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https://www.readbyqxmd.com/read/28230861/ripk3-interactions-with-mlkl-and-camkii-mediate-oligodendrocytes-death-in-the-developing-brain
#1
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/28215597/ripk1-a-key-survival-factor-for-hepatocytes
#2
EDITORIAL
Camille Blériot, Marc Lecuit
No abstract text is available yet for this article.
February 16, 2017: Journal of Hepatology
https://www.readbyqxmd.com/read/28212752/caspase-8-acts-in-a-non-enzymatic-role-as-a-scaffold-for-assembly-of-a-pro-inflammatory-faddosome-complex-upon-trail-stimulation
#3
Conor M Henry, Seamus J Martin
TRAIL is a potent inducer of apoptosis and has been studied almost exclusively in this context. However, TRAIL can also induce NFκB-dependent expression of multiple pro-inflammatory cytokines and chemokines. Surprisingly, whereas inhibition of caspase activity blocked TRAIL-induced apoptosis, but not cytokine production, knock down or deletion of caspase-8 suppressed both outcomes, suggesting that caspase-8 participates in TRAIL-induced inflammatory signaling in a scaffold role. Consistent with this, introduction of a catalytically inactive caspase-8 mutant into CASP-8 null cells restored TRAIL-induced cytokine production, but not cell death...
February 16, 2017: Molecular Cell
https://www.readbyqxmd.com/read/28160766/phenytoin-induced-gingival-overgrowth-caused-by-death-receptor-pathway-malfunction
#4
Reiri Takeuchi, Hiroko Matsumoto, Kazumune Arikawa, Chieko Taguchi, Ryuji Nakayama, Ikuo Nasu, Koichi Hiratsuka
OBJECTIVE: In this study, we investigated the role of phenytoin (PHT) in death receptor-induced apoptosis of gingival fibroblasts to clarify the mechanism of PHT-induced gingival overgrowth. METHODS: Human gingival fibroblasts were cultured to semi-confluence and treated with PHT (0.025, 0.1, 0.25, and 1.0 μM) for 48 h, and then the apoptotic cell numbers were relatively determined by absorptiometry. After 24 h of 0.25 μM PHT treatment, caspase activity was measured by absorptiometry, apoptotic and cell cycle phase distribution was analyzed by flow cytometry, expression levels of apoptotic genes were quantified by real-time qPCR, and expression of apoptotic proteins was detected by western blot analysis...
February 4, 2017: Oral Diseases
https://www.readbyqxmd.com/read/28159673/ripk1-binds-to-vitamin-d-receptor-and-decreases-vitamin-d-induced-growth-suppression
#5
Waise Quarni, Panida Lungchukiet, Anfernee Tse, Pei Wang, Yuefeng Sun, Ravi Kasiappan, Jheng-Yu Wu, Xiaohong Zhang, Wenlong Bai
Receptor interacting protein kinase 1 (RIPK1) is an enzyme acting downstream of tumor necrosis factor alpha to control cell survival and death. RIPK1 expression has been reported to cause drug resistance in cancer cells, but so far, no published studies have investigated the role of RIPK1 in vitamin D signaling. In the present study, we investigated whether RIPK1 plays any roles in 1,25-dihydroxyvitamin D3 (1,25D3)-induced growth suppression. In our studies, RIPK1 decreased the transcriptional activity of vitamin D receptor (VDR) in luciferase reporter assays independent of its kinase activity, suggesting a negative role of RIPK1 in 1,25D3 action...
February 1, 2017: Journal of Steroid Biochemistry and Molecular Biology
https://www.readbyqxmd.com/read/28151480/ripk1-ripk3-promotes-vascular-permeability-to-allow-tumor-cell-extravasation-independent-of-its-necroptotic-function
#6
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/28140659/protective-effect-of-mild-induced-hypothermia-against-moderate-traumatic-brain-injury-in-rats-involved-in-necroptotic-and-apoptotic-pathways
#7
Hai-Bo Zhang, Shi-Xiang Cheng, Yue Tu, Sai Zhang, Shi-Ke Hou, Zhen Yang
AIM: To investigate the protective effect of hypothermia (HT) on brain injury in moderate traumatic brain injury (TBI) rat models and the potential mechanisms, especially the involvement of RIPK1 in apoptosis and necroptosis. METHODS: Adult Sprague-Dawley rats were randomized to four groups: sham+normothermia (sham+NT), sham+hypothermia (sham+HT), moderate TBI+normothermia (TBI+NT) and moderate TBI+hypothermia (TBI+HT). The sham+HT and TBI+HT groups were submitted to 32°C for 6 hours...
