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https://www.readbyqxmd.com/read/28415572/inhibition-of-iron-overload-induced-apoptosis-and-necrosis-of-bone-marrow-mesenchymal-stem-cells-by-melatonin
#1
Fan Yang, Yuan Li, Gege Yan, Tianyi Liu, Chao Feng, Rui Gong, Ye Yuan, Fengzhi Ding, Lai Zhang, Elina Idiiatullina, Valentin Pavlov, Zhenbo Han, Wenya Ma, Qi Huang, Ying Yu, Zhengyi Bao, Xiuxiu Wang, Bingjie Hua, Zhimin Du, Benzhi Cai, Lei Yang
Iron overload induces severe damage to several vital organs such as the liver, heart and bone, and thus contributes to the dysfunction of these organs. The aim of this study is to investigate whether iron overload causes the apoptosis and necrosis of bone marrow mesenchymal stem cells (BMSCs) and melatonin may prevent its toxicity. Perls' Prussion blue staining showed that exposure to increased concentrations of ferric ammonium citrate (FAC) induced a gradual increase of intracellular iron level in BMSCs. Trypan blue staining demonstrated that FAC decreased the viability of BMSCs in a concentration-dependent manner...
March 19, 2017: Oncotarget
https://www.readbyqxmd.com/read/28414098/cytosolic-calcium-mediates-rip1-rip3-complex-dependent-necroptosis-through-jnk-activation-and-mitochondrial-ros-production-in-human-colon-cancer-cells
#2
Wen Sun, Xiaxia Wu, Hongwei Gao, Jie Yu, Wenwen Zhao, Jin-Jian Lu, Jinhua Wang, Guanhua Du, Xiuping Chen
Necroptosis is a form of programmed necrosis mediated by signaling complexes with receptor-interacting protein 1 (RIP1) and RIP3 kinases as the main mediators. However, the underlying execution pathways of this phenomenon have yet to be elucidated in detail. In this study, a RIP1/RIP3 complex was formed in 2-methoxy-6-acetyl-7-methyljuglone (MAM)-treated HCT116 and HT29 colon cancer cells. With this formation, mitochondrial reactive oxygen species (ROS) levels increased, mitochondrial depolarization occurred, and ATP concentrations decreased...
April 14, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28404866/combined-antiangiogenic-and-anti-pd-l1-therapy-stimulates-tumor-immunity-through-hev-formation
#3
Elizabeth Allen, Arnaud Jabouille, Lee B Rivera, Inge Lodewijckx, Rindert Missiaen, Veronica Steri, Kevin Feyen, Jaime Tawney, Douglas Hanahan, Iacovos P Michael, Gabriele Bergers
Inhibitors of VEGF (vascular endothelial growth factor)/VEGFR2 (vascular endothelial growth factor receptor 2) are commonly used in the clinic, but their beneficial effects are only observed in a subset of patients and limited by induction of diverse relapse mechanisms. We describe the up-regulation of an adaptive immunosuppressive pathway during antiangiogenic therapy, by which PD-L1 (programmed cell death ligand 1), the ligand of the negative immune checkpoint regulator PD-1 (programmed cell death protein 1), is enhanced by interferon-γ-expressing T cells in distinct intratumoral cell types in refractory pancreatic, breast, and brain tumor mouse models...
April 12, 2017: Science Translational Medicine
https://www.readbyqxmd.com/read/28404865/dual-angiopoietin-2-and-vegfa-inhibition-elicits-antitumor-immunity-that-is-enhanced-by-pd-1-checkpoint-blockade
#4
Martina Schmittnaegel, Nicolò Rigamonti, Ece Kadioglu, Antonino Cassará, Céline Wyser Rmili, Anna Kiialainen, Yvonne Kienast, Hans-Joachim Mueller, Chia-Huey Ooi, Damya Laoui, Michele De Palma
Pathological angiogenesis is a hallmark of cancer and a therapeutic target. Vascular endothelial growth factor A (VEGFA) and angiopoietin-2 (ANGPT2; also known as ANG2) are proangiogenic cytokines that sustain tumor angiogenesis and limit antitumor immunity. We show that combined ANGPT2 and VEGFA blockade by a bispecific antibody (A2V) provided superior therapeutic benefits, as compared to the single agents, in both genetically engineered and transplant tumor models, including metastatic breast cancer (MMTV-PyMT), pancreatic neuroendocrine tumor (RIP1-Tag2), and melanoma...
April 12, 2017: Science Translational Medicine
https://www.readbyqxmd.com/read/28396243/mechanical-force-mediated-pathological-cartilage-thinning-is-regulated-by-necroptosis-and-apoptosis
#5
C Zhang, S Lin, T Li, Y Jiang, Z Huang, J Wen, W Cheng, H Li
OBJECTIVE: This study aimed to identify the mechanisms underlying mandibular chondrocyte cell death and cartilage thinning in response to mechanical force. MATERIAL AND METHODS: An in vivo model (compressive mechanical force) and an in vitro model (TNF-α+cycloheximide) were used to induce mandibular chondrocyte necroptosis. Hematoxylin and eosin staining and transmission electron microscopy were used to assess histological and subcellular changes in mandibular chondrocyte...
