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https://read.qxmd.com/read/30770794/mir-451a-suppressing-bap31-can-inhibit-proliferation-and-increase-apoptosis-through-inducing-er-stress-in-colorectal-cancer
#1
Ke Xu, Bin Han, Yang Bai, Xiu-Ying Ma, Zhen-Ni Ji, Yao Xiong, Shi-Kun Miao, Yuan-Yuan Zhang, Li-Ming Zhou
The global morbidity and mortality of colorectal cancer (CRC) are ranked the third among gastrointestinal tumors in the world. MiR-451a is associated with several types of cancer, including CRC. However, the roles and mechanisms of miR-451a in CRC have not been elucidated. BAP31 is a predicted target gene of miR-451a in our suppression subtractive hybridization library. Its relationship with miR-451a and function in CRC are unclear. We hypothesized that miR-451a could induce apoptosis through suppressing BAP31 in CRC...
February 15, 2019: Cell Death & Disease
https://read.qxmd.com/read/30760707/fisetin-induces-autophagy-in-pancreatic-cancer-cells-via-endoplasmic-reticulum-stress-and-mitochondrial-stress-dependent-pathways
#2
Shengnan Jia, Xiaodong Xu, Senhao Zhou, Yan Chen, Guoping Ding, Liping Cao
Pancreatic cancer is one of the most aggressive tumors and patients have poor survival rates. Fisetin, a natural flavonoid, was recently reported to have antitumor effects in various cancer models. Autophagy is a conserved catabolic process that maintains cellular homoeostasis in response to stress, and together with apoptosis, determines cell fate. Herein, we examined the effect of fisetin on pancreatic cancer. We reveal that fisetin inhibits PANC-1 cell proliferation using a real-time cell analysis system...
February 13, 2019: Cell Death & Disease
https://read.qxmd.com/read/30760285/mesencephalic-astrocyte-derived-neurotrophic-factor-manf-protects-against-a%C3%AE-toxicity-via-attenuating-a%C3%AE-induced-endoplasmic-reticulum-stress
#3
Shengchun Xu, Zemin Di, Yufeng He, Runjie Wang, Yuyang Ma, Rui Sun, Jing Li, Tao Wang, Yujun Shen, Shengyun Fang, Lijie Feng, Yuxian Shen
BACKGROUND: Extracellular accumulation of amyloid β-peptide (Aβ) is one of pathological hallmarks of Alzheimer's disease (AD) and contributes to the neuronal loss. Mesencephalic astrocyte-derived neurotrophic factor (MANF) is an endoplasmic reticulum (ER) stress-inducible neurotrophic factor. Many groups, including ours, have proved that MANF rescues neuronal loss in several neurological disorders, such as Parkinson's disease and cerebral ischemia. However, whether MANF exerts its protective effect against Aβ neurotoxicity in AD remains unknown...
February 13, 2019: Journal of Neuroinflammation
https://read.qxmd.com/read/30760074/small-variations-in-nanoparticle-structure-dictate-differential-cellular-stress-responses-and-mode-of-cell-death
#4
Marzena Szwed, Tonje Sønstevold, Anders Øverbye, Nikolai Engedal, Beata Grallert, Ýrr Mørch, Einar Sulheim, Tore-Geir Iversen, Tore Skotland, Kirsten Sandvig, Maria L Torgersen
For optimal exploitation of nanoparticles (NPs) in biomedicine, and to predict nanotoxicity, detailed knowledge of the cellular responses to cell-bound or internalized NPs is imperative. The final outcome of NP-cell interaction is dictated by the type and magnitude of the NP insult and the cellular response. Here, this has been systematically studied by using poly(alkylcyanoacrylate) (PACA) particles differing only in their alkyl side chains; butyl (PBCA), ethylbutyl (PEBCA), or octyl (POCA), respectively. Surprisingly, these highly similar NPs induced different stress responses and modes of cell death in human cell lines...
February 14, 2019: Nanotoxicology
https://read.qxmd.com/read/30755590/dj-1-modulates-the-unfolded-protein-response-and-cell-death-via-upregulation-of-atf4-following-er-stress
#5
Jungwoo Yang, Kwang Soo Kim, Grace O Iyirhiaro, Paul C Marcogliese, Steve M Callaghan, Dianbo Qu, Woo Jae Kim, Ruth S Slack, David S Park
The unfolded protein response (UPR) triggered by endoplasmic reticulum (ER) stress is a feature of many neurodegenerative diseases including Alzheimer's disease, Huntington's disease and Parkinson's disease (PD). Although the vast majority of PD is sporadic, mutations in a number of genes including PARK7 which encodes the protein DJ-1 have been linked to early-onset, familial PD. In this regard, both PD of sporadic and genetic origins exhibit markers of ER stress-induced UPR. However, the relationship between pathogenic mutations in PARK7 and ER stress-induced UPR in PD pathogenesis remains unclear...
