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https://www.readbyqxmd.com/read/29775589/better-together-a-hybrid-amyloid-signals-necroptosis
#1
Dan Li, Cong Liu
A new solid-state NMR study determines the high-resolution hetero-amyloid structure of the RIPK1-RIPK3 signaling complex that is involved in mediating necroptosis. The structure demonstrates specific formation of hetero-amyloids over homo-amyloids and the structural basis for a functional amyloid to act as a platform to recruit and activate downstream partners in intracellular signaling.
May 17, 2018: Cell
https://www.readbyqxmd.com/read/29772481/vascular-peroxide-1-promotes-ox-ldl-induced-programmed-necrosis-in-endothelial-cells-through-a-mechanism-involving-%C3%AE-catenin-signaling
#2
Yin-Zhuang Zhang, Lei Wang, Jie-Jie Zhang, Xiao-Ming Xiong, Di Zhang, Xuan-Meng Tang, Xiu-Ju Luo, Qi-Lin Ma, Jun Peng
BACKGROUND AND AIMS: Vascular peroxidase 1 (VPO1) plays a key role in mediation of cardiovascular oxidative injury. This study aims to determine whether VPO1 can promote programmed necrosis of endothelial cells and the underlying mechanisms. METHODS AND RESULTS: Human umbilical vein endothelial cells (HUVECs) were incubated with oxidized low-density lipoprotein (ox-LDL, 100 μg/mL) for 48 h to induce cell injury, which showed an elevation in cell necrosis (reflected by the increased propidium iodide (PI) positive-staining cells, LDH release and decreased cell viability), concomitant with an increase in programmed necrosis-relevant proteins including receptor-interacting protein kinase 1/3 (RIPK1/3), p-RIPK3 and mixed lineage kinase domain like (MLKL); these phenomena were attenuated by necrostatin-1(Nec-1) and RIPK3 siRNA...
May 3, 2018: Atherosclerosis
https://www.readbyqxmd.com/read/29760660/ophiopogonin-d-a-natural-product-from-radix-ophiopogonis-induces-in-vitro-and-in-vivo-ripk1-dependent-and-caspase-independent-apoptotic-death-in-androgen-independent-human-prostate-cancer-cells
#3
Zongliang Lu, He Wang, Mingxing Zhu, Wei Song, Jiajia Wang, Changpeng Wu, Ya Kong, Jing Guo, Na Li, Jie Liu, Yanwu Li, Hongxia Xu
Objective: The purpose of this study was to evaluate the anticancer effects of Ophiopogonin D' (OPD', a natural product extracted from a traditional Chinese medicine ( Radix Ophiopogonis ) against androgen-independent prostate cancer cells and to explore the underlying molecular mechanism(s) of action. Methods: The CCK-8 assay was used to assess the viability of prostate cancer cells. The cell morphology was examined by an ultrastructural analysis via transmission electron microscopy. Cells in apoptosis (early and late stages) were detected using an Annexin V-FITC/propidium iodide kit with a FACSCaliber flow cytometer...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29735703/correction-for-martin-sanchez-et-al-tweak-and-ripk1-mediate-a-second-wave-of-cell-death-during-aki
#4
(no author information available yet)
No abstract text is available yet for this article.
May 7, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29729104/the-impact-of-diet-induced-hepatic-steatosis-in-a-murine-model-of-hepatic-ischemia-reperfusion-injury
#5
Kim H H Liss, Kyle S McCommis, Kari T Chambers, Terri A Pietka, George G Schweitzer, Sara L Park, ILKe Nalbantoglu, Carla J Weinheimer, Angela M Hall, Brian N Finck
The prevalence of obesity-associated nonalcoholic fatty liver disease has significantly increased over the past decade and end stage liver disease secondary to nonalcoholic steatohepatitis has become one of the most common indications for liver transplantation. This both increases the demand for organs and decreases the availability of donor livers deemed suitable for transplantation. While in the past many steatotic livers were discarded due to concerns over enhanced susceptibility to ischemia reperfusion injury and organ failure, the discrepancy between supply and demand has resulted in increasing use of expanded criteria donor organs including steatotic livers...
