, Vishva M Dixit
Receptor-interacting protein kinase 1 (RIPK1) promotes cell survival-mice lacking RIPK1 die perinatally, exhibiting aberrant caspase-8-dependent apoptosis and mixed lineage kinase-like (MLKL)-dependent necroptosis. However, mice expressing catalytically inactive RIPK1 are viable, and an ill-defined pro-survival function for the RIPK1 scaffold has therefore been proposed. Here we show that the RIP homotypic interaction motif (RHIM) in RIPK1 prevents the RHIM-containing adaptor protein ZBP1 (Z-DNA binding protein 1; also known as DAI or DLM1) from activating RIPK3 upstream of MLKL...
December 1, 2016: Nature
https://www.readbyqxmd.com/read/27819681/ripk1-counteracts-zbp1-mediated-necroptosis-to-inhibit-inflammation
#13
Juan Lin, Snehlata Kumari, Chun Kim, Trieu-My Van, Laurens Wachsmuth, Apostolos Polykratis, Manolis Pasparakis
Receptor-interacting protein kinase 1 (RIPK1) regulates cell death and inflammation through kinase-dependent and -independent functions. RIPK1 kinase activity induces caspase-8-dependent apoptosis and RIPK3 and mixed lineage kinase like (MLKL)-dependent necroptosis. In addition, RIPK1 inhibits apoptosis and necroptosis through kinase-independent functions, which are important for late embryonic development and the prevention of inflammation in epithelial barriers. The mechanism by which RIPK1 counteracts RIPK3-MLKL-mediated necroptosis has remained unknown...
December 1, 2016: Nature
https://www.readbyqxmd.com/read/27816051/molecular-features-of-the-cytotoxicity-of-an-nhe-inhibitor-evidence-of-mitochondrial-alterations-ros-overproduction-and-dna-damage
#14
Francesca Aredia, Sebastian Czaplinski, Simone Fulda, A Ivana Scovassi
BACKGROUND: NH exchangers (NHEs) play a crucial role in regulating intra/extracellular pH, which is altered in cancer cells, and are therefore suitable targets to alter cancer cell metabolism in order to inhibit cell survival and proliferation. Among NHE inhibitors, amiloride family members are commonly used in clinical practice as diuretics; we focused on the amiloride HMA, reporting a net cytotoxic effect on a panel of human cancer cell lines; now we aim to provide new insights into the molecular events leading to cell death by HMA...
November 5, 2016: BMC Cancer
https://www.readbyqxmd.com/read/27815445/neutrophil-necroptosis-is-triggered-by-ligation-of-adhesion-molecules-following-gm-csf-priming
#15
Xiaoliang Wang, Zhaoyue He, He Liu, Shida Yousefi, Hans-Uwe Simon
Apoptosis is the most common form of neutrophil death under both physiological and inflammatory conditions. However, forms of nonapoptotic neutrophil death have also been observed. In the current study, we report that human neutrophils undergo necroptosis after exposure to GM-CSF followed by the ligation of adhesion receptors such as CD44, CD11b, CD18, or CD15. Using a pharmacological approach, we demonstrate the presence of a receptor-interacting protein kinase-3 (RIPK3)-a mixed lineage kinase-like (MLKL) signaling pathway in neutrophils which, following these treatments, first activates p38 MAPK and PI3K, that finally leads to the production of high levels of reactive oxygen species (ROS)...
November 15, 2016: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/27811014/regulated-necrosis-related-molecule-mrna-expression-in-humans-mice-and-murine-acute-tissue-injury-systemic-autoimmunity-leading-to-progressive-organ-damage-and-progressive-fibrosis
#16
Mohsen Honarpisheh, Jyaysi Desai, Julian A Marschner, Marc Weidenbusch, Maciej Lech, Volker Vielhauer, Hans-Joachim Anders, Shrikant R Mulay
The species-specific, as well as organ-specific expression of regulated necrosis (RN)-related molecules, is not known. We determined the expression levels of TNFR1, RIPK1, RIPK3, MLKL, CASP8, FADD, CIAP1, CIAP2, GPX4, CYPD, CASP1, NLRP3, and PARP1 in human and mouse solid organs. We observed significant differences in expression of these molecules between human and mice. In addition, we characterized their expression profiles in acute as well as persistent tissue injury and chronic tissue remodeling using acute and chronic kidney injury models...
