keyword
MENU ▼
Read by QxMD icon Read
search

RIPK3

keyword
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
#1
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
#2
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
#3
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 14, 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28407477/a-riptide-protects-neurons-from-infection
#4
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
#5
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
#6
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
#7
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
https://www.readbyqxmd.com/read/28342910/receptor-interacting-protein-kinase-3-controls-keratinocyte-activation-in-a-necroptosis-independent-manner-and-promotes-psoriatic-dermatitis-in-mice
#8
Tetsuya Honda, Osamu Yamamoto, Yu Sawada, Gyohei Egawa, Akihiko Kitoh, Atsushi Otsuka, Teruki Dainichi, Saeko Nakajima, Yoshiki Miyachi, Kenji Kabashima
RIPK3 in keratinocytes facilitates psoriatic inflammation by promoting cytokine and chemokine production, independent of the induction of necroptosis. Control of RIPK3 activation may be a novel therapeutic target for psoriasis.
March 22, 2017: Journal of Allergy and Clinical Immunology
https://www.readbyqxmd.com/read/28297660/progesterone-prevents-high-grade-serous-ovarian-cancer-by-inducing-necroptosis-of-p53-defective-fallopian-tube-epithelial-cells
#9
Na-Yiyuan Wu, Hsuan-Shun Huang, Tung Hui Chao, Hsien Ming Chou, Chao Fang, Chong-Zhen Qin, Chueh-Yu Lin, Tang-Yuan Chu, Hong Hao Zhou
High-grade serous ovarian carcinoma (HGSOC) originates mainly from the fallopian tube (FT) epithelium and always carries early TP53 mutations. We previously reported that tumors initiate in the FT fimbria epithelium because of apoptotic failure and the expansion of cells with DNA double-strand breaks (DSB) caused by bathing of the FT epithelial cells in reactive oxygen species (ROSs) and hemoglobin-rich follicular fluid (FF) after ovulation. Because ovulation is frequent and HGSOC is rare, we hypothesized that luteal-phase progesterone (P4) could eliminate p53-defective FT cells...
March 14, 2017: Cell Reports
https://www.readbyqxmd.com/read/28292903/mouse-cytomegalovirus-m36-and-m45-death-suppressors-cooperate-to-prevent-inflammation-resulting-from-antiviral-programmed-cell-death-pathways
#10
Lisa P Daley-Bauer, Linda Roback, Lynsey N Crosby, A Louise McCormick, Yanjun Feng, William J Kaiser, Edward S Mocarski
The complex interplay between caspase-8 and receptor-interacting protein (RIP) kinase RIP 3 (RIPK3) driving extrinsic apoptosis and necroptosis is not fully understood. Murine cytomegalovirus triggers both apoptosis and necroptosis in infected cells; however, encoded inhibitors of caspase-8 activity (M36) and RIP3 signaling (M45) suppress these antiviral responses. Here, we report that this virus activates caspase-8 in macrophages to trigger apoptosis that gives rise to secondary necroptosis. Infection with double-mutant ΔM36/M45mutRHIM virus reveals a signaling pattern in which caspase-8 activates caspase-3 to drive apoptosis with subsequent RIP3-dependent activation of mixed lineage kinase domain-like (MLKL) leading to necroptosis...
March 28, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28292463/key-players-of-the-necroptosis-pathway-ripk1-and-sirt2-are-altered-in-placenta-from-preeclampsia-and-fetal-growth-restriction
#11
Natalie J Hannan, Sally Beard, Natalie K Binder, Kenji Onda, Tu'uhevaha J Kaitu'u-Lino, Qi Chen, Laura Tuohey, Manarangi De Silva, Stephen Tong
INTRODUCTION: Preeclampsia (PE) and fetal growth restriction (FGR) are among the leading causes of perinatal morbidity and mortality. Placental insufficiency is central to these conditions. The mechanisms underlying placental insufficiency are poorly understood. Apoptosis has long been considered the only form of regulated cell death, recent research has identified an alternate process of programmed cell death known as necroptosis [1]. Necroptosis is distinct from apoptosis, relying on the deacetylase sirtuin-2 [2], receptor interacting kinases RIPK1 and 3, and the pseudokinase MLKL [3]...
March 2017: Placenta
https://www.readbyqxmd.com/read/28289909/ripk1-ripk3-mlkl-mediated-necroptosis-contributes-to-compression-induced-rat-nucleus-pulposus-cells-death
#12
Songfeng Chen, Xiao Lv, Binwu Hu, Zengwu Shao, Baichuan Wang, Kaige Ma, Hui Lin, Min Cui
The aim of this study was to systematically investigate the role of necroptosis in compression-induced rat nucleus pulposus (NP) cells death, as well as explore the underlying mechanisms involved. Rat NP cells underwent various periods of exposure to 1.0 MPa pressure. Cell viability and cell death were quantified by using cell counting kit-8 (CCK-8), and Calcein-AM/propidium iodine (PI) staining respectively. Necroptosis-associated target molecules receptor-interacing protein kinase 1 (RIPK1), phosphorylated RIPK1 (pRIPK1), receptor-interacing protein kinase 3 (RIPK3), phosphorylated RIPK3 (pRIPK3) and mixed lineage kinase domain-like (MLKL) were analyzed by Western-blot and RT-PCR...