May 5, 2018: Liver Transplantation
https://www.readbyqxmd.com/read/29725301/necrostatin-1-attenuates-cisplatin-induced-nephrotoxicity-through-suppression-of-apoptosis-and-oxidative-stress-and-retains-klotho-expression
#6
Yichun Ning, Yiqin Shi, Jing Chen, Nana Song, Jieru Cai, Yi Fang, Xiaofang Yu, Jun Ji, Xiaoqiang Ding
Aim: Cisplatin is an effective chemotherapeutic drug, but the application in clinical is greatly limited by its nephrotoxicity. Necrostatin-1 (Nec-1), an inhibitor of RIP1 kinase, has been reported to inhibit RIP-mediated necroptosis. The aim of this study is to detect the protective effects of Nec-1 on the nephrotoxicity of cisplatin and to investigate its renoprotection mechanism. Methods: 8-week-old male C57BL/6 mice were randomly assigned into four groups: Control, Nec-1, Cisplatin, and Cisplatin+Nec-1...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29710643/pm-2-5-induces-male-reproductive-toxicity-via-mitochondrial-dysfunction-dna-damage-and-ripk1-mediated-apoptotic-signaling-pathway
#7
Jin Zhang, Jianhui Liu, Lihua Ren, Jialiu Wei, Junchao Duan, Lefeng Zhang, Xianqing Zhou, Zhiwei Sun
Recent years, air pollution has been a serious problem, and PM2.5 is the main air particulate pollutant. Studies have investigated that PM2.5 is a risky factor to the deterioration of semen quality in males. But, the related mechanism is still unclear. To explore the effect of PM2.5 , Sprague Dawley (SD) rats were exposed to PM2.5 (0, 1.8, 5.4 and 16.2mg/kg.bw.) through intratracheal instillation. The exposure was performed once every 3days and continued for 30days. In vitro, GC-2spd cells were treated using 0, 50, 100, 200μg/mL PM2...
April 13, 2018: Science of the Total Environment
https://www.readbyqxmd.com/read/29706658/actn4-regulates-the-stability-of-ripk1-in-melanoma
#8
Yuan Yuan Zhang, Hessam Tabataba, Xiao Ying Liu, Jia Yu Wang, Xu Guang Yan, Margaret Farrelly, Chen Chen Jiang, Su Tang Guo, Tao Liu, Hung-Ying Kao, Rick F Thorne, Xu Dong Zhang, Lei Jin
The actin crosslinking protein α-actinin-4 (ACTN4) is emerging as an important contributor to the pathogenesis of cancer. This has largely been attributed to its role in regulating cytoskeleton organization and its involvement in transcriptional regulation of gene expression. Here we report a novel function of ACTN4 as a scaffold necessary for stabilization of receptor-interacting protein kinase 1 (RIPK1) that we have recently found to be an oncogenic driver in melanoma. ACTN4 bound to RIPK1 and cellular inhibitor of apoptosis protein 1 (cIAP1) with its actin-binding domain at the N-terminus and the CaM-like domain at the C-terminus, respectively...
April 30, 2018: Oncogene
https://www.readbyqxmd.com/read/29705943/critical-contribution-of-ripk1-mediated-mitochondrial-dysfunction-and-oxidative-stress-to-compression-induced-rat-nucleus-pulposus-cells-necroptosis-and-apoptosis
#9
Songfeng Chen, Xiao Lv, Binwu Hu, Lei Zhao, Shuai Li, Zhiliang Li, Xiangcheng Qing, Hongjian Liu, Jianzhong Xu, Zengwu Shao
The aim of this study was to investigate whether RIPK1 mediated mitochondrial dysfunction and oxidative stress contributed to compression-induced nucleus pulposus (NP) cells necroptosis and apoptosis, together with the interplay relationship between necroptosis and apoptosis in vitro. Rat NP cells underwent various periods of 1.0 MPa compression. To determine whether compression affected mitochondrial function, we evaluated the mitochondrial membrane potential, mitochondrial permeability transition pore (mPTP), mitochondrial ultrastructure and ATP content...
April 28, 2018: Apoptosis: An International Journal on Programmed Cell Death
https://www.readbyqxmd.com/read/29703889/necroptosis-promotes-cell-autonomous-activation-of-proinflammatory-cytokine-gene-expression
#10
Kezhou Zhu, Wei Liang, Zaijun Ma, Daichao Xu, Shuangyi Cao, Xiaojuan Lu, Nan Liu, Bing Shan, Lihui Qian, Junying Yuan
Necroptosis, a form of regulated necrotic cell death, is mediated by receptor interacting protein 1 (RIPK1), RIPK3, and mixed lineage kinase domain-like protein (MLKL). However, the mechanism by which necroptosis promotes inflammation is still unclear. Here we report that the expression of cytokines is robustly upregulated in a cell-autonomous manner during necroptosis induced by tumor necrosis factor alpha (TNFα). We demonstrate that TNFα-induced necroptosis leads to two waves of cytokine production. The first wave, more transient and weaker than the second, is in response to TNFα alone; whereas the second wave depends upon the necroptotic signaling...
April 27, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29696779/necroptosis-increases-with-age-and-is-reduced-by-dietary-restriction
#11
Sathyaseelan S Deepa, Archana Unnikrishnan, Stephanie Matyi, Niran Hadad, Arlan Richardson
Necroptosis is a newly identified programmed cell death pathway that is highly proinflammatory due to the release of cellular components that promote inflammation. To determine whether necroptosis might play a role in inflammaging, we studied the effect of age and dietary restriction (DR) on necroptosis in the epididymal white adipose tissue (eWAT), a major source of proinflammatory cytokines. Phosphorylated MLKL and RIPK3, markers of necroptosis, were increased 2.7- and 1.9-fold, respectively, in eWAT of old mice compared to adult mice, and DR reduced P-MLKL and P-RIPK3 to levels similar to adult mice...