November 3, 2016: Bioscience Reports
https://www.readbyqxmd.com/read/27788734/-programmed-necrosis-mediated-by-receptor-interacting-protein-3-a-new-target-for-liver-disease-research
#17
J Zhang, Y Jing, Y N Li, L Zhou, B M Wang
Hepatocyte death mainly includes apoptosis and necrosis and is a critical process in the pathophysiological mechanism of liver injury caused by various reasons. Recent studies have shown that key regulatory molecules in the inhibition of apoptosis such as caspase cannot be used as targets for inhibiting disease progression in clinical practice. In recent years, programmed necrosis mediated by receptor-interacting protein 3(RIP3)becomes a new hot research topic. It not only plays an important role in inducing inflammatory response, but also is closely regulated by intracellular signal factors, and it is a type of active cell death which can be interfered with...
September 20, 2016: Zhonghua Gan Zang Bing za Zhi, Zhonghua Ganzangbing Zazhi, Chinese Journal of Hepatology
https://www.readbyqxmd.com/read/27778032/activation-of-necroptosis-in-a-rat-model-of-acute-respiratory-distress-syndrome-induced-by-oleic-acid
#18
Long Pan, Dun-Chen Yao, Yu-Zhong Yu, Bing-Jun Chen, Sheng-Jie Li, Gui-He Hu, Chang Xi, Zi-Hui Wang, Jian-Hua Li, Jie Long, Yong-Sheng Tu
The present study was aimed to investigate the role of necroptosis in the pathogenesis of acute respiratory distress syndrome (ARDS). The rat model of ARDS was induced by intravenous injection of oleic acid (OA), and observed for 4 h. The lung injury was evaluated by arterial blood gas, lung wet-dry weight ratio (W/D) and histological analyses. Simultaneously, bronchoalveolar lavage fluid (BALF) was collected for total and differential cell analysis and total protein determination. Tumor necrosis factor alpha (TNF-α) level in BALF was determined with a rat TNF-α ELISA kit...
October 25, 2016: Sheng Li Xue Bao: [Acta Physiologica Sinica]
https://www.readbyqxmd.com/read/27760053/a-murder-mystery-in-the-liver-who-done-it-and-how
#19
Lily Dara, Zhang-Xu Liu, Neil Kaplowitz
Hepatocyte death, which can be apoptosis or necrosis depending on the context, is a prominent feature of liver disease. The lectin concanavalin A (ConA) activates immune cells, resulting in inflammatory liver injury and hepatocyte necrosis. In this issue of the JCI, Günther et al. demonstrate that the pseudokinase mixed lineage kinase domain-like protein (MLKL) participates in hepatocyte death in ConA injury and that MLKL-mediated death is independent of the receptor-interacting protein kinase RIPK3. RIPK3 was absent in hepatocytes, and MLKL-deficient mice, but not RIPK3-deficient mice, were protected from ConA-induced liver injury...
November 1, 2016: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/27756752/tsc2-deficiency-unmasks-a-novel-necrosis-pathway-that-is-suppressed-by-the-rip1-rip3-mlkl-signaling-cascade
#20
Piotr T Filipczak, Cynthia L Thomas, Wenshu Chen, Andrew Salzman, Jacob D McDonald, Yong Lin, Steven A Belinsky
Tuberous sclerosis complex (TSC) is a genetic multi-organ disorder characterized by the development of neoplastic lesions in kidney, lung, brain, heart and skin. It is caused by an inactivating mutation in tumor suppressor genes coding the TSC1/TSC2 complex, resulting in hyperactivation of mTOR- and Raf/MEK/MAPK-dependent signaling that stimulates tumor cell proliferation and metastasis. Despite its oncogenic effect, cells with TSC deficiency were more sensitive to oxidative stress and dependent on mitochondrial metabolism, providing a rationale for a new therapeutic approach...
October 18, 2016: Cancer Research
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