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https://www.readbyqxmd.com/read/28749466/knockout-of-march2-inhibits-the-growth-of-hct116-colon-cancer-cells-by-inducing-endoplasmic-reticulum-stress
#1
Dan Xia, Wanli Ji, Chentong Xu, Xin Lin, Xiaokun Wang, Yan Xia, Ping Lv, Quansheng Song, Dalong Ma, Yingyu Chen
Membrane-associated RING-CH protein 2 (MARCH2), a member of the MARCH family, functions in vesicle trafficking and autophagy regulation. In this study, we established MARCH2 knockout HCT116 cell lines using CRISPR/Cas9-mediated genome editing to evaluate the role of MARCH2 in colon cancer in vitro and in vivo. Knockout of MARCH2 suppressed cell proliferation, and promoted autophagy, apoptosis and G2/M phase cell cycle arrest. These effects were associated with activation of endoplasmic reticulum (ER) stress...
July 27, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28748751/update-on-nitazoxanide-a-multifunctional-chemotherapeutic-agent
#2
Anshul Shakya, Hans Raj Bhat, Surjit Kumar Ghosh
The thiazolide nitazoxanide (NTZ) is a broad-spectrum anti-infective drug that adversely affects viability, growth, and proliferation of a range of extracellular and intracellular protozoan, helminths, anaerobic and microaerophilic bacteria, and viruses. Current review compiled the potential chemotherapeutic efficacy of NTZ against a variety of such disease-causing macro and/or micro-organisms as well as neoplastic cells. The most accepted anti-infective mechanism of NTZ involves impairment of the energy metabolism in anaerobic pathogens by inhibition of the pyruvate: ferredoxin/flavodoxin oxidoreductase (PFOR)...
July 27, 2017: Current Drug Discovery Technologies
https://www.readbyqxmd.com/read/28747426/intestinal-epithelial-cell-endoplasmic-reticulum-stress-promotes-mult1-up-regulation-and-nkg2d-mediated-inflammation
#3
Shuhei Hosomi, Joep Grootjans, Markus Tschurtschenthaler, Niklas Krupka, Juan D Matute, Magdalena B Flak, Eduardo Martinez-Naves, Manuel Gomez Del Moral, Jonathan N Glickman, Mizuki Ohira, Lewis L Lanier, Arthur Kaser, Richard Blumberg
Endoplasmic reticulum (ER) stress is commonly observed in intestinal epithelial cells (IECs) and can, if excessive, cause spontaneous intestinal inflammation as shown by mice with IEC-specific deletion of X-box-binding protein 1 (Xbp1), an unfolded protein response-related transcription factor. In this study, Xbp1 deletion in the epithelium (Xbp1(ΔIEC) ) is shown to cause increased expression of natural killer group 2 member D (NKG2D) ligand (NKG2DL) mouse UL16-binding protein (ULBP)-like transcript 1 and its human orthologue cytomegalovirus ULBP via ER stress-related transcription factor C/EBP homology protein...
July 26, 2017: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/28741046/erratum-to-exposure-of-vital-cells-to-necrotic-cell-lysates-induce-the-ire1%C3%AE-branch-of-the-unfolded-protein-response-and-cell-proliferation
#4
Philipp Rohne, Steven Wolf, Carolin Dörr, Julia Ringen, Andrew Holtz, René Gollan, Benjamin Renner, Hans Prochnow, Markus Baiersdörfer, Claudia Koch-Brandt
No abstract text is available yet for this article.
July 24, 2017: Cell Stress & Chaperones
https://www.readbyqxmd.com/read/28739804/role-of-the-disulfide-bond-in-stabilizing-and-folding-of-the-fimbrial-protein-drae-from-uropathogenic-escherichia-coli
#5
Justyna Pilipczuk, Beata Zalewska-Piątek, Piotr Bruździak, Jacek Czub, Milosz Wieczór, Marcin Olszewski, Marta Wanarska, Bogdan Nowicki, Danuta Augustin-Nowacka, Rafal Piątek
Dr fimbriae are homopolymeric adhesive organelles of uropathogenic Escherichia coli composed of DraE subunits, responsible for the attachment to host cells. These structures are characterized by enormously high stability resulting from the structural properties of an Ig-like fold of DraE. One feature of DraE and other fimbrial subunits that makes them peculiar among Ig-like domain-containing proteins is a conserved disulfide bond that joins their A and B strands. Here, we investigated how this disulfide bond affects the stability and folding/unfolding pathway of DraE...
