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https://www.readbyqxmd.com/read/28715128/sibiriline-a-new-small-chemical-inhibitor-of-receptor-interacting-protein-kinase-1-prevents-immune-dependent-hepatitis
#1
Fabienne Le Cann, Claire Delehouzé, Sabrina Penna-Leverrier, Aveline Filliol, Arnaud Comte, Olivier Delalande, Nathalie Desban, Blandine Baratte, Isabelle Gallais, Claire Piquet-Pellorce, Florence Faurez, Marion Bonnet, Yvette Mettey, Peter Goekjian, Michel Samson, Peter Vandenabeele, Stéphane Bach, Marie-Thérèse Dimanche-Boitrel
Necroptosis is a regulated form of cell death involved in several disease models including in particular liver diseases. Receptor-Interacting Protein Kinases, RIPK1 and RIPK3, are the main serine/threonine kinases driving this cell death pathway. We screened a non-commercial kinase-focused chemical library allowed us to identify Sibiriline as new inhibitor of necroptosis induced by TNF in Fas-Associated protein with Death Domain (FADD)-deficient Jurkat cells. Moreover, Sib inhibits necroptotic cell death induced by various death ligands in human or mouse cells while not protecting from caspase-dependent apoptosis...
July 17, 2017: FEBS Journal
https://www.readbyqxmd.com/read/28708137/fas-apoptotic-inhibitory-molecule-2-is-a-stress-induced-intrinsic-neuroprotective-factor-in-the-retina
#2
Mercy Pawar, Boris Busov, Aaruran Chandrasekhar, Jingyu Yao, David N Zacks, Cagri G Besirli
We report the neuroprotective role of FAS apoptotic inhibitory molecule 2 (FAIM2), an inhibitor of the FAS signaling pathway, during stress-induced photoreceptor apoptosis. Retinal detachment resulted in increased FAIM2 levels in photoreceptors with higher amounts detected at the tips of outer segments. Activation of FAS death receptor via FAS-ligand led to JNK-mediated FAIM2 phosphorylation, decreased proteasome-mediated degradation and increased association with the FAS receptor. Photoreceptor apoptosis was accelerated in Faim2 knockout mice following experimental retinal detachment...
July 14, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28701375/spata2-regulates-the-activation-of-ripk1-by-modulating-linear-ubiquitination
#3
Ran Wei, Lily Wen Xu, Jianping Liu, Yanxia Li, Pei Zhang, Bing Shan, Xiaojuan Lu, Lihui Qian, Zheming Wu, Kangyun Dong, Hong Zhu, Lifeng Pan, Junying Yuan, Heling Pan
Stimulation of cells with TNFα leads to the formation of the TNF-R1 signaling complex (TNF-RSC) to mediate downstream cellular fate decision. Activation of the TNF-RSC is modulated by different types of ubiquitination and may lead to cell death, including apoptosis and necroptosis, in both RIPK1-dependent and RIPK1-independent manners. Spata2 (spermatogenesis-associated 2) is an adaptor protein recruited into the TNF-RSC to modulate the interaction between the linear ubiquitin chain assembly complex (LUBAC) and the deubiquitinase CYLD (cylindromatosis)...
July 12, 2017: Genes & Development
https://www.readbyqxmd.com/read/28689299/4-o-methylhonokiol-protects-from-alcohol-carbon-tetrachloride-induced-liver-injury-in-mice
#4
Eleonora Patsenker, Andrea Chicca, Vanessa Petrucci, Sheida Moghadamrad, Andrea de Gottardi, Jochen Hampe, Jürg Gertsch, Nasser Semmo, Felix Stickel
Alcoholic liver disease (ALD) is a leading cause of liver cirrhosis, liver cancer, and related mortality. The endocannabinoid system contributes to the development of chronic liver diseases, where cannabinoid receptor 2 (CB2) has been shown to have a protecting role. Thus, here, we investigated how CB2 agonism by 4'-O-methylhonokiol (MHK), a biphenyl from Magnolia grandiflora, affects chronic alcohol-induced liver fibrosis and damage in mice. A combination of alcohol (10% vol/vol) and CCl4 (1 ml/kg) was applied to C57BL/6 mice for 5 weeks...