February 12, 2019: Cell Death & Disease
https://read.qxmd.com/read/30753517/microrna-24-promotes-pancreatic-beta-cells-toward-dedifferentiation-to-avoid-endoplasmic-reticulum-stress-induced-apoptosis
#6
Yunxia Zhu, Yi Sun, Yuncai Zhou, Yan Zhang, Tao Zhang, Yating Li, Weiyan You, Xiaoai Chang, Li Yuan, Xiao Han
Current research indicates that beta cell loss in type 2 diabetes may be attributed to beta cell dedifferentiation rather than apoptosis; however, the mechanisms by which this occurs remain poorly understood. Our previous study demonstrated that elevation of microRNA-24 (miR-24) in a diabetic setting caused beta cell dysfunction and replicative deficiency. In this study, we focused on the role of miR-24 in beta cell apoptosis and dedifferentiation under endoplasmic reticulum (ER) stress conditions. We found that miR-24 overabundance protected beta cells from thapsigargin (TG)-induced apoptosis at the cost of accelerating the impairment of glucose-stimulated insulin secretion (GSIS) and enhancing the presence of dedifferentiation markers...
February 12, 2019: Journal of Molecular Cell Biology
https://read.qxmd.com/read/30742128/targeting-kpnb1-overcomes-trail-resistance-by-regulating-dr5-mcl-1-and-flip-in-glioblastoma-cells
#7
Zhi-Chuan Zhu, Ji-Wei Liu, Can Yang, Ming-Jie Li, Rong-Jie Wu, Zhi-Qi Xiong
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a cytokine with potential anticancer effect, but innate and adaptive TRAIL resistance in majority of cancers limit its clinical application. Karyopherin β1 (KPNB1) inhibition in cancer cells has been reported to abrogate the nuclear import of TRAIL receptor DR5 and facilitate its localization on the cell surface ready for TRAIL stimulation. However, our study reveals a more complicated mechanism. Genetic or pharmacological inhibition of KPNB1 potentiated TRAIL-induced apoptosis selectively in glioblastoma cells mainly by unfolded protein response (UPR)...
February 11, 2019: Cell Death & Disease
https://read.qxmd.com/read/30721430/activation-of-endoplasmic-reticulum-stress-in-rat-brain-following-low-intensity-microwave-exposure
#8
Ranjeet Kumar, Pravin S Deshmukh, Sonal Sharma, BasuDev Banerjee
The present study was designed to explore the effects of low-intensity microwave radiation on endoplasmic reticulum stress and unfolded protein response. Experiments were performed on male Wistar rats exposed to microwave radiation for 30 days at 900 MHz, 1800 MHz, and 2450 MHz frequencies on four groups of animal: sham-exposed group, 900 MHz exposed (SAR 5.84 × 10-4 W/kg), 1800 MHz exposed (SAR 5.94 × 10-4 W/kg), and 2450 MHz exposed (SAR 6.7 × 10-4 W/kg) groups. Expressions of mRNA were estimated at the end of exposure in rat brain by real-time quantitative PCR...
February 5, 2019: Environmental Science and Pollution Research International
https://read.qxmd.com/read/30719230/atf4-contributes-to-autophagy-and-survival-in-sunitinib-treated-brain-tumor-initiating-cells-btics
#9
Sylvia Moeckel, Kelly LaFrance, Julia Wetsch, Corinna Seliger, Markus J Riemenschneider, Martin Proescholdt, Peter Hau, Arabel Vollmann-Zwerenz
Receptor tyrosine kinase (RTK) pathways are known to play an important role in tumor cell proliferation of glioblastoma (GBM). Cellular determinants of RTK-inhibitor sensitivity are important to optimize and tailor treatment strategies. The stress response gene activating transcription factor 4 (ATF4) is involved in homeostasis and cellular protection. However, little is known about its function in GBM. We found that the ATF4/p-eIF2α pathway is activated in response to Sunitinib in primary tumor initiating progenitor cell cultures (BTICs)...
January 8, 2019: Oncotarget
https://read.qxmd.com/read/30718659/environmental-stresses-suppress-nonsense-mediated-mrna-decay-nmd-and-affect-cells-by-stabilizing-nmd-targeted-gene-expression
#10
Fusako Usuki, Akio Yamashita, Masatake Fujimura
Nonsense-mediated mRNA decay (NMD) is a cellular mechanism that eliminates mRNAs that harbor premature translation termination codons (PTCs). Here, we investigated the effects of environmental stresses (oxidative stress and endoplasmic reticulum (ER) stress) on NMD activity. Methylmercury (MeHg) was used to cause oxidative stress and thapsigargin to stress the ER. NMD suppression, evidenced by upregulation of NMD-sensitive mRNAs and a decrease in UPF1 phosphorylation, was observed in MeHg-treated myogenic cells, cerebral cortical neuronal cells, and astroglial cells...
