keyword
MENU ▼
Read by QxMD icon Read
search

RIPK3

keyword
https://www.readbyqxmd.com/read/28592892/noncanocial-cell-death-program-independent-of-caspase-activation-cascade-and-necroptotic-modules-is-elicited-by-loss-of-tgf%C3%AE-activated-kinase-1
#1
September R Mihaly, Yosuke Sakamachi, Jun Ninomiya-Tsuji, Sho Morioka
Programmed cell death (PCD) occurs in several forms including apoptosis and necroptosis. Apoptosis is executed by the activation of caspases, while necroptosis is dependent on the receptor interacting protein kinase 3 (RIPK3). Precise control of cell death is crucial for tissue homeostasis. Indeed, necroptosis is triggered by caspase inhibition to ensure cell death. Here we identified a previously uncharacterized cell death pathway regulated by TAK1, which is unexpectedly provoked by inhibition of caspase activity and necroptosis cascades...
June 7, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28539327/quantitative-phospho-proteomic-analysis-of-tnf%C3%AE-nf%C3%AE%C2%BAb-signaling-reveals-a-role-for-ripk1-phosphorylation-in-suppressing-necrotic-cell-death
#2
Firaz Mohideen, Joao Paolo, Alban Ordureau, Steve P Gygi, J Wade Harper
TNFα is a potent inducer of inflammation due to its ability to promote gene expression, in part via the NFκB pathway. Moreover, in some contexts, TNFα promotes Caspase-dependent apoptosis or RIPK1/RIPK3/MLKL-dependent necrosis. Engagement of the TNF Receptor Signaling Complex (TNF-RSC), which contains multiple kinase activities, promotes phosphorylation of several downstream components, including TAK1, IKKα/IKKβ, IκBα, and NFκB. However, immediate downstream phosphorylation events occurring in response to TNFα signaling are poorly understood at a proteome-wide level...
May 24, 2017: Molecular & Cellular Proteomics: MCP
https://www.readbyqxmd.com/read/28524164/ripped-for-neuroinflammation
#3
Bart Tummers, Douglas R Green
Activation of the receptor interacting serine/threonine kinase (RIPK) 3 mediates an inflammatory type of cell death called necroptosis; in addition, RIPK3 has necroptosis-independent roles in inflammation, although these are not well defined. In a recent study published in Cell, Daniels and colleagues demonstrate that RIPK3 controls West Nile virus infection by promoting neuroinflammation in the central nervous system without affecting neuronal death.
May 19, 2017: Cell Research
https://www.readbyqxmd.com/read/28511054/synthesis-and-in-vitro-anticancer-activity-of-new-2-thioxo-oxazolidin-4-one-derivatives
#4
Júlia Furtado Campos, Michelly Cristiny Pereira, Wanessa Layssa Batista de Sena, Caio Gomes de Barros Martins, Jamerson Ferreira de Oliveira, Cezar Augusto da Cruz Amorim, Moacyr Jesus Barreto de Melo Rêgo, Marina Galdino da Rocha Pitta, Maria do Carmo Alves de Lima, Maira Galdino da Rocha Pitta, Ivan da Rocha Pitta
BACKGROUND: Oxazolidinones derivatives exhibit different biological properties, including anticancer activity. This work aimed to investigate the anticancer potential of five novel 2-Thioxo-oxazolidin-4-one derivatives. METHODS: Cytotoxicity assays were performed in human peripheral blood mononuclear cells (PBMCs) from healthy individuals and seven tumor cell lines. Apoptosis detection and cell cycle were evaluated by flow cytometry and the expression of genes involved in cell death processes by Real-Time PCR...
March 18, 2017: Pharmacological Reports: PR
https://www.readbyqxmd.com/read/28507808/pro-necrotic-molecules-impact-local-immunosurveillance-in-human-breast-cancer
#5
Gautier Stoll, Yuting Ma, Heng Yang, Oliver Kepp, Laurence Zitvogel, Guido Kroemer
Necrosis culminates in spilling cellular content through the permeabilized plasma membrane, thereby releasing potentially immunostimulatory molecules in the pericellular space of dead cells. Accordingly, molecules involved in necroptotic signaling, such as receptor-interacting serine/threonine-protein kinase 3 (RIPK3) and mixed lineage kinase-like (MLKL) have been found to stimulate anticancer immune responses in mouse models of chemotherapy. mRNAs encoding prominent pro-necrotic gene products (RIPK1, RIPK3, MLKL, PGAM5 and DFNA5) were correlated with immune-related metagenes in several cancer types (breast, colorectal, lung, ovary, melanoma), revealing the strongest associations in breast cancer...
