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https://www.readbyqxmd.com/read/28739531/oxidative-and-er-stress-dependent-ask1-activation-in-steatotic-hepatocytes-and-kupffer-cells-sensitizes-mice-fatty-liver-to-ischemia-reperfusion-injury
#1
Chiara Imarisio, Elisa Alchera, Bangalore R Chandrashekar, Guido Valente, Antonia Follenzi, Elena Trisolini, Renzo Boldorini, Rita Carini
Steatosis intensifies hepatic ischemia/reperfusion (I/R) injury increasing hepatocyte damage and hepatic inflammation. This study evaluates if this process is associated to a differential response of steatotic hepatocytes (HP) and Kupffer cells (KC) to I/R injury and investigates the molecular mechanisms involved. Control or steatotic (treated with 50 μmol palmitic acid, PA) mouse HP or KC were exposed to hypoxia/reoxygenation (H/R). C57BL/6 mice fed 9 week with control or High Fat diet underwent to partial hepatic IR...
July 21, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28732559/socs-1-is-involved-in-tnf-%C3%AE-induced-mitochondrial-dysfunction-and-apoptosis-in-renal-tubular-epithelial-cells
#2
Chunyang Du, Fang Yao, Yunzhuo Ren, Yunxia Du, Jinying Wei, Haijiang Wu, Huijun Duan, Yonghong Shi
Tumor necrosis factor-α (TNF-α) is suggested to induce mitochondrial dysfunction and apoptosis of renal tubular epithelial cells that possibly exacerbates renal function in chronic kidney disease (CKD). Here we investigated whether suppressor of cytokine signaling-1 (SOCS-1), an inhibitor of cytokine signaling, was involved in TNF-α-induced human renal tubular epithelial cells (HKCs) oxidative stress and apoptosis. TNF-α promoted the protein and mRNA expression of SOCS-1 in a time and dose dependent manner, along with increased cell apoptosis and activation of apoptosis signal regulating kinase-1(ASK1) in HKCs...
June 30, 2017: Tissue & Cell
https://www.readbyqxmd.com/read/28702328/ask1-map3k5-is-transcriptionally-upregulated-by-e2f1-in-adipose-tissue-in-obesity-molecularly-defining-a-human-dys-metabolic-obese-phenotype
#3
Yulia Haim, Matthias Blüher, Daniel Konrad, Nir Goldstein, Nora Klöting, Ilana Harman-Boehm, Boris Kirshtein, Doron Ginsberg, Tanya Tarnovscki, Yftach Gepner, Iris Shai, Assaf Rudich
OBJECTIVE: Obesity variably disrupts human health, but molecular-based patients' health-risk stratification is limited. Adipose tissue (AT) stresses may link obesity with metabolic dysfunction, but how they signal in humans remains poorly-characterized. We hypothesized that a transcriptional AT stress-signaling cascade involving E2F1 and ASK1 (MAP3K5) molecularly defines high-risk obese subtype. METHODS: ASK1 expression in human AT biopsies was determined by real-time PCR analysis, and chromatin immunoprecipitation (ChIP) adopted to AT explants was used to evaluate the binding of E2F1 to the ASK1 promoter...
July 2017: Molecular Metabolism
https://www.readbyqxmd.com/read/28669716/the-regulatory-and-signaling-mechanisms-of-the-ask-family
#4
REVIEW
Takuto Nishida, Kazuki Hattori, Kengo Watanabe
Apoptosis signal-regulating kinase 1 (ASK1) was identified as a MAP3K that activates the JNK and p38 pathways, and subsequent studies have reported ASK2 and ASK3 as members of the ASK family. The ASK family is activated by various intrinsic and extrinsic stresses, including oxidative stress, ER stress and osmotic stress. Numerous lines of evidence have revealed that members of the ASK family are critical for signal transduction systems to control a wide range of stress responses such as cell death, differentiation and cytokine induction...
May 22, 2017: Advances in Biological Regulation
https://www.readbyqxmd.com/read/28661486/the-role-of-map2-kinases-and-p38-kinase-in-acute-murine-liver-injury-models
#5
Jun Zhang, Robert W M Min, Khanh Le, Sheng Zhou, Mariam Aghajan, Tin A Than, Sanda Win, Neil Kaplowitz
c-Jun N-terminal kinase (JNK) mediates hepatotoxicity through interaction of its phospho-activated form with a mitochondrial outer membrane protein, Sh3bp5 or Sab, leading to dephosphorylation of intermembrane Src and consequent impaired mitochondrial respiration and enhanced ROS release. ROS production from mitochondria activates MAP3 kinases, such as MLK3 and ASK1, which continue to activate a pathway to sustain JNK activation, and amplifies the toxic effect of acetaminophen (APAP) and TNF/galactosamine (TNF/GalN)...