February 4, 2019: Scientific Reports
https://read.qxmd.com/read/30709400/oligodendrocyte-specific-atf4-inactivation-does-not-influence-the-development-of-eae
#11
Yuan Yue, Milos Stanojlovic, Yifeng Lin, Gerard Karsenty, Wensheng Lin
BACKGROUND: Multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), are inflammatory demyelinating and neurodegenerative diseases of the CNS. Although recent studies suggest the neuroprotective effects of oligodendrocytes in neurodegenerative diseases, it remains unknown whether oligodendrocyte death induced by inflammatory attacks contributes to neurodegeneration in MS and EAE. Upon endoplasmic reticulum (ER) stress, activation of pancreatic ER kinase (PERK) promotes cell survival through induction of activating transcription factor 4 (ATF4) by phosphorylating eukaryotic translation initiation factor 2α (eIF2α)...
February 1, 2019: Journal of Neuroinflammation
https://read.qxmd.com/read/30707413/pollen-typhae-total-flavone-inhibits-endoplasmic-reticulum-stress-induced-apoptosis-in-human-aortic-vascular-smooth-muscle-cells-through-down-regulating-perk-eif2%C3%AE-atf4-chop-pathway
#12
Ming-Tai Chen, Ruo-Lan Huang, Li-Jun Ou, Ying-Nan Chen, Ling Men, Xiao Chang, Ling Wang, Yu-Zhu Yang, Zhong Zhang
OBJECTIVE: To test the hypothesis that the inhibition of endoplasmic reticulum (ER) stress-induced apoptosis in oxidized low-density lipoproteins (ox-LDL)-induced human aortic-vascular smooth muscle cells (HA-VSMCs) was associated with suppression of the protein kinase RNA-like ER kinase (PERK)-eukaryotic translation initiation factor 2α (eIF2α)-activating transcription factor 4 (ATF4)-CCAAT/enhancer binding protein homologous protein (CHOP) signaling pathway by Pollen Typhae total flavone (PTF)...
February 1, 2019: Chinese Journal of Integrative Medicine
https://read.qxmd.com/read/30705506/role-of-the-isr-atf4-pathway-and-its-cross-talk-with-nrf2-in-mitochondrial-quality-control
#13
REVIEW
Shuya Kasai, Hiromi Yamazaki, Kunikazu Tanji, Máté János Engler, Tomoh Matsumiya, Ken Itoh
Recent investigations have clarified the importance of mitochondria in various age-related degenerative diseases, including late-onset Alzheimer's disease and Parkinson's disease. Although mitochondrial disturbances can be involved in every step of disease progression, several observations have demonstrated that a subtle mitochondrial functional disturbance is observed preceding the actual appearance of pathophysiological alterations and can be the target of early therapeutic intervention. The signals from damaged mitochondria are transferred to the nucleus, leading to the altered expression of nuclear-encoded genes, which includes mitochondrial proteins (i...
January 2019: Journal of Clinical Biochemistry and Nutrition
https://read.qxmd.com/read/30703445/er-stress-activation-impairs-the-expression-of-circadian-clock-and-clock-controlled-genes-in-nih3t3-cells-via-an-atf4-dependent-mechanism
#14
Lei Gao, Huatao Chen, Cuimei Li, Yaoyao Xiao, Dan Yang, Manhui Zhang, Dong Zhou, Wei Liu, Aihua Wang, Yaping Jin
Endoplasmic reticulum (ER) stress and circadian clockwork signaling pathways mutually regulate various cellular functions, but the details regarding the cross-talk between these pathways in mammalian cells are unclear. In this study, whether perturbation of ER stress signaling affects the cellular circadian clockwork and transcription of clock-controlled genes was investigated in NIH3T3 mouse fibroblasts. An NIH3T3 cell model stably expressing luciferase (Luc) under the control of the Bmal1 clock gene promoter was established using a lentiviral system...
January 28, 2019: Cellular Signalling
https://read.qxmd.com/read/30674717/neuron-specific-perk-inactivation-exacerbates-neurodegeneration-during-experimental-autoimmune-encephalomyelitis
#15
Sarrabeth Stone, Yuan Yue, Milos Stanojlovic, Shuangchan Wu, Gerard Karsenty, Wensheng Lin
Multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), are chronic inflammatory demyelinating and neurodegenerative diseases of the CNS. Although neurodegeneration is the major contributor to chronic disability in MS, mechanisms governing the viability of axons and neurons in MS and EAE remain elusive. Data indicate that activation of pancreatic endoplasmic reticulum kinase (PERK) influences, positively or negatively, neuron and axon viability in various neurodegenerative diseases through induction of ATF4...