January 31, 2017: Brain Injury: [BI]
https://www.readbyqxmd.com/read/28138023/distinct-roles-of-the-anti-apoptotic-effectors-nleb-and-nlef-from-enteropathogenic-escherichia-coli
#8
Georgina L Pollock, Clare V L Oates, Cristina Giogha, Tania Wong Fok Lung, Sze Ying Ong, Jaclyn S Pearson, Elizabeth L Hartland
During infection, enteropathogenic Escherichia coli (EPEC) translocates effector proteins directly into the cytosol of infected enterocytes using a type III secretion system (T3SS). Once inside the host cell, these effector proteins subvert various immune signaling pathways including death receptor-induced apoptosis. One such effector protein is the Non-LEE encoded effector NleB1, which inhibits extrinsic apoptotic signaling via the FAS death receptor. NleB1 transfers a single GlcNAc residue to Arg117 in the death domain of FADD and inhibits FAS ligand (FasL) stimulated caspase-8 cleavage...
January 30, 2017: Infection and Immunity
https://www.readbyqxmd.com/read/28126382/complex-pathologic-roles-of-ripk1-and-ripk3-moving-beyond-necroptosis
#9
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
#10
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/28106882/combination-of-iap-antagonist-and-ifn%C3%AE-activates-novel-caspase-10-and-ripk1-dependent-cell-death-pathways
#11
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/28092460/a-three-dimensional-lymphatic-endothelial-cell-tube-formation-assay-to-identify-novel-kinases-involved-in-lymphatic-vessel-remodeling
#12
T Jessica Gambino, Steven P Williams, Carol Caesar, Daniel Resnick, Cameron J Nowell, Rae H Farnsworth, Marc G Achen, Steven A Stacker, Tara Karnezis
The lymphatic system is a series of vessels that transport cells and excess fluid from tissues to the blood vascular system. Normally quiescent, the lymphatics can grow or remodel in response to developmental, immunological, or cells pathological stimuli. Lymphatic vessels comprise lymphatic endothelial cells (LECs) that can respond to external growth factors by undergoing proliferation, migration, adhesion, and tube and lumen formation into new vessel structures, a process known as lymphangiogenesis. To understand the key gene and signaling pathways necessary for lymphangiogenesis and lymphatic vessel remodeling, we have developed a three-dimensional LEC tube formation assay to explore the role of kinase signaling in these processes...
January 2017: Assay and Drug Development Technologies
https://www.readbyqxmd.com/read/28088582/ripk1-protects-hepatocytes-from-kupffer-cells-mediated-tnf-induced-apoptosis-in-mouse-models-of-pamp-induced-hepatitis
#13
Aveline Filliol, Claire Piquet-Pellorce, Céline Raguénès-Nicol, Sarah Dion, Muhammad Farooq, Catherine Lucas-Clerc, Peter Vandenabeele, Mathieu J M Bertrand, Jacques Le Seyec, Michel Samson
BACKGROUND & AIMS: The severity of liver diseases is exacerbated by the death of hepatocytes, which can be induced by the sensing of Pathogen Associated Molecular Patterns (PAMPs) derived from the gut microbiota. The molecular mechanisms regulating these cell death pathways are poorly documented. In this study, we investigated the role of the Receptor Interacting Protein Kinase 1 (RIPK1), a protein known to regulate cell fate decisions, in the death of hepatocytes using two in vivo models of PAMP-induced hepatitis...
January 11, 2017: Journal of Hepatology
https://www.readbyqxmd.com/read/28087739/tnf-signaling-through-rip1-kinase-enhances-sn38-induced-death-in-colon-adenocarcinoma
#14
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/28069809/the-receptor-interacting-serine-threonine-protein-kinase-1-ripk1-regulates-progranulin-levels
#15
Amanda R Mason, Lisa P Elia, Steven Finkbeiner
Progranulin (PGRN), a secreted growth factor, is a key regulator of inflammation and is genetically linked to two common and devastating neurodegenerative diseases. Haploinsufficiency mutations in GRN, the gene encoding PGRN, cause frontotemporal dementia (FTD) and a GRN SNP confers significantly increased risk for Alzheimer's disease (AD). Because cellular and animal data indicate that increasing PGRN can reverse phenotypes of both FTD and AD, modulating PGRN level has been proposed as a therapeutic strategy for both diseases...