June 29, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28656265/bioinformatic-analysis-reveals-potential-properties-of-human-claudin-6-regulation-and-functions
#6
Dongjing Lin, Yaxiong Guo, Yanru Li, Yang Ruan, Mingzi Zhang, Xiangshu Jin, Minlan Yang, Yan Lu, Peiye Song, Shuai Zhao, Bing Dong, Yinping Xie, Qihua Dang, Chengshi Quan
Claudin-6 (CLDN6) is an integral component of the tight junction proteins in polarized epithelial and endothelial cells and plays a crucial role in maintaining cell integrity. Deregulation of CLDN6 expression and distribution in tumor tissues have been widely documented and correlated with cancer progression and metastasis. However, a complete mechanistic understanding of CLDN6 regulation and function remains to be studied. Herein, we show new potential properties of CLDN6 regulation and functions from bioinformatics analysis...
June 27, 2017: Oncology Reports
https://www.readbyqxmd.com/read/28651161/connexin-43-mediates-changes-in-protein-phosphorylation-in-hk-2-cells-during-chronic-cadmium-exposure
#7
Zehe Ge, Haipeng Diao, Maohui Yu, Xiaoli Ji, Qingping Liu, Xiuli Chang, Qing Wu
Connexin 43 (Cx43) is believed to play a role in the mechanisms of toxicity of many chemical species, include cadmium (Cd). In this study, human renal proximal tubule (HK-2) cells were exposed to Cd (1μM, 10 days). Of the 584 protein residues detected using a Phospho Explorer antibody microarray (PEX100), more than half changed their levels of phosphorylation after chronic Cd exposure. Cx43 siRNA attenuated Cd-induced apoptosis and inhibited proliferation, while also attenuating changes in the levels of phosphorylation of many protein residues...
July 2017: Environmental Toxicology and Pharmacology
https://www.readbyqxmd.com/read/28647884/fluoxetine-induces-apoptosis-through-endoplasmic-reticulum-stress-via-mitogen-activated-protein-kinase-activation-and-histone-hyperacetylation-in-sk-n-be-2-m17-human-neuroblastoma-cells
#8
Ji Hyun Choi, Yeon Ju Jeong, Ah-Ran Yu, Kyung-Sik Yoon, Wonchae Choe, Joohun Ha, Sung Soo Kim, Eui-Ju Yeo, Insug Kang
Fluoxetine (FLX) is an antidepressant drug that belongs to the class of selective serotonin reuptake inhibitors. FLX is known to induce apoptosis in multiple types of cancer cells. In this study, the molecular mechanisms underlying the anti-cancer effects of FLX were investigated in SK-N-BE(2)-M17 human neuroblastoma cells. FLX induced apoptotic cell death, activation of caspase-4, -9, and -3, and expression of endoplasmic reticulum (ER) stress-associated proteins, including C/EBP homologous protein (CHOP)...
June 24, 2017: Apoptosis: An International Journal on Programmed Cell Death
https://www.readbyqxmd.com/read/28616035/neuroprotective-effects-of-activin-a-on-endoplasmic-reticulum-stress-mediated-apoptotic-and-autophagic-pc12-cell-death
#9
Long-Xing Xue, Hong-Yu Liu, Yang Cui, Yue Dong, Jiao-Qi Wang, Qiu-Ye Ji, Jin-Ting He, Min Yao, Ying-Ying Wang, Yan-Kun Shao, Jing Mang, Zhong-Xin Xu
Activin A, a member of the transforming growth factor-beta superfamily, plays a neuroprotective role in multiple neurological diseases. Endoplasmic reticulum (ER) stress-mediated apoptotic and autophagic cell death is implicated in a wide range of diseases, including cerebral ischemia and neurodegenerative diseases. Thapsigargin was used to induce PC12 cell death, and Activin A was used for intervention. Our results showed that Activin A significantly inhibited morphological changes in thapsigargin-induced apoptotic cells, and the expression of apoptosis-associated proteins [cleaved-caspase-12, C/EBP homologous protein (CHOP) and cleaved-caspase-3] and biomarkers of autophagy (Beclin-1 and light chain 3), and downregulated the expression of thapsigargin-induced ER stress-associated proteins [inositol requiring enzyme-1 (IRE1), tumor necrosis factor receptor-associated factor 2 (TRAF2), apoptosis signal-regulating kinase 1 (ASK1), c-Jun N-terminal kinase (JNK) and p38]...