January 24, 2019: JCI Insight
https://read.qxmd.com/read/30674641/nupr1-regulates-palmitate-induced-apoptosis-in-human-articular-chondrocytes
#16
Li Tan, Raghunatha R Yammani
Obesity, a major risk factor for the development of osteoarthritis (OA), is associated with increased circulating levels of free fatty acids (FFA). However, the role of these FFAs in OA pathophysiology is not clearly understood.  In this study, we found that palmitate treatment of human primary articular chondrocytes increased the expression of ER stress markers [activating transcription factor 4 (ATF4), C/EBP homologous protein (CHOP)] and apoptosis markers [cytochrome c and cleaved caspase-3 (CC3)]. Palmitate treatment also increased the expression of Nuclear protein 1 (Nupr1) and tribbles related protein 3 (TRB3), which are known as negative regulators of cell survival pathways...
January 23, 2019: Bioscience Reports
https://read.qxmd.com/read/30671754/mir-214-is-stretch-sensitive-in-aortic-valve-and-inhibits-aortic-valve-calcification
#17
Md Tausif Salim, Joan Fernández Esmerats, Sivakkumar Arjunon, Nicolas Villa-Roel, Robert M Nerem, Hanjoong Jo, Ajit P Yoganathan
miR-214 has been recently found to be significantly downregulated in calcified human aortic valves (AVs). ER stress, especially the ATF4-mediated pathway, has also been shown to be significantly upregulated in calcific AV disease. Since elevated cyclic stretch is one of the major mechanical stimuli for AV calcification and ATF4 is a validated target of miR-214, we investigated the effect of cyclic stretch on miR-214 expression as well as those of ATF4 and two downstream genes (CHOP and BCL2L1). Porcine aortic valve (PAV) leaflets were cyclically stretched at 15% for 48 h in regular medium and for 1 week in osteogenic medium to simulate the early remodeling and late calcification stages of stretch-induced AV disease, respectively...
January 22, 2019: Annals of Biomedical Engineering
https://read.qxmd.com/read/30670351/insulin-action-in-the-brain-regulates-mitochondrial-stress-responses-and-reduces-diet-induced-weight-gain
#18
Kristina Wardelmann, Sabine Blümel, Michaela Rath, Eugenia Alfine, Chantal Chudoba, Mareike Schell, Weikang Cai, Robert Hauffe, Kathrin Warnke, Tanina Flore, Katrin Ritter, Jürgen Weiß, C Ronald Kahn, André Kleinridders
OBJECTIVE: Insulin action in the brain controls metabolism and brain function, which is linked to proper mitochondrial function. Conversely, brain insulin resistance associates with mitochondrial stress and metabolic and neurodegenerative diseases. In the present study, we aimed to decipher the impact of hypothalamic insulin action on mitochondrial stress responses, function and metabolism. METHODS: To investigate the crosstalk of insulin action and mitochondrial stress responses (MSR), namely the mitochondrial unfolded protein response (UPRmt) and integrated stress response (ISR), qPCR, western blotting, and mitochondrial activity assays were performed...
January 6, 2019: Molecular Metabolism
https://read.qxmd.com/read/30670030/the-unfolded-protein-response-induced-by-tembusu-virus-infection
#19
Dongmin Zhao, Jing Yang, Kaikai Han, Qingtao Liu, Huili Wang, Yuzhuo Liu, Xinmei Huang, Lijiao Zhang, Yin Li
BACKGROUND: Tembusu virus (TMUV), classified in the genus Flavivirus, causes reduced egg production and neurological problems in poultry. Flavivirus replication depends on the host endoplasmic reticulum (ER) and induces ER stress that leads to activation of the cellular unfolded protein response (UPR), an important signalling pathway that regulates many biological functions involved in viral pathogenesis and innate immunity. However, the mechanism of TMUV-induced UPR activation remains unclear...
January 22, 2019: BMC Veterinary Research
https://read.qxmd.com/read/30669692/hydrogen-indirectly-suppresses-increases-in-hydrogen-peroxide-in-cytoplasmic-hydroxyl-radical-induced-cells-and-suppresses-cellular-senescence
#20
Takahiro Sakai, Ryosuke Kurokawa, Shin-Ichi Hirano, Jun Imai
Bacteria inhabiting the human gut metabolize microbiota-accessible carbohydrates (MAC) contained in plant fibers and subsequently release metabolic products. Gut bacteria produce hydrogen (H₂), which scavenges the hydroxyl radical (•OH). Because H₂ diffuses within the cell, it is hypothesized that H₂ scavenges cytoplasmic •OH (cyto •OH) and suppresses cellular senescence. However, the mechanisms of cyto •OH-induced cellular senescence and the physiological role of gut bacteria-secreted H₂ have not been elucidated...
January 21, 2019: International Journal of Molecular Sciences
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