July 8, 2017: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
https://www.readbyqxmd.com/read/28676433/the-neurotoxicant-pcb-95-by-increasing-the-neuronal-transcriptional-repressor-rest-down-regulates-caspase-8-and-increases-ripk1-ripk3-and-mlkl-expression-determining-necroptotic-neuronal-death
#5
Natascia Guida, Giusy Laudati, Angelo Serani, Luigi Mascolo, Pasquale Molinaro, Paolo Montuori, Gianfranco Di Renzo, Lorella Mt Canzoniero, Luigi Formisano
Our previous study showed that the environmental neurotoxicant non-dioxin-like polychlorinated biphenyl (PCB)-95 increases RE1-Silencing Transcription Factor (REST) expression, which is related to necrosis, but not apoptosis, of neurons. Meanwhile, necroptosis is a type of a programmed necrosis that is positively regulated by receptor interacting protein kinase 1 (RIPK1), RIPK3 and mixed lineage kinase domain-like (MLKL) and negatively regulated by caspase-8. Here we evaluated whether necroptosis contributes to PCB-95-induced neuronal death through REST up-regulation...
July 1, 2017: Biochemical Pharmacology
https://www.readbyqxmd.com/read/28663335/mitochondrial-quality-control-in-alveolar-epithelial-cells-damaged-by-s-aureus-pneumonia-in-mice
#6
Hagir B Suliman, Bryan D Kraft, Raquel R Bartz, Lingye Chen, Karen E Welty-Wolf, Claude A Piantadosi
(242 words) Mitochondrial damage is often overlooked in acute lung injury (ALI), but most of the lung's physiological processes, such as airway tone, muco-ciliary clearance, Va/Q matching, and immune surveillance require aerobic energy provision. Because the cell's processes of mitochondrial quality control (QC) regulate the elimination and replacement of damaged mitochondria to support cell survival, we evaluated mitochondrial biogenesis and mitophagy in the alveolar region of mice in a validated S. aureus pneumonia model...
June 29, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28661484/sorafenib-tosylate-inhibits-directly-necrosome-complex-formation-and-protects-in-mouse-models-of-inflammation-and-tissue-injury
#7
Sofie Martens, Manhyung Jeong, Wulf Tonnus, Friederike Feldmann, Sam Hofmans, Vera Goossens, Nozomi Takahashi, Jan Hinrich Bräsen, Eun-Woo Lee, Pieter Van der Veken, Jurgen Joossens, Koen Augustyns, Simone Fulda, Andreas Linkermann, Jaewhan Song, Peter Vandenabeele
Necroptosis contributes to the pathophysiology of several inflammatory, infectious and degenerative disorders. TNF-induced necroptosis involves activation of the receptor-interacting protein kinases 1 and 3 (RIPK1/3) in a necrosome complex, eventually leading to the phosphorylation and relocation of mixed lineage kinase domain like protein (MLKL). Using a high-content screening of small compounds and FDA-approved drug libraries, we identified the anti-cancer drug Sorafenib tosylate as a potent inhibitor of TNF-dependent necroptosis...
June 29, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28647349/inhibitor-of-apoptosis-proteins-iaps-limit-ripk1-mediated-skin-inflammation
#8
H Anderton, J A Rickard, G A Varigos, N Lalaoui, J Silke
Inhibitor of Apoptosis Proteins (IAPs) are critical regulators of cell death and survival pathways. Mice lacking cellular IAP (cIAP) 1 and either cIAP2 or X-linked IAP (XIAP) die in utero, and myeloid lineage-specific deletion of all IAPs causes sterile inflammation, but their role in the skin is unknown. We generated epidermal-specific IAPs deficient mice and found that combined genetic deletion of cIAP1 in keratinocytes and ubiquitous cIAP2 deletion (cIap1(EKO/EKO).cIap2(-/-)) caused profound skin inflammation and keratinocyte death, lethal by post-partum day 10...