March 13, 2017: Apoptosis: An International Journal on Programmed Cell Death
https://www.readbyqxmd.com/read/28279333/dai-another-way-necroptotic-control-of-viral-infection
#13
Jason W Upton, William J Kaiser
Interrogation of murine cytomegalovirus (MCMV)-encoded cell-death suppressors revealed that necroptosis functions as a trap door to eliminate virally infected cells. This crucial host defense pathway is orchestrated by the sensing of infection by DAI/ZBP-1, engagement of the kinase RIPK3, and subsequent membrane permeablization by the pseudokinase MLKL.
March 8, 2017: Cell Host & Microbe
https://www.readbyqxmd.com/read/28273458/distinct-kinase-independent-role-of-ripk3-in-cd11c-mononuclear-phagocytes-in-cytokine-induced-tissue-repair
#14
Kenta Moriwaki, Sakthi Balaji, John Bertin, Peter J Gough, Francis Ka-Ming Chan
Receptor interacting protein kinase 3 (RIPK3) induces necroptosis, a type of regulated necrosis, through its kinase domain and receptor interacting protein (RIP) homotypic interaction motif (RHIM). In addition, RIPK3 has been shown to regulate NLRP3 inflammasome and nuclear factor κB (NF-κB) activation. However, the relative contribution of these signaling pathways to RIPK3-dependent inflammation in distinct immune effectors is unknown. To investigate these questions, we generated RIPK3-GFP reporter mice...
March 7, 2017: Cell Reports
https://www.readbyqxmd.com/read/28260192/polyphyllin-d-a-steroidal-saponin-in-paris-polyphylla-induces-apoptosis-and-necroptosis-cell-death-of-neuroblastoma-cells
#15
Shunsuke Watanabe, Tatuya Suzuki, Fujio Hara, Toshihiro Yasui, Naoko Uga, Atuki Naoe
PURPOSE: Neuroblastoma is a refractory pediatric malignant solid tumor. The previous studies demonstrated that Polyphyllin D, the main constituent of Paris polyphylla, a traditional Chinese medicine, exerts an anti-tumor effect on many tumors. However, its effects against neuroblastomas are unclear. METHODS: We examined the anti-tumor effect of polyphyllin D in human neuroblastoma using IMR-32 and LA-N-2 cells, which exhibit MYCN gene amplification, and NB-69 cells, which do not exhibit MYCN gene amplification...
March 4, 2017: Pediatric Surgery International
https://www.readbyqxmd.com/read/28258062/the-linear-ubiquitin-chain-assembly-complex-regulates-trail-induced-gene-activation-and-cell%C3%A2-death
#16
Elodie Lafont, Chahrazade Kantari-Mimoun, Peter Draber, Diego De Miguel, Torsten Hartwig, Matthias Reichert, Sebastian Kupka, Yutaka Shimizu, Lucia Taraborrelli, Maureen Spit, Martin R Sprick, Henning Walczak
The linear ubiquitin chain assembly complex (LUBAC) is the only known E3 ubiquitin ligase which catalyses the generation of linear ubiquitin linkages de novo LUBAC is a crucial component of various immune receptor signalling pathways. Here, we show that LUBAC forms part of the TRAIL-R-associated complex I as well as of the cytoplasmic TRAIL-induced complex II In both of these complexes, HOIP limits caspase-8 activity and, consequently, apoptosis whilst being itself cleaved in a caspase-8-dependent manner. Yet, by limiting the formation of a RIPK1/RIPK3/MLKL-containing complex, LUBAC also restricts TRAIL-induced necroptosis...
March 3, 2017: EMBO Journal
https://www.readbyqxmd.com/read/28238799/inhibition-of-drp1-hyper-activation-is-protective-in-animal-models-of-experimental-multiple-sclerosis
#17
Fucheng Luo, Karl Herrup, Xin Qi, Yan Yang
Multiple Sclerosis (MS), a leading neurological disorder of young adults, is characterized by the loss of oligodendrocytes (OLs), demyelination, inflammation and neuronal degeneration. Here we show that dynamin-related protein 1 (Drp1), a mitochondrial fission protein, is activated in primary OL cells exposed to TNF-α induced inflammation or oxidative stress, as well as in EAE-immunized and cuprizone toxicity-induced demyelinating mouse models. Inhibition of Drp1 hyper-activation by the selective inhibitor P110 abolishes Drp1 translocation to the mitochondria, reduces mitochondrial fragmentation and stems necrosis in primary OLs exposed to TNF-α and H2O2...
February 24, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28230861/ripk3-interactions-with-mlkl-and-camkii-mediate-oligodendrocytes-death-in-the-developing-brain
#18
Yi Qu, Jun Tang, Huiqing Wang, Shiping Li, Fengyan Zhao, Li Zhang, Q Richard Lu, Dezhi Mu
Oligodendrocyte progenitor cells (OPCs) death is a key contributor to cerebral white matter injury (WMI) in the developing brain. A previous study by our group indicated that receptor-interacting proteins (RIPs) are crucial in mediating necroptosis in developing neurons. However, whether this mechanism is involved in OPCs death is unclear. We aimed to explore the mechanisms of RIP-mediated oligodendrocytes (OLs) death in the developing brain. Oligodendrocytes necroptosis was induced by oxygen-glucose deprivation plus caspase inhibitor zVAD treatment (OGD/zVAD) in vitro...
February 23, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28197335/caspase-8-not-so-silently-deadly
#19
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/28151480/ripk1-ripk3-promotes-vascular-permeability-to-allow-tumor-cell-extravasation-independent-of-its-necroptotic-function
#20
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
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"