April 7, 2017: Osteoarthritis and Cartilage
https://www.readbyqxmd.com/read/28395284/indole-3-carbinol-induces-apoptosis-of-hepatic-stellate-cells-through-k63-de-ubiquitination-of-rip1-in-rats
#6
Bin Li, Meng Cong, Yanan Zhu, Ying Xiong, Wenyi Jin, Yang Wan, Yunjiao Zhou, Ying Ao, Hui Wang
BACKGROUND/AIMS: The apoptosis of activated hepatic stellate cells (HSCs) is the central event in the reversal of liver fibrosis. K63 de-ubiquitinated receptor-interacting protein (RIP)1 promotes apoptosis in tumor necrosis factor (TNF)-α signaling pathway. In the previous study, we have proved that indole-3-carbinol (I3C) could reverse different models of liver fibrosis in rats, but the mechanism is still unclear. Thus, the present research aimed to demonstrate the induction of I3C on apoptosis of HSCs and the underlying molecular mechanism...
March 24, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28392570/human-t-cell-lymphotropic-virus-type-1-and-its-oncogenesis
#7
REVIEW
Lan-Lan Zhang, Jing-Yun Wei, Long Wang, Shi-le Huang, Ji-Long Chen
Human T-cell lymphotropic virus type 1 (HTLV-1) is the etiologic agent of adult T-cell leukemia/lymphoma (ATL), a rapidly progressing clonal malignancy of CD4+ T lymphocytes. Exploring the host-HTLV-1 interactions and the molecular mechanisms underlying HTLV-1-mediated tumorigenesis is critical for developing efficient therapies against the viral infection and associated leukemia/lymphoma. It has been demonstrated to date that several HTLV-1 proteins play key roles in the cellular transformation and immortalization of infected T lymphocytes...
April 10, 2017: Acta Pharmacologica Sinica
https://www.readbyqxmd.com/read/28387756/pore-forming-toxin-mediated-ion-dysregulation-leads-to-death-receptor-independent-necroptosis-of-lung-epithelial-cells-during-bacterial-pneumonia
#8
Norberto González-Juarbe, Kelley Margaret Bradley, Anukul Taranath Shenoy, Ryan Paul Gilley, Luis Felipe Reyes, Cecilia Anahí Hinojosa, Marcos Ignacio Restrepo, Peter Herman Dube, Molly Ann Bergman, Carlos Javier Orihuela
We report that pore-forming toxins (PFTs) induce respiratory epithelial cell necroptosis independently of death receptor signaling during bacterial pneumonia. Instead, necroptosis was activated as a result of ion dysregulation arising from membrane permeabilization. PFT-induced necroptosis required RIP1, RIP3 and MLKL, and could be induced in the absence or inhibition of TNFR1, TNFR2 and TLR4 signaling. We detected activated MLKL in the lungs from mice and nonhuman primates experiencing Serratia marcescens and Streptococcus pneumoniae pneumonia, respectively...
April 7, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28380356/necroptosis-execution-is-mediated-by-plasma-membrane-nanopores-independent-of-calcium
#9
Uris Ros, Aida Peña-Blanco, Kay Hänggi, Ulrich Kunzendorf, Stefan Krautwald, W Wei-Lynn Wong, Ana J García-Sáez
Necroptosis is a form of regulated necrosis that results in cell death and content release after plasma membrane permeabilization. However, little is known about the molecular events responsible for the disruption of the plasma membrane. Here, we find that early increase in cytosolic calcium in TNF-induced necroptosis is mediated by treatment with a Smac mimetic via the TNF/RIP1/TAK1 survival pathway. This does not require the activation of the necrosome and is dispensable for necroptosis. Necroptosis induced by the activation of TLR3/4 pathways does not trigger early calcium flux...
April 4, 2017: Cell Reports
https://www.readbyqxmd.com/read/28377500/innate-immune-signaling-in-drosophila-is-regulated-by-tgf%C3%AE-activated-kinase-tak1-triggered-ubiquitin-editing
#10
Li Chen, Nicholas Paquette, Shahan Mamoor, Florentina Rus, Anubhab Nandy, John Leszyk, Scott A Shaffer, Neal Silverman
Coordinated regulation of innate immune responses is necessary in all metazoans. In Drosophila, the Imd pathway detects gram-negative bacterial infections through recognition of DAP-type peptidoglycan and activation of the NF-κB precursor Relish, which drives robust antimicrobial peptide (AMP) gene expression. Imd is a receptor-proximal adaptor protein homologous to mammalian RIP1 that is regulated by proteolytic cleavage and K63-polyubiquitination. However, the precise events and molecular mechanisms that control the post-translational modification of Imd remain unclear...