June 21, 2017: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/28628031/kinase-independent-functions-of-ripk1-regulate-hepatocyte-survival-and-liver-carcinogenesis
#9
Trieu-My Van, Apostolos Polykratis, Beate Katharina Straub, Vangelis Kondylis, Nikoletta Papadopoulou, Manolis Pasparakis
The mechanisms that regulate cell death and inflammation play an important role in liver disease and cancer. Receptor-interacting protein kinase 1 (RIPK1) induces apoptosis and necroptosis via kinase-dependent mechanisms and exhibits kinase-independent prosurvival and proinflammatory functions. Here, we have used genetic mouse models to study the role of RIPK1 in liver homeostasis, injury, and cancer. While ablating either RIPK1 or RelA in liver parenchymal cells (LPCs) did not cause spontaneous liver pathology, mice with combined deficiency of RIPK1 and RelA in LPCs showed increased hepatocyte apoptosis and developed spontaneous chronic liver disease and cancer that were independent of TNF receptor 1 (TNFR1) signaling...
June 30, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28616581/the-enigma-of-ripk1-in-the-liver-more-than-just-a-kinase
#10
Mihael Vucur, Anne T Schneider, Jérémie Gautheron, Tom Luedde
Receptor interacting protein kinase 1 (RIPK1) represents a key molecule in cell death. Here, we discuss our recent data on RIPK1 in liver injury and hepatocellular carcinoma development and put these into relation to previous experimental findings to underpin that it exerts opposing kinase-dependent and kinase independent functions in liver cells.
2017: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/28603092/crosstalk-of-liver-immune-cells-and-cell-death-mechanisms-in-different-murine-models-of-liver-injury-and-its-clinical-relevance
#11
Hilal Ahmad Khan, Muhammad Zishan Ahmad, Junaid Ali Khan, Muhammad Imran Arshad
BACKGROUND: Liver inflammation or hepatitis is a result of pluripotent interactions of cell death molecules, cytokines, chemokines and the resident immune cells collectively called as microenvironment. The interplay of these inflammatory mediators and switching of immune responses during hepatotoxic, viral, drug-induced and immune cell-mediated hepatitis decide the fate of liver pathology. The present review aimed to describe the mechanisms of liver injury, its relevance to human liver pathology and insights for the future therapeutic interventions...
June 2017: Hepatobiliary & Pancreatic Diseases International: HBPD INT
https://www.readbyqxmd.com/read/28593135/evaluation-of-cell-death-pathways-initiated-by-antitumor-drugs-melatonin-and-valproic-acid-in-bladder-cancer-cells
#12
Siwei Liu, Bilin Liang, Huiting Jia, Yuhan Jiao, Zhongqiu Pang, Yongye Huang
Effective drug combinations have the potential to strengthen therapeutic efficacy and combat drug resistance. Both melatonin and valproic acid (VPA) exhibit antitumor activities in various cancer cells. The aim of this study was to evaluate the cell death pathways initiated by anticancer combinatorial effects of melatonin and VPA in bladder cancer cells. The results demonstrated that the combination of melatonin and VPA leads to significant synergistic growth inhibition of UC3 bladder cancer cells. Gene expression studies revealed that cotreatment with melatonin and VPA triggered the up-regulation of certain genes related to apoptosis (TNFRSF10A and TNFRSF10B), autophagy (BECN, ATG3 and ATG5) and necrosis (MLKL, PARP-1 and RIPK1)...
June 2017: FEBS Open Bio
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
#13
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/28582465/differential-regulation-of-cell-death-pathways-by-the-microenvironment-correlates-with-chemoresistance-and-survival-in-leukaemia
#14
Malak Yahia Qattan, Emyr Yosef Bakker, Ramkumar Rajendran, Daphne Wei-Chen Chen, Vaskar Saha, Jizhong Liu, Leo Zeef, Jean-Marc Schwartz, Luciano Mutti, Constantinos Demonacos, Marija Krstic-Demonacos
Glucocorticoids (GCs) and topoisomerase II inhibitors are used to treat acute lymphoblastic leukaemia (ALL) as they induce death in lymphoid cells through the glucocorticoid receptor (GR) and p53 respectively. Mechanisms underlying ALL cell death and the contribution of the bone marrow microenvironment to drug response/resistance remain unclear. The role of the microenvironment and the identification of chemoresistance determinants were studied by transcriptomic analysis in ALL cells treated with Dexamethasone (Dex), and Etoposide (Etop) grown in the presence or absence of bone marrow conditioned media (CM)...