May 2017: Neural Regeneration Research
https://www.readbyqxmd.com/read/28615513/thioredoxin-plays-a-key-role-in-retinal-neuropathy-prior-to-endothelial-damage-in-diabetic-mice
#10
Xiang Ren, Chen Li, Junli Liu, Chenghong Zhang, Yuzhen Fu, Nina Wang, Haiying Ma, Heyuan Lu, Hui Kong, Li Kong
Diabetes is a chronic metabolic syndrome that results in changes in carbohydrate, lipid and protein metabolism. With diabetes for a long time, it increases the risk of diabetic retinopathy (DR) and long-term morbidity and mortality. Moreover, emerging evidence suggests that neuron damage occurs earlier than microvascular complications in DR patients, but the underlying mechanism is unclear. We investigated diabetes-induced retinal neuropathy and elucidated key molecular events to identify new therapeutic targets for the clinical treatment and prevention of DR...
May 24, 2017: Oncotarget
https://www.readbyqxmd.com/read/28604593/melatonin-modulates-neuronal-cell-death-induced-by-endoplasmic-reticulum-stress-under-insulin-resistance-condition
#11
Juhyun Song, Oh Yoen Kim
Insulin resistance (IR) is an important stress factor in the central nervous system, thereby aggravating neuropathogenesis and triggering cognitive decline. Melatonin, which is an antioxidant phytochemical and synthesized by the pineal gland, has multiple functions in cellular responses such as apoptosis and survival against stress. This study investigated whether melatonin modulates the signaling of neuronal cell death induced by endoplasmic reticulum (ER) stress under IR condition using SH-SY5Y neuroblastoma cells...
June 10, 2017: Nutrients
https://www.readbyqxmd.com/read/28600984/impaired-cross-talk-between-the-thioredoxin-and-glutathione-systems-is-related-to-ask-1-mediated-apoptosis-in-neuronal-cells-exposed-to-mercury
#12
Vasco Branco, Lucia Coppo, Susana Solá, Jun Lu, Cecília M P Rodrigues, Arne Holmgren, Cristina Carvalho
Mercury (Hg) compounds target both cysteine (Cys) and selenocysteine (Sec) residues in peptides and proteins. Thus, the components of the two major cellular antioxidant systems - glutathione (GSH) and thioredoxin (Trx) systems - are likely targets for mercurials. Hg exposure results in GSH depletion and Trx and thioredoxin reductase (TrxR) are prime targets for mercury. These systems have a wide-range of common functions and interaction between their components has been reported. However, toxic effects over both systems are normally treated as isolated events...
June 1, 2017: Redox Biology
https://www.readbyqxmd.com/read/28562156/neuritin-attenuates-early-brain-injury-in-rats-after-experimental-subarachnoid-hemorrhage
#13
Hang Zhang, Xuejun He, Yezhong Wang, Xiaokun Sun, Licang Zhu, Chao Lei, Jiangwen Yin, Xiaotian Li, Fandi Hou, Wengao He, Dong Zhao
OBJECTIVES: Early brain injury (EBI) is central to the pathological progress of subarachnoid hemorrhage (SAH). In this study, we determined if neuritin protects the brain against EBI in rats and discussed the role of apoptosis pathway mediated by endoplasmic reticulum stress in this neuroprotective route. METHODS: A total of 96 male Sprague Dawley rats were divided into control, sham, SAH and SAH + neuritin groups. The rat SAH model was induced by injection 0.3 mL of nonheparinized arterial blood into the prechiasmatic cistern...
June 14, 2017: International Journal of Neuroscience
https://www.readbyqxmd.com/read/28552582/proteasome-activation-by-small-molecules
#14
Yves Leestemaker, Annemieke de Jong, Katharina F Witting, Renske Penning, Karianne Schuurman, Boris Rodenko, Esther A Zaal, Bert van de Kooij, Stefan Laufer, Albert J R Heck, Jannie Borst, Wiep Scheper, Celia R Berkers, Huib Ovaa
Drugs that increase 26S proteasome activity have potential therapeutic applications in the treatment of neurodegenerative diseases. A chemical genetics screen of over 2,750 compounds using a proteasome activity probe as a readout in a high-throughput live-cell fluorescence-activated cell sorting-based assay revealed more than ten compounds that increase proteasome activity, with the p38 MAPK inhibitor PD169316 being one of the most potent ones. Genetic and chemical inhibition of either p38 MAPK, its upstream regulators, ASK1 and MKK6, and downstream target, MK2, enhance proteasome activity...
June 22, 2017: Cell Chemical Biology
https://www.readbyqxmd.com/read/28552579/ask-family-and-cancer
#15
REVIEW
Hiroki Ryuno, Isao Naguro, Miki Kamiyama
Cancer is a major problem in public health and is one of the leading causes of mortality worldwide. Many types of cancer cells exhibit aberrant cellular signal transduction in response to stress, which often leads to oncogenesis. Mitogen-activated protein kinase (MAPK) signal cascades are one of the important intracellular stress signaling pathways closely related to cancer. The key molecules in MAPK signal cascades that respond to various types of stressors are apoptosis signal-regulating kinase (ASK) family members; ASK1, ASK2 and ASK3...