April 4, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28337828/tradd-traf2-rip1-and-tak1-are-required-for-tnf-%C3%AE-induced-pro-labour-mediators-in-human-primary-myometrial-cells
#11
Ratana Lim, Gillian Barker, Martha Lappas
PROBLEM: TNF-α plays a central role in the processes of human labour and delivery. This study sought to determine the role of the adaptor proteins TNFR1-associated death domain protein (TRADD), TNF receptor-associated factor 2 (TRAF2), receptor interacting protein 1 (RIP1) and transforming growth factor beta-activated kinase 1 (TAK1) in TNF-α-induced formation of pro-labour mediators. METHOD OF STUDY: Human primary myometrial cells were transfected with siRNA against TRADD (siTRADD), TRAF2 (siTRAF2), RIP1 (siRIP1) or TAK1 (siTAK1), treated with TNF-α, and assayed for pro-inflammatory mediators expression...
March 24, 2017: American Journal of Reproductive Immunology: AJRI
https://www.readbyqxmd.com/read/28330474/hypercholesterolemia-downregulates-autophagy-in-the-rat-heart
#12
Zoltán Giricz, Gábor Koncsos, Tomáš Rajtík, Zoltán V Varga, Tamás Baranyai, Csaba Csonka, Adrián Szobi, Adriana Adameová, Roberta A Gottlieb, Péter Ferdinandy
BACKGROUND: We have previously shown that efficiency of ischemic conditioning is diminished in hypercholesterolemia and that autophagy is necessary for cardioprotection. However, it is unknown whether isolated hypercholesterolemia disturbs autophagy or the mammalian target of rapamycin (mTOR) pathways. Therefore, we investigated whether isolated hypercholesterolemia modulates cardiac autophagy-related pathways or programmed cell death mechanisms such as apoptosis and necroptosis in rat heart...
March 23, 2017: Lipids in Health and Disease
https://www.readbyqxmd.com/read/28315674/dichotomy-between-receptor-interacting-protein-1-and-receptor-interacting-protein-3-mediated-necroptosis-in-experimental-pancreatitis
#13
Jianghong Wu, Tunike Mulatibieke, Jianbo Ni, Xiao Han, Bin Li, Yue Zeng, Rong Wan, Xingpeng Wang, Guoyong Hu
Pancreatic acinar cell necrosis and inflammatory responses are two key pathologic processes in acute pancreatitis (AP), which determines the severity and outcome of the disease. Recent studies suggest that necroptosis, a programed form of necrosis, is involved in the pathogenesis of AP, but the underlying mechanisms remain unknown. We investigated the expression of necrosome components, including receptor-interacting protein (RIP) 1, RIP3, and mixed lineage kinase domain-like (MLKL), and the molecular mechanisms in pancreatitis-associated necroptosis...
March 15, 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/28300832/deletion-of-xiap-reduces-the-severity-of-acute-pancreatitis-via-regulation-of-cell-death-and-nuclear-factor-%C3%AE%C2%BAb-activity
#14
Yong Liu, Xiao-Dong Chen, Jiang Yu, Jun-Lin Chi, Fei-Wu Long, Hong-Wei Yang, Ke-Ling Chen, Zhao-Ying Lv, Bin Zhou, Zhi-Hai Peng, Xiao-Feng Sun, Yuan Li, Zong-Guang Zhou
Severe acute pancreatitis (SAP) still remains a clinical challenge, not only for its high mortality but the uncontrolled inflammatory progression from acute pancreatitis (AP) to SAP. Cell death, including apoptosis and necrosis are critical pathology of AP, since the severity of pancreatitis correlates directly with necrosis and inversely with apoptosis Therefore, regulation of cell death from necrosis to apoptosis may have practicably therapeutic value. X-linked inhibitor of apoptosis protein (XIAP) is the best characterized member of the inhibitor of apoptosis proteins (IAP) family, but its function in AP remains unclear...
March 16, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28300624/neurotoxicity-of-the-steroidal-alkaloids-tomatine-and-tomatidine-is-rip1-kinase-and-caspase-independent-and-involves-the-eif2%C3%AE-branch-of-the-endoplasmic-reticulum
#15
Daniela Correia da Silva, Paula B Andrade, Patrícia Valentão, David M Pereira
Steroidal alkaloids are a class of natural products that occur in several species of the Solanaceae family. In the case of tomato plant (Lycopersicon esculentum Mill.), tomatine and its aglycone, tomatidine, are the most representative molecules. These steroidal alkaloids have already shown several potentially useful biological activities, from anticancer to anti-inflammatory or antibacterial. In this work, the toxicity of these molecules in neuronal cells, namely in the neuroblastoma cell line SH-SY5Y, was assessed, emphasis being given to the cellular mechanisms underlying the effects observed...