2017: Oncoimmunology
https://www.readbyqxmd.com/read/28498367/initiation-and-execution-mechanisms-of-necroptosis-an-overview
#6
REVIEW
Sasker Grootjans, Tom Vanden Berghe, Peter Vandenabeele
Necroptosis is a form of regulated cell death, which is induced by ligand binding to TNF family death domain receptors, pattern recognizing receptors and virus sensors. The common feature of these receptor systems is the implication of proteins, which contain a receptor interaction protein kinase (RIPK) homology interaction motif (RHIM) mediating recruitment and activation of receptor-interacting protein kinase 3 (RIPK3), which ultimately activates the necroptosis executioner mixed lineage kinase domain-like (MLKL)...
May 12, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28462531/the-interplay-of-ikk-nf-%C3%AE%C2%BAb-and-ripk1-signaling-in-the-regulation-of-cell-death-tissue-homeostasis-and-inflammation
#7
REVIEW
Vangelis Kondylis, Snehlata Kumari, Katerina Vlantis, Manolis Pasparakis
Regulated cell death pathways have important functions in host defense and tissue homeostasis. Studies in genetic mouse models provided evidence that cell death could cause inflammation in different tissues. Inhibition of RIPK3-MLKL-dependent necroptosis by FADD and caspase-8 was identified as a key mechanism preventing inflammation in epithelial barriers. Moreover, the interplay between IKK/NF-κB and RIPK1 signaling was recognized as a critical determinant of tissue homeostasis and inflammation. NEMO was shown to regulate RIPK1 kinase activity-mediated apoptosis by NF-κB-dependent and -independent functions, which are critical for averting chronic tissue injury and inflammation in the intestine and the liver...
May 2017: Immunological Reviews
https://www.readbyqxmd.com/read/28462528/the-in-vivo-evidence-for-regulated-necrosis
#8
REVIEW
Wulf Tonnus, Andreas Linkermann
Necrosis is a hallmark of several widespread diseases or their direct complications. In the past decade, we learned that necrosis can be a regulated process that is potentially druggable. RIPK3- and MLKL-mediated necroptosis represents by far the best studied pathway of regulated necrosis. During necroptosis, the release of damage-associated molecular patterns (DAMPs) drives a phenomenon referred to as necroinflammation, a common consequence of necrosis. However, most studies of regulated necrosis investigated cell lines in vitro in a cell autonomous manner, which represents a non-physiological situation...
May 2017: Immunological Reviews
https://www.readbyqxmd.com/read/28462524/ripk3-driven-cell-death-during-virus-infections
#9
REVIEW
Jason W Upton, Maria Shubina, Siddharth Balachandran
The programmed self-destruction of infected cells is a powerful antimicrobial strategy in metazoans. For decades, apoptosis represented the dominant mechanism by which the virus-infected cell was thought to undergo programmed cell death. More recently, however, new mechanisms of cell death have been described that are also key to host defense. One such mechanism in vertebrates is programmed necrosis, or "necroptosis", driven by receptor-interacting protein kinase 3 (RIPK3). Once activated by innate immune stimuli, including virus infections, RIPK3 phosphorylates the mixed lineage kinase domain-like protein (MLKL), which then disrupts cellular membranes to effect necroptosis...
May 2017: Immunological Reviews
https://www.readbyqxmd.com/read/28462521/ripk3-in-cell-death-and-inflammation-the-good-the-bad-and-the-ugly
#10
REVIEW
Susana Orozco, Andrew Oberst
Necroptosis is a form of cell death that can be observed downstream of death receptor or pattern recognition receptor signaling under certain cellular contexts, or in response to some viral and bacterial infections. The receptor interacting protein kinases-1 (RIPK1) and RIPK3 are at the core of necroptotic signaling, among other proteins. Because this pathway is normally halted by the pro-apoptotic protease caspase-8 and the IAP ubiquitin ligases, how and when necroptosis is triggered in physiological settings are ongoing questions...