January 9, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28017612/ripk1-suppresses-a-traf2-dependent-pathway-to-liver-cancer
#16
Anne T Schneider, Jérémie Gautheron, Maria Feoktistova, Christoph Roderburg, Sven H Loosen, Sanchari Roy, Fabian Benz, Peter Schemmer, Markus W Büchler, Ueli Nachbur, Ulf P Neumann, Rene Tolba, Mark Luedde, Jessica Zucman-Rossi, Diana Panayotova-Dimitrova, Martin Leverkus, Christian Preisinger, Frank Tacke, Christian Trautwein, Thomas Longerich, Mihael Vucur, Tom Luedde
Receptor-interacting protein kinase 1 (RIPK1) represents an essential signaling node in cell death and inflammation. Ablation of Ripk1 in liver parenchymal cells (LPC) did not cause a spontaneous phenotype, but led to tumor necrosis factor (TNF)-dependent hepatocyte apoptosis and liver injury without affecting inducible nuclear factor κB (NF-κB) activation. Loss of Ripk1 induced the TNF-dependent proteasomal degradation of the E3-ligase, TNF receptor-associated factor 2 (TRAF2), in a kinase-independent manner, thereby activating caspase-8...
January 9, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28004776/a20-curtails-primary-but-augments-secondary-cd8-t-cell-responses-in-intracellular-bacterial-infection
#17
Sissy Just, Gopala Nishanth, Jörn H Buchbinder, Xu Wang, Michael Naumann, Inna Lavrik, Dirk Schlüter
The ubiquitin-modifying enzyme A20, an important negative feedback regulator of NF-κB, impairs the expansion of tumor-specific CD8(+) T cells but augments the proliferation of autoimmune CD4(+) T cells. To study the T cell-specific function of A20 in bacterial infection, we infected T cell-specific A20 knockout (CD4-Cre A20(fl/fl)) and control mice with Listeria monocytogenes. A20-deficient pathogen-specific CD8(+) T cells expanded stronger resulting in improved pathogen control at day 7 p.i. Imaging flow cytometry revealed that A20-deficient Listeria-specific CD8(+) T cells underwent increased apoptosis and necroptosis resulting in reduced numbers of memory CD8(+) T cells...
December 22, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27999438/necroptosis-in-development-inflammation-and-disease
#18
REVIEW
Ricardo Weinlich, Andrew Oberst, Helen M Beere, Douglas R Green
In the early 2000s, receptor-interacting serine/threonine protein kinase 1 (RIPK1), a molecule already recognized as an important regulator of cell survival, inflammation and disease, was attributed an additional function: the regulation of a novel cell death pathway that came to be known as necroptosis. Subsequently, the related kinase RIPK3 and its substrate mixed-lineage kinase domain-like protein (MLKL) were also implicated in the necroptotic pathway, and links between this pathway and apoptosis were established...
2017: Nature Reviews. Molecular Cell Biology
https://www.readbyqxmd.com/read/27980222/ripk1-prevents-aberrant-zbp1-initiated-necroptosis
#19
EDITORIAL
Tom Vanden Berghe, William J Kaiser
No abstract text is available yet for this article.
January 3, 2017: Oncotarget
https://www.readbyqxmd.com/read/27929749/critical-role-of-x-box-binding-protein-1-in-nadph-oxidase-4-triggered-cardiac-hypertrophy-is-mediated-by-receptor-interacting-protein-kinase-1
#20
Li Chen, Mingyue Zhao, Junli Li, Yu Wang, Qinxue Bao, Siyuan Wu, Xueqin Deng, Xiaoju Tang, Wenchao Wu, Xiaojing Liu
NADPH oxidase 4 (NOX4) and the NOX4-related redox signaling are implicated in cardiac hypertrophy. NOX4 is interrelated with endoplasmic reticulum stress (ERS). Spliced X-box binding protein 1 (Xbp1s) is a key mediator of ERS while its role in cardiac hypertrophy is still poorly understood. Recently, receptor interacting protein kinase 1(RIPK1) has been increasingly reported to be associated with ERS. Therefore, we aimed to test the hypothesis that Xbp1s mediates NOX4-triggered cardiac hypertrophy via RIPK1 signaling...
February 16, 2017: Cell Cycle
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