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https://www.readbyqxmd.com/read/28330474/hypercholesterolemia-downregulates-autophagy-in-the-rat-heart
#1
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
#2
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
#3
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
#4
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
#5
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...
March 13, 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
#6
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
#7
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
#8
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
#9
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
https://www.readbyqxmd.com/read/28260985/involvement-of-necroptosis-a-newly-recognized-cell-death-type-in-steroid-induced-osteonecrosis-in-a-rabbit-model
#10
Toru Ichiseki, Shusuke Ueda, Yoshimichi Ueda, Masanobu Tuchiya, Ayumi Kaneuji, Norio Kawahara
We investigated the role of programmed necrosis (necroptosis), a newly recognized form of cell necrosis that has been implicated in the development of steroid-induced osteonecrosis. We used an osteonecrosis model in which 30 Japanese white rabbits each weighing 3.5kg were injected once with methylprednisolone at 20 mg/kg body weight into the right gluteal muscle. Ten animals killed 14 days thereafter were designated as S14d groups, while another 10 animals injected with necroptosis, a specific inhibitor of necrostatin-1 i...
2017: International Journal of Medical Sciences
https://www.readbyqxmd.com/read/28256219/mapping-the-broad-structural-and-mechanical-properties-of-amyloid-fibrils
#11
Guillaume Lamour, Roy Nassar, Patrick H W Chan, Gunes Bozkurt, Jixi Li, Jennifer M Bui, Calvin K Yip, Thibault Mayor, Hongbin Li, Hao Wu, Jörg A Gsponer
Amyloids are fibrillar nanostructures of proteins that are assembled in several physiological processes in human cells (e.g., hormone storage) but also during the course of infectious (prion) and noninfectious (nonprion) diseases such as Creutzfeldt-Jakob and Alzheimer's diseases, respectively. How the amyloid state, a state accessible to all proteins and peptides, can be exploited for functional purposes but also have detrimental effects remains to be determined. Here, we measure the nanomechanical properties of different amyloids and link them to features found in their structure models...
February 28, 2017: Biophysical Journal
https://www.readbyqxmd.com/read/28252651/role-for-rip1-in-mediating-necroptosis-in-experimental-intracerebral-hemorrhage-model-both-in-vivo-and-in-vitro
#12
Haitao Shen, Chenglin Liu, Dongping Zhang, Xiyang Yao, Kai Zhang, Haiying Li, Gang Chen
Cell death is a hallmark of second brain injury after intracerebral hemorrhage (ICH); however, the mechanism still has not been fully illustrated. In this study, we explored whether necroptosis, a type of regulated necrosis, has an essential role in brain injury after ICH. We found that inhibiting receptor-interacting protein 1 (RIP1) - a core element of the necroptotic pathway - by a specific chemical inhibitor or genetic knockdown attenuated brain injury in a rat model of ICH. Furthermore, necroptosis of cultured neurons could be induced by conditioned medium from microglia stimulated with oxygen hemoglobin, and this effect could be inhibited by TNF-α inhibitor, indicating that TNF-α secreted from activated microglia is an important factor in inducing necroptosis of neurons...
March 2, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28250973/mpp-induces-necrostatin-1-and-ferrostatin-1-sensitive-necrotic-death-of-neuronal-sh-sy5y-cells
#13
Keisuke Ito, Yutaka Eguchi, Yusuke Imagawa, Shuji Akai, Hideki Mochizuki, Yoshihide Tsujimoto
Regulation of cell death is potentially a powerful treatment modality for intractable diseases such as neurodegenerative diseases. Although there have been many reports about the possible involvement of various types of cell death in neurodegenerative diseases, it is still unclear exactly how neurons die in patients with these diseases, thus treatment strategies based on cell death regulation have not been established yet. To obtain some insight into the mechanisms of cell death involved in neurodegenerative diseases, we studied the effect of 1-methyl-4-phenylpyridinium (MPP+) on the human neuroblastoma cell line SH-SY5Y (a widely used model of Parkinson's disease)...