May 2017: Immunological Reviews
https://www.readbyqxmd.com/read/28461567/kinase-activities-of-ripk1-and-ripk3-can-direct-ifn-%C3%AE-synthesis-induced-by-lipopolysaccharide
#11
Danish Saleh, Malek Najjar, Matija Zelic, Saumil Shah, Shoko Nogusa, Apostolos Polykratis, Michelle K Paczosa, Peter J Gough, John Bertin, Michael Whalen, Katherine A Fitzgerald, Nikolai Slavov, Manolis Pasparakis, Siddharth Balachandran, Michelle Kelliher, Joan Mecsas, Alexei Degterev
The innate immune response is a central element of the initial defense against bacterial and viral pathogens. Macrophages are key innate immune cells that upon encountering pathogen-associated molecular patterns respond by producing cytokines, including IFN-β. In this study, we identify a novel role for RIPK1 and RIPK3, a pair of homologous serine/threonine kinases previously implicated in the regulation of necroptosis and pathologic tissue injury, in directing IFN-β production in macrophages. Using genetic and pharmacologic tools, we show that catalytic activity of RIPK1 directs IFN-β synthesis induced by LPS in mice...
June 1, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28451648/necroptosis-and-cancer
#12
Ayaz Najafov, Hongbo Chen, Junying Yuan
Necroptosis is a programmed lytic cell death pathway, deregulation of which is linked to various inflammatory disorders. Escape from programmed cell death and inflammation play a significant role in cancer, and therefore, investigating the role of necroptosis in cancer has been of high interest. Necroptosis has been shown to promote cancer metastasis and T cells death. Escape from necroptosis via loss of RIPK3 expression is a feature of some cancers. While necroptosis is a promising novel target for cancer therapies, further investigation into its biological role in carcinogenesis is warranted...
April 2017: Trends in Cancer
https://www.readbyqxmd.com/read/28445730/ripk3-mediates-necroptosis-during-embryonic-development-and-postnatal-inflammation-in-fadd-deficient-mice
#13
Qun Zhao, XianJun Yu, HaiWei Zhang, YongBo Liu, XiXi Zhang, XiaoXia Wu, Qun Xie, Ming Li, Hao Ying, Haibing Zhang
RIPK3 mediates cell death and regulates inflammatory responses. Although genetic studies have suggested that RIPK3-MLKL-mediated necroptosis leads to embryonic lethality in Fadd or Caspase-8-deficient mice, the exact mechanisms are not fully understood. Here, we generated Ripk3 mutant mice by altering the RIPK3 kinase domain (Ripk3(Δ/Δ) mice), thus abolishing its kinase activity. Ripk3(Δ/Δ) cells were resistant to necroptosis stimulation in vitro, and Ripk3(Δ/Δ) mice were protected from necroptotic diseases...
April 25, 2017: Cell Reports
https://www.readbyqxmd.com/read/28428949/p2x1-p2x4-and-p2x7-receptor-knock-out-mice-expose-differential-outcome-of-sepsis-induced-by-%C3%AE-haemolysin-producing-escherichia-coli
#14
Anne-Sofie Greve, Marianne Skals, Steen K Fagerberg, Wulf Tonnus, Svend Ellermann-Eriksen, Richard J Evans, Andreas Linkermann, Helle A Praetorius
α-haemolysin (HlyA)-producing Escherichia coli commonly inflict severe urinary tract infections, including pyelonephritis, which comprises substantial risk for sepsis. In vitro, the cytolytic effect of HlyA is mainly mediated by ATP release through the HlyA pore and subsequent P2X1/P2X7 receptor activation. This amplification of the lytic process is not unique to HlyA but is observed by many other pore-forming proteins including complement-induced haemolysis. Since free hemoglobin in the blood is known to be associated with a worse outcome in sepsis one could speculate that inhibition of P2X receptors would ameliorate the course of sepsis...
2017: Frontiers in Cellular and Infection Microbiology
https://www.readbyqxmd.com/read/28412393/adhesion-induced-eosinophil-cytolysis-requires-the-ripk3-mlkl-signaling-pathway-which-is-counter-regulated-by-autophagy
#15
Susanne Radonjic-Hoesli, Xiaoliang Wang, Elisabeth de Graauw, Christina Stoeckle, Beata Styp-Rekowska, Ruslan Hlushchuk, Dagmar Simon, Peter J Spaeth, Shida Yousefi, Hans-Uwe Simon
BACKGROUND: Eosinophils are a subset of granulocytes which can be involved in the pathogenesis of different diseases, including allergy. Their effector functions are closely linked to their cytotoxic granule proteins. The release takes place by several different mechanisms, one of which is cytolysis, which is associated with the release of intact granules, so-called clusters of free eosinophil granules. The mechanism underlying this activation-induced form of cell death in eosinophils has remained unclear...