2017: PloS One
https://www.readbyqxmd.com/read/28574505/the-small-molecule-that-packs-a-punch-ubiquitin-mediated-regulation-of-ripk1-fadd-caspase-8-complexes
#15
REVIEW
Rebecca Feltham, John Silke
The mechanisms that underpin the production of small molecules and cytokines that lead to inflammation or programmed cell death are intricately intertwined. So much so that some of the proteins that contribute to the transcriptional up regulation of cytokines can switch their role in the right circumstances to generate cell death-inducing complexes. This entwinement is reflected in the fact that inflammation helps an organism fight pathogens and that therefore pathogens are under an evolutionary pressure to interfere with this process...
June 2, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28562322/characterization-of-a-novel-androgen-receptor-ar-coregulator-ripk1-and-related-chemicals-that-suppress-ar-mediated-prostate-cancer-growth-via-peptide-and-chemical-screening
#16
Cheng-Lung Hsu, Jai-Shin Liu, Ting-Wei Lin, Ying-Hsu Chang, Yung-Chia Kuo, An-Chi Lin, Huei-Ju Ting, See-Tong Pang, Li-Yu Lee, Wen-Lung Ma, Chun-Cheng Lin, Wen-Guey Wu
Using bicalutamide-androgen receptor (AR) DNA binding domain-ligand binding domain as bait, we observed enrichment of FxxFY motif-containing peptides. Protein database searches revealed the presence of receptor-interacting protein kinase 1 (RIPK1) harboring one FxxFY motif. RIPK1 interacted directly with AR and suppressed AR transactivation in a dose-dependent manner. Domain mapping experiments showed that the FxxFY motif in RIPK1 is critical for interactions with AR and the death domain of RIPK1 plays a crucial role in its inhibitory effect on transactivation...
May 13, 2017: Oncotarget
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
#17
Firaz Mohideen, Joao A Paulo, 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...
July 2017: Molecular & Cellular Proteomics: MCP
https://www.readbyqxmd.com/read/28520112/proapoptotic-signaling-induced-by-ripk1-and-traf2-deletion-results-in-liver-carcinogenesis
#18
Petra Hirsova, Maria Eugenia Guicciardi, Gregory J Gores
No abstract text is available yet for this article.
May 18, 2017: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/28507808/pro-necrotic-molecules-impact-local-immunosurveillance-in-human-breast-cancer
#19
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/28506461/mk2-phosphorylates-ripk1-to-prevent-tnf-induced-cell-death
#20
Isabel Jaco, Alessandro Annibaldi, Najoua Lalaoui, Rebecca Wilson, Tencho Tenev, Lucie Laurien, Chun Kim, Kunzah Jamal, Sidonie Wicky John, Gianmaria Liccardi, Diep Chau, James M Murphy, Gabriela Brumatti, Rebecca Feltham, Manolis Pasparakis, John Silke, Pascal Meier
TNF is an inflammatory cytokine that upon binding to its receptor, TNFR1, can drive cytokine production, cell survival, or cell death. TNFR1 stimulation causes activation of NF-κB, p38α, and its downstream effector kinase MK2, thereby promoting transcription, mRNA stabilization, and translation of target genes. Here we show that TNF-induced activation of MK2 results in global RIPK1 phosphorylation. MK2 directly phosphorylates RIPK1 at residue S321, which inhibits its ability to bind FADD/caspase-8 and induce RIPK1-kinase-dependent apoptosis and necroptosis...
June 1, 2017: Molecular Cell
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