2017: Cell Death Discovery
https://www.readbyqxmd.com/read/28249776/lack-of-interaction-between-between-nemo-and-sharpin-impairs-linear-ubiquitination-and-nf-%C3%AE%C2%BAb-activation-and-leads-to-incontinentia-pigmenti
#14
E Bal, E Laplantine, Y Hamel, V Dubosclard, B Boisson, A Pesacatore, C Picard, S Hadj-Rabia, G Royer, J Steffann, J P Bonnefont, V M Ursini, P Vabres, A Munnich, J L Casanova, C Bodemer, R Weil, F Agou, A Smahi
BACKGROUND: Incontinentia pigmenti (IP; MIM308300) is a severe, male-lethal, X-linked, dominant genodermatosis resulting from loss-of-function mutations in the IKBKG gene encoding NF-κB essential modulator (NEMO, the regulatory subunit of the IKK complex). In 80% of cases of IP, the deletion of exons 4 to 10 leads to the absence of NEMO and total inhibition of NF-κB signaling. Here, we described a new IKBKG mutation responsible for IP resulting in an inactive truncated form of NEMO...
February 26, 2017: Journal of Allergy and Clinical Immunology
https://www.readbyqxmd.com/read/28213559/an-organelle-rna-recognition-motif-protein-is-required-for-photosynthetic-subunit-psbf-transcript-editing
#15
Justin B Hackett, Xiaowen Shi, Amy T Kobylarz, Meriah K Lucas, Ryan L Wessendorf, Kevin M Hines, Stephane Bentolila, Maureen Hanson, Yan Lu
Loss-of-function mutations in Organelle RNA Recognition Motif Protein 6 (ORRM6) result in near absence of RNA editing of psbF-C77 and reduction in accD-C794 editing in Arabidopsis (Arabidopsis thaliana). The orrm6 mutants have decreased levels of PSII proteins, especially PsbF, lower PSII activity, pale green pigmentation, smaller leaf and plant sizes, and retarded growth. Stable expression of ORRM6 rescues orrm6 editing defects and mutant phenotype. Unlike ORRM1, the other known ORRM plastid editing factor, ORRM6 does not contain RNA editing interacting protein/multiple organellar RNA editing factor (RIP/MORF) boxes, which are required for ORRM1 to interact with site-specific pentatricopeptide repeat (PPR) protein editing factors...
February 17, 2017: Plant Physiology
https://www.readbyqxmd.com/read/28186202/inhibition-of-receptor-interacting-protein-kinase-1-with-necrostatin-1s-ameliorates-disease-progression-in-elastase-induced-mouse-abdominal-aortic-aneurysm-model
#16
Qiwei Wang, Ting Zhou, Zhenjie Liu, Jun Ren, Noel Phan, Kartik Gupta, Danielle M Stewart, Stephanie Morgan, Carmel Assa, K Craig Kent, Bo Liu
Abdominal aortic aneurysm (AAA) is a common aortic disease with a progressive nature. There is no approved pharmacological treatment to effectively slow aneurysm growth or prevent rupture. Necroptosis is a form of programmed necrosis that is regulated by receptor-interacting protein kinases (RIPs). We have recently demonstrated that the lack of RIP3 in mice prevented aneurysm formation. The goal of the current study is to test whether perturbing necroptosis affects progression of existing aneurysm using the RIP1 inhibitors Necrostatin-1 (Nec-1) and an optimized form of Nec-1, 7-Cl-O-Nec-1 (Nec-1s)...
February 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28176780/rip1-autophosphorylation-is-promoted-by-mitochondrial-ros-and-is-essential-for-rip3-recruitment-into-necrosome
#17
Yingying Zhang, Sheng Sean Su, Shubo Zhao, Zhentao Yang, Chuan-Qi Zhong, Xin Chen, Qixu Cai, Zhang-Hua Yang, Deli Huang, Rui Wu, Jiahuai Han
Necroptosis is a type of programmed cell death with great significance in many pathological processes. Tumour necrosis factor-α(TNF), a proinflammatory cytokine, is a prototypic trigger of necroptosis. It is known that mitochondrial reactive oxygen species (ROS) promote necroptosis, and that kinase activity of receptor interacting protein 1 (RIP1) is required for TNF-induced necroptosis. However, how ROS function and what RIP1 phosphorylates to promote necroptosis are largely unknown. Here we show that three crucial cysteines in RIP1 are required for sensing ROS, and ROS subsequently activates RIP1 autophosphorylation on serine residue 161 (S161)...