March 11, 2017: Journal of Steroid Biochemistry and Molecular Biology
https://www.readbyqxmd.com/read/28289160/prolonged-ischemia-triggers-necrotic-depletion-of-tissue-resident-macrophages-to-facilitate-inflammatory-immune-activation-in-liver-ischemia-reperfusion-injury
#16
Shi Yue, Haoming Zhou, Xuehao Wang, Ronald W Busuttil, Jerzy W Kupiec-Weglinski, Yuan Zhai
Although mechanisms of immune activation against liver ischemia reperfusion (IR) injury (IRI) have been studied extensively, questions regarding liver-resident macrophages, that is, Kupffer cells (KCs), remain controversial. Recent progress in the biology of tissue-resident macrophages implicates homeostatic functions of KCs. This study aims to dissect responses and functions of KCs in liver IRI. In a murine liver partial warm ischemia model, we analyzed liver-resident versus infiltrating macrophages by FACS and immunofluorescence staining...
May 1, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28288569/endothelial-dll4-overexpression-reduces-vascular-response-and-inhibits-tumor-growth-and-metastasization-in-vivo
#17
Alexandre Trindade, Dusan Djokovic, Joana Gigante, Liliana Mendonça, António Duarte
BACKGROUND: The inhibition of Delta-like 4 (Dll4)/Notch signaling has been shown to result in excessive, nonfunctional vessel proliferation and significant tumor growth suppression. However, safety concerns emerged with the identification of side effects resulting from chronic Dll4/Notch blockade. Alternatively, we explored the endothelial Dll4 overexpression using different mouse tumor models. METHODS: We used a transgenic mouse model of endothelial-specific Dll4 overexpression, previously produced...
March 14, 2017: BMC Cancer
https://www.readbyqxmd.com/read/28281536/laser-mediated-rupture-of-chlamydial-inclusions-triggers-pathogen-egress-and-host-cell-necrosis
#18
Markus C Kerr, Guillermo A Gomez, Charles Ferguson, Maria C Tanzer, James M Murphy, Alpha S Yap, Robert G Parton, Wilhelmina M Huston, Rohan D Teasdale
Remarkably little is known about how intracellular pathogens exit the host cell in order to infect new hosts. Pathogenic chlamydiae egress by first rupturing their replicative niche (the inclusion) before rapidly lysing the host cell. Here we apply a laser ablation strategy to specifically disrupt the chlamydial inclusion, thereby uncoupling inclusion rupture from the subsequent cell lysis and allowing us to dissect the molecular events involved in each step. Pharmacological inhibition of host cell calpains inhibits inclusion rupture, but not subsequent cell lysis...
March 10, 2017: Nature Communications
https://www.readbyqxmd.com/read/28274274/a-novel-form-of-necrosis-triad-occurs-in-human-huntington-s-disease
#19
Emiko Yamanishi, Kazuko Hasegawa, Kyota Fujita, Shizuko Ichinose, Saburo Yagishita, Miho Murata, Kazuhiko Tagawa, Takumi Akashi, Yoshinobu Eishi, Hitoshi Okazawa
We previously reported transcriptional repression-induced atypical cell death of neuron (TRIAD), a new type of necrosis that is mainly regulated by Hippo pathway signaling and distinct from necroptosis regulated by RIP1/3 pathway. Here, we examined the ultrastructural and biochemical features of neuronal cell death in the brains of human HD patients in parallel with the similar analyses using mutant Htt-knock-in (Htt-KI) mice. LATS1 kinase, the critical regulator and marker of TRIAD, is actually activated in cortical neurons of postmortem human HD and of Htt-KI mouse brains, while apoptosis promoter kinase Plk1 was inactivated in human HD brains...
March 8, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28270653/rip-1-c-flipl-induce-hepatic-cancer-cell-apoptosis-through-regulating-tumor-necrosis-factor-related-apoptosis-inducing-ligand-trail
#20
Jichun Sun, Xiao Yu, Changfa Wang, Can Yu, Zhiqiang Li, Wanpin Nie, Xundi Xu, Xiongying Miao, Xiaoxin Jin
BACKGROUND Almost all hepatic cancer cells have resistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. c-FLIPL and RIP-1 are apoptotic negative regulatory factors. This study investigated the role of c-FLIPL and RIP-1 in hepatic cancer cell resistance to TRAIL-induced apoptosis. MATERIAL AND METHODS HepG2 cells were treated by TRAIL, RIP-1 siRNA, and/or BY11-7082. Cell viability was detected by MTT assay. Cell apoptosis was tested by flow cytometry. DISC component proteins, RIP-1, and p-p65 were measured by Western blot...
March 8, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
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