April 25, 2018: Aging Cell
https://www.readbyqxmd.com/read/29695863/lubac-is-essential-for-embryogenesis-by-preventing-cell-death-and-enabling-haematopoiesis
#12
Nieves Peltzer, Maurice Darding, Antonella Montinaro, Peter Draber, Helena Draberova, Sebastian Kupka, Eva Rieser, Amanda Fisher, Ciaran Hutchinson, Lucia Taraborrelli, Torsten Hartwig, Elodie Lafont, Tobias L Haas, Yutaka Shimizu, Charlotta Böiers, Aida Sarr, James Rickard, Silvia Alvarez-Diaz, Michael T Ashworth, Allison Beal, Tariq Enver, John Bertin, William Kaiser, Andreas Strasser, John Silke, Philippe Bouillet, Henning Walczak
The linear ubiquitin chain assembly complex (LUBAC) is required for optimal gene activation and prevention of cell death upon activation of immune receptors, including TNFR1 1 . Deficiency in the LUBAC components SHARPIN or HOIP in mice results in severe inflammation in adulthood or embryonic lethality, respectively, owing to deregulation of TNFR1-mediated cell death2-8 . In humans, deficiency in the third LUBAC component HOIL-1 causes autoimmunity and inflammatory disease, similar to HOIP deficiency, whereas HOIL-1 deficiency in mice was reported to cause no overt phenotype9-11 ...
May 2018: Nature
https://www.readbyqxmd.com/read/29686306/anisomycin-prevents-ogd-induced-necroptosis-by-regulating-the-e3-ligase-chip
#13
Mi-Bo Tang, Yu-Sheng Li, Shao-Hua Li, Yuan Cheng, Shuo Zhang, Hai-Yang Luo, Cheng-Yuan Mao, Zheng-Wei Hu, Jonathan C Schisler, Chang-He Shi, Yu-Ming Xu
Necroptosis is an essential pathophysiological process in cerebral ischemia-related diseases. Therefore, targeting necroptosis may prevent cell death and provide a much-needed therapy. Ansiomycin is an inhibitor of protein synthesis which can also activate c-Jun N-terminal kinases. The present study demonstrated that anisomycin attenuated necroptosis by upregulating CHIP (carboxyl terminus of Hsc70-interacting protein) leading to the reduced levels of receptor-interacting protein kinase 1 (RIPK1) and receptor-interacting protein kinase 3 (RIPK3) proteins in two in vitro models of cerebral ischemia...
April 23, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29686269/lysosomal-damage-after-spinal-cord-injury-causes-accumulation-of-ripk1-and-ripk3-proteins-and-potentiation-of-necroptosis
#14
Shuo Liu, Yun Li, Harry M C Choi, Chinmoy Sarkar, Eugene Y Koh, Junfang Wu, Marta M Lipinski
Necroptosis, a regulated necrosis pathway mediated by the receptor-interacting protein kinases 1 and 3 (RIPK1 and RIPK3), is induced following spinal cord injury (SCI) and thought to contribute to neuronal and glial cell death. However, mechanisms leading to activation of necroptosis after SCI remain unclear. We have previously shown that autophagy, a catabolic pathway facilitating degradation of cytoplasmic proteins and organelles in a lysosome-dependent manner, is inhibited following SCI in rats. Our current data confirm that inhibition of autophagy also occurs after thoracic contusive SCI in the mouse model, as indicated by accumulation of both the autophagosome marker, LC3-II and autophagy cargo protein, p62/SQSTM1...
April 23, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29681787/the-response-to-neoadjuvant-chemoradiotherapy-with-5-fluorouracil-in-locally-advanced-rectal-cancer-patients-a-predictive-proteomic-signature
#15
Anaïs Chauvin, Chang-Shu Wang, Sameh Geha, Perrine Garde-Granger, Alex-Ane Mathieu, Vincent Lacasse, François-Michel Boisvert
Background: Colorectal cancer is the third most common and the fourth most lethal cancer in the world. In the majority of cases, patients are diagnosed at an advanced stage or even metastatic, thus explaining the high mortality. The standard treatment for patients with locally advanced non-metastatic rectal cancer is neoadjuvant radio-chemotherapy (NRCT) with 5-fluorouracil (5-FU) followed by surgery, but the resistance rate to this treatment remains high with approximately 30% of non-responders...