May 20, 2017: Advances in Biological Regulation
https://www.readbyqxmd.com/read/28551792/mechanistic-role-of-thioredoxin-2-in-heart-failure
#16
Chaofei Chen, Haixuan Chen, Huanjiao Jenny Zhou, Weidong Ji, Wang Min
Thioredoxin 2 (Trx2) is a pivotal mitochondrial protein that regulates redox signaling. The mitochondrial Trx2 is expressed ubiquitously, but it is found at the highest levels in metabolically active tissues like the heart. Global gene knockout of Trx2 results in embryonic lethality, likely due to the increased cellular oxidative stress. Moreover, mice with cardiac-specific Trx2 deletion develop spontaneous dilated cardiomyopathy (DCM), correlating with increased apoptosis stress kinase-1 (ASK1) signaling and increased cardiomyocyte apoptosis...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28537893/alpha-mangostin-induces-apoptosis-through-activation-of-reactive-oxygen-species-and-ask1-p38-signaling-pathway-in-cervical-cancer-cells
#17
Chien-Hsing Lee, Tsung-Ho Ying, Hui-Ling Chiou, Shu-Ching Hsieh, Shiua-Hua Wen, Ruey-Hwang Chou, Yi-Hsien Hsieh
Alpha-mangostin, a natural xanthonoid, has been reported to possess the anti-cancer property in various types of human cancer. However, its effects and mechanism of α-mangostin in cervical cancer remain unclear. We found that α-mangostin effectively inhibited cell viability, resulted in loss of mitochondrial membrane potential (MMP), release of cytochrome C, increase of Bax, decrease of Bcl-2, and activation of caspase-9/caspase-3 cascade in cervical cancer cells. Alpha-mangostin elevated the contents of reactive oxygen species (ROS) to activate p38...
May 7, 2017: Oncotarget
https://www.readbyqxmd.com/read/28526890/a-heteromeric-molecular-complex-regulates-the-migration-of-lung-alveolar-epithelial-cells-during-wound-healing
#18
Manik C Ghosh, Patrudu S Makena, Joseph Kennedy, Bin Teng, Charlean Luellen, Scott E Sinclair, Christopher M Waters
Alveolar type II epithelial cells (ATII) are instrumental in early wound healing in response to lung injury, restoring epithelial integrity through spreading and migration. We previously reported in separate studies that focal adhesion kinase-1 (FAK) and the chemokine receptor CXCR4 promote epithelial repair mechanisms. However, potential interactions between these two pathways were not previously considered. In the present study, we found that wounding of rat ATII cells promoted increased association between FAK and CXCR4...
May 19, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28508477/the-novel-intracellular-protein-creg-inhibits-hepatic-steatosis-obesity-and-insulin-resistance
#19
Quan-Yu Zhang, Ling-Ping Zhao, Xiao-Xiang Tian, Cheng-Hui Yan, Yang Li, Yan-Xia Liu, Pi-Xiao Wang, Xiao-Jing Zhang, Ya-Ling Han
Cellular repressor of E1A-stimulated genes (CREG), a novel cellular glycoprotein, has been identified as a suppressor of various cardiovascular diseases (CVDs) because of its capacity to reduce hyperplasia, maintain vascular homeostasis, and promote endothelial restoration. However, the effects and mechanism of CREG in metabolic disorder and hepatic steatosis remain unknown. Here, we report that hepatocyte-specific CREG deletion dramatically exacerbates high fat diet (HFD) and leptin deficiency-induced (ob/ob) adverse effects such as obesity, hepatic steatosis and metabolic disorders, whereas a beneficial effect is conferred by CREG overexpression...
May 15, 2017: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/28505379/analysis-of-cfb-a-cytokinin-responsive-gene-of-arabidopsis-thaliana-encoding-a-novel-f-box-protein-regulating-sterol-biosynthesis
#20
Wolfram G Brenner, Jan Erik Leuendorf, Anne Cortleven, Laetitia B B Martin, Hubert Schaller, Thomas Schmülling
Protein degradation by the ubiquitin-26S proteasome pathway is important for the regulation of cellular processes, but the function of most F-box proteins relevant to substrate recognition is unknown. We describe the analysis of the gene Cytokinin-induced F-box encoding (CFB, AT3G44326), identified in a meta-analysis of cytokinin-related transcriptome studies as one of the most robust cytokinin response genes. F-box domain-dependent interaction with the E3 ubiquitin ligase complex component ASK1 classifies CFB as a functional F-box protein...
May 12, 2017: Journal of Experimental Botany
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