February 8, 2017: Nature Communications
https://www.readbyqxmd.com/read/28151659/discovery-of-a-first-in-class-receptor-interacting-protein-1-rip1-kinase-specific-clinical-candidate-gsk2982772-for-the-treatment-of-inflammatory-diseases
#18
Philip A Harris, Scott B Berger, Jae U Jeong, Rakesh Nagilla, Deepak Bandyopadhyay, Nino Campobasso, Carol A Capriotti, Julie A Cox, Lauren Dare, Xiaoyang Dong, Patrick M Eidam, Joshua N Finger, Sandra J Hoffman, James Kang, Viera Kasparcova, Bryan W King, Ruth Lehr, Yunfeng Lan, Lara K Leister, John D Lich, Thomas T MacDonald, Nathan A Miller, Michael T Ouellette, Christina S Pao, Attiq Rahman, Michael A Reilly, Alan R Rendina, Elizabeth J Rivera, Michelle C Schaeffer, Clark A Sehon, Robert R Singhaus, Helen H Sun, Barbara A Swift, Rachel D Totoritis, Anna Vossenkämper, Paris Ward, David D Wisnoski, Daohua Zhang, Robert W Marquis, Peter J Gough, John Bertin
RIP1 regulates necroptosis and inflammation and may play an important role in contributing to a variety of human pathologies, including immune-mediated inflammatory diseases. Small-molecule inhibitors of RIP1 kinase that are suitable for advancement into the clinic have yet to be described. Herein, we report our lead optimization of a benzoxazepinone hit from a DNA-encoded library and the discovery and profile of clinical candidate GSK2982772 (compound 5), currently in phase 2a clinical studies for psoriasis, rheumatoid arthritis, and ulcerative colitis...
February 10, 2017: Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/28151467/augmented-trophoblast-cell-death-in-preeclampsia-can-proceed-via-ceramide-mediated-necroptosis
#19
Liane Jennifer Bailey, Sruthi Alahari, Andrea Tagliaferro, Martin Post, Isabella Caniggia
Preeclampsia, a serious hypertensive disorder of pregnancy, is characterized by elevated ceramide (CER) content that is responsible for heightened trophoblast cell death rates via apoptosis and autophagy. Whether trophoblast cells undergo necroptosis, a newly characterized form of regulated necrosis, and the potential role of CER in this process remain to be established. Herein, we report that exposure of both JEG3 cells and primary isolated cytotrophoblasts to C16:0 CER in conjunction with a caspase-8 inhibitor (Q-VD-OPh) promoted necroptotic cell death, as evidenced by increased expression and association of receptor-interacting protein kinases RIP1 and RIP3, as well as phosphorylation of mixed lineage kinase domain-like (MLKL) protein...
February 2, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28139737/histone-h4-expression-is-cooperatively-maintained-by-ikk%C3%AE-and-akt1-which-attenuates-cisplatin-induced-apoptosis-through-the-dna-pk-rip1-iaps-signaling-cascade
#20
Ruixue Wang, Xuelian Zheng, Lei Zhang, Bin Zhou, Huaizhong Hu, Zhiping Li, Lin Zhang, Yong Lin, Xia Wang
While chromatin remodeling mediated by post-translational modification of histone is extensively studied in carcinogenesis and cancer cell's response to chemotherapy and radiotherapy, little is known about the role of histone expression in chemoresistance. Here we report a novel chemoresistance mechanism involving histone H4 expression. Extended from our previous studies showing that concurrent blockage of the NF-κB and Akt signaling pathways sensitizes lung cancer cells to cisplatin-induced apoptosis, we for the first time found that knockdown of Akt1 and the NF-κB-activating kinase IKKβ cooperatively downregulated histone H4 expression, which increased cisplatin-induced apoptosis in lung cancer cells...
January 31, 2017: Scientific Reports
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