2018: Clinical Proteomics
https://www.readbyqxmd.com/read/29681455/the-structure-of-the-necrosome-ripk1-ripk3-core-a-human-hetero-amyloid-signaling-complex
#16
Miguel Mompeán, Wenbo Li, Jixi Li, Ségolène Laage, Ansgar B Siemer, Gunes Bozkurt, Hao Wu, Ann E McDermott
The RIPK1-RIPK3 necrosome is an amyloid signaling complex that initiates TNF-induced necroptosis, serving in human immune defense, cancer, and neurodegenerative diseases. RIPK1 and RIPK3 associate through their RIP homotypic interaction motifs with consensus sequences IQIG (RIPK1) and VQVG (RIPK3). Using solid-state nuclear magnetic resonance, we determined the high-resolution structure of the RIPK1-RIPK3 core. RIPK1 and RIPK3 alternately stack (RIPK1, RIPK3, RIPK1, RIPK3, etc.) to form heterotypic β sheets...
April 16, 2018: Cell
https://www.readbyqxmd.com/read/29666472/caspase-8-deficiency-in-mouse-embryos-triggers-chronic-ripk1-dependent-activation-of-inflammatory-genes-independently-of-ripk3
#17
Tae-Bong Kang, Ju-Seong Jeong, Seung-Hoon Yang, Andrew Kovalenko, David Wallach
Deletion of the Casp8 gene in epithelial tissues of mice results in severe inflammatory pathologies. Its ubiquitous deletion, or its specific deletion in endothelial cells, results in intrauterine death associated with capillary damage. These pathologies are all preventable by co-deletion of Casp8 and the genes encoding either the RIPK1 or the RIPK3 protein kinase. Since activation of RIPK3 in Caspase-8-deficient cells can trigger necroptotic cell death, and since RIPK1 can activate RIPK3, it is widely assumed that the inflammatory states resulting from Caspase-8 deficiency occur as a consequence of RIPK3-induced necroptosis...
April 17, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29664014/rip-kinase-1-dependent-endothelial-necroptosis-underlies-systemic-inflammatory-response-syndrome
#18
Matija Zelic, Justine E Roderick, Joanne A O'Donnell, Jesse Lehman, Sung Eun Lim, Harish P Janardhan, Chinmay M Trivedi, Manolis Pasparakis, Michelle A Kelliher
Receptor interacting protein kinase 1 (RIPK1) has important kinase-dependent and kinase-independent scaffolding functions that activate or prevent apoptosis or necroptosis in a cell context-dependent manner. The kinase activity of RIPK1 mediates hypothermia and lethality in a mouse model of TNF-induced shock, reflecting the hyperinflammatory state of systemic inflammatory response syndrome (SIRS), where the proinflammatory "cytokine storm" has long been viewed as detrimental. Here, we demonstrate that cytokine and chemokine levels did not predict survival and, importantly, that kinase-inactive Ripk1D138N/D138N hematopoietic cells afforded little protection from TNF- or TNF/zVAD-induced shock in reconstituted mice...
April 16, 2018: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/29661487/ripk1-downregulation-in-keratinocyte-enhances-trail-signaling-in-psoriasis
#19
Nao Saito, Masaru Honma, Takashi Shibuya, Shin Iinuma, Satomi Igawa, Mari Kishibe, Akemi Ishida-Yamamoto
BACKGROUND: Psoriasis, a common inflammatory skin disorder characterized by scaly erythema and plaques, is induced by dysregulation of dendritic cell- and T cell-mediated immune reaction. Receptor-interacting protein kinase 1 (RIPK1) regulates inflammatory signaling in response to stimuli such as TNF-α, TRAIL, and TLRs, resulting in apoptosis, necroptosis and NF-κB activation. However, the physiological relevance in human epidermis remains elusive. OBJECTIVE: In this study, we examined whether RIPK1 is involved in the pathogenesis of psoriasis vulgaris...
April 10, 2018: Journal of Dermatological Science
https://www.readbyqxmd.com/read/29629899/ask1-2-signaling-promotes-inflammation-in-a-mouse-model-of-neutrophilic-dermatosis
#20
Sarang Tartey, Prajwal Gurung, Tejasvi Krishna Dasari, Amanda Burton, Thirumala-Devi Kanneganti
Mice homozygous for the Tyr208Asn amino acid substitution in the carboxy terminus of Src homology region 2 (SH2) domain-containing phosphatase 1 (SHP-1) (referred to as Ptpn6spin mice) spontaneously develop a severe inflammatory disease resembling neutrophilic dermatosis in humans. Disease in Ptpn6spin mice is characterized by persistent footpad swelling and suppurative inflammation. Recently, in addition to IL-1α and IL-1R signaling, we demonstrated a pivotal role for several kinases such as SYK, RIPK1, and TAK1 in promoting inflammatory disease in Ptpn6spin mice...
April 9, 2018: Journal of Clinical Investigation
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