April 12, 2017: Journal of Allergy and Clinical Immunology
https://www.readbyqxmd.com/read/28410401/ripk3-interacts-with-mavs-to-regulate-type-i-ifn-mediated-immunity-to-influenza-a-virus-infection
#16
Jeffrey Downey, Erwan Pernet, François Coulombe, Benoit Allard, Isabelle Meunier, Joanna Jaworska, Salman Qureshi, Donald C Vinh, James G Martin, Philippe Joubert, Maziar Divangahi
The type I interferon pathway plays a critical role in both host defense and tolerance against viral infection and thus requires refined regulatory mechanisms. RIPK3-mediated necroptosis has been shown to be involved in anti-viral immunity. However, the exact role of RIPK3 in immunity to Influenza A Virus (IAV) is poorly understood. In line with others, we, herein, show that Ripk3-/- mice are highly susceptible to IAV infection, exhibiting elevated pulmonary viral load and heightened morbidity and mortality...
April 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28407477/a-riptide-protects-neurons-from-infection
#17
COMMENT
Ryan P Gilley, William J Kaiser
RIPK3 and RIPK1 limit virus spread by executing either apoptotic or necroptotic cell death in response to infection. In a recent issue of Cell, Daniels et al. (2017) unveil an unexpected cell death-independent requirement of RIP kinase activity in coordinating neuroinflammation, restricting West Nile virus pathogenesis in neurons.
April 12, 2017: Cell Host & Microbe
https://www.readbyqxmd.com/read/28401933/bcl-xl-mediates-ripk3-dependent-necrosis-in-m-tuberculosis-infected-macrophages
#18
X Zhao, N Khan, H Gan, F Tzelepis, T Nishimura, S-Y Park, M Divangahi, H G Remold
Virulent Mycobacterium tuberculosis (Mtb) triggers necrosis in host Mϕ, which is essential for successful pathogenesis in tuberculosis. Here we demonstrate that necrosis of Mtb-infected Mϕ is dependent on the action of the cytosolic Receptor Interacting Protein Kinase 3 (RIPK3) and the mitochondrial Bcl-2 family member protein B-cell lymphoma-extra large (Bcl-xL). RIPK3-deficient Mϕ are able to better control bacterial growth in vitro and in vivo. Mechanistically, cytosolic RIPK3 translocates to the mitochondria where it promotes necrosis and blocks caspase 8-activation and apoptosis via Bcl-xL...
April 12, 2017: Mucosal Immunology
https://www.readbyqxmd.com/read/28388412/escrt-iii-acts-downstream-of-mlkl-to-regulate-necroptotic-cell-death-and-its-consequences
#19
Yi-Nan Gong, Cliff Guy, Hannes Olauson, Jan Ulrich Becker, Mao Yang, Patrick Fitzgerald, Andreas Linkermann, Douglas R Green
The activation of mixed lineage kinase-like (MLKL) by receptor-interacting protein kinase-3 (RIPK3) results in plasma membrane (PM) disruption and a form of regulated necrosis, called necroptosis. Here, we show that, during necroptosis, MLKL-dependent calcium (Ca(2+)) influx and phosphatidylserine (PS) exposure on the outer leaflet of the plasma membrane preceded loss of PM integrity. Activation of MLKL results in the generation of broken, PM "bubbles" with exposed PS that are released from the surface of the otherwise intact cell...
April 6, 2017: Cell
https://www.readbyqxmd.com/read/28366204/ripk3-restricts-viral-pathogenesis-via-cell-death-independent-neuroinflammation
#20
COMMENT
Brian P Daniels, Annelise G Snyder, Tayla M Olsen, Susana Orozco, Thomas H Oguin, Stephen W G Tait, Jennifer Martinez, Michael Gale, Yueh-Ming Loo, Andrew Oberst
Receptor-interacting protein kinase-3 (RIPK3) is an activator of necroptotic cell death, but recent work has implicated additional roles for RIPK3 in inflammatory signaling independent of cell death. However, while necroptosis has been shown to contribute to antiviral immunity, death-independent roles for RIPK3 in host defense have not been demonstrated. Using a mouse model of West Nile virus (WNV) encephalitis, we show that RIPK3 restricts WNV pathogenesis independently of cell death. Ripk3(-/-) mice exhibited enhanced mortality compared to wild-type (WT) controls, while mice lacking the necroptotic effector MLKL, or both MLKL and caspase-8, were unaffected...
April 6, 2017: Cell
keyword
keyword
37620
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"