July 24, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28739408/inhibition-of-amyloid-fibrillation-and-destabilization-of-fibrils-of-human-%C3%AE-d-crystallin-by-direct-red-80-and-orange-g
#6
Vandna Sharma, Kalyan Sundar Ghosh
Inhibition of amyloid fibril formation by a lens protein namely human γD-crystallin (HGD) under stressful conditions was targeted by using some small molecules like direct red 80 (DR), orange G (OG) and rhodamine B (RH). The protein itself was found to form matured fibrils after 48hours of incubation at pH 3.0 at 37°C. Various fluorescence based assays (thioflavinT assay, ANS binding assay, intrinsic Trp fluorescence determination), circular dichroism and microscopic imaging techniques were used in the inhibition studies...
July 21, 2017: International Journal of Biological Macromolecules
https://www.readbyqxmd.com/read/28731225/decreased-levels-of-pdi-and-p5-in-oligodendrocytes-in-alzheimer-s-disease
#7
Yasuyuki Honjo, Takashi Ayaki, Takami Tomiyama, Tomohisa Horibe, Hidefumi Ito, Hiroshi Mori, Ryosuke Takahashi, Koji Kawakami
Protein disulfide isomerase (PDI) is a chaperone protein located in the endoplasmic reticulum (ER). Nitric oxide-induced S-nitrosylation of PDI inhibits its enzymatic activity, leading to protein accumulation and activation of the unfolded protein response. Protein disulfide isomerase P5 (P5) is a member of the PDI family that mostly localizes to the ER lumen. Both S-nitrosylated PDI and S-nitrosylated P5 are found in Alzheimer's disease (AD) brain. Previously, we showed that expression of the ER stress marker, growth arrest, and DNA damage protein (GADD34) was significantly increased in neurons and oligodendrocytes in AD brain...
July 21, 2017: Neuropathology: Official Journal of the Japanese Society of Neuropathology
https://www.readbyqxmd.com/read/28731040/er-stress-and-the-unfolded-protein-response-in-neurodegeneration
#8
REVIEW
Claudio Hetz, Smita Saxena
The clinical manifestation of neurodegenerative diseases is initiated by the selective alteration in the functionality of distinct neuronal populations. The pathology of many neurodegenerative diseases includes accumulation of misfolded proteins in the brain. In physiological conditions, the proteostasis network maintains normal protein folding, trafficking and degradation; alterations in this network - particularly disturbances to the function of endoplasmic reticulum (ER) - are thought to contribute to abnormal protein aggregation...
July 21, 2017: Nature Reviews. Neurology
https://www.readbyqxmd.com/read/28729917/autophagy-endoplasmic-reticulum-stress-and-the-unfolded-protein-response-in-intracerebral-hemorrhage
#9
Mingming Niu, Xiaohong Dai, Wei Zou, Xueping Yu, Wei Teng, Qiuxin Chen, Xiaowei Sun, Weiwei Yu, Huihui Ma, Peng Liu
Intracerebral hemorrhage (ICH) is a subtype of stroke that is followed by primary and secondary brain injury. As a result of the injury, cell metabolism is disrupted and a series of stress responses are activated, such as endoplasmic reticulum (ER) stress and the unfolded protein response (UPR), leading to the re-establishment of cell homeostasis or cell death. As an important mechanism of cell homeostasis, autophagy has been widely studied, and the associations between autophagy, ER stress, and the UPR have also been demonstrated...
2017: Translational Neuroscience
https://www.readbyqxmd.com/read/28729712/unfolded-protein-response-reacting-to-membrane-stress
#10
Paulina Strzyz
No abstract text is available yet for this article.
July 21, 2017: Nature Reviews. Molecular Cell Biology
https://www.readbyqxmd.com/read/28729348/a-new-target-for-caffeine-in-the-developing-lung-endoplasmic-reticulum-stress
#11
Philipp Rath, Claudio Nardiello, Rory E Morty
The utility of caffeine to manage apnea of prematurity is widely accepted, however, much controversy surrounds the potential for caffeine to drive post-natal lung maturation in settings of arrested lung development. Many studies have reported pathways relevant to lung injury and lung development are modulated by caffeine in vitro and in vivo, leading to the application of caffeine in experimental animal models of bronchopulmonary dysplasia (BPD). These studies have generated exciting, but at times confusing data...
July 20, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28727885/sustained-activation-of-the-unfolded-protein-response-induces-cell-death-in-fuchs-endothelial-corneal-dystrophy
#12
Naoki Okumura, Miu Kitahara, Hirokazu Okuda, Keisuke Hashimoto, Emi Ueda, Makiko Nakahara, Shigeru Kinoshita, Robert D Young, Andrew J Quantock, Theofilos Tourtas, Ursula Schlötzer-Schrehardt, Friedrich Kruse, Noriko Koizumi
Purpose: The unfolded protein response (UPR) is believed to play a role in the pathogenesis of Fuchs' endothelial corneal dystrophy (FECD). The purpose of this study was to investigate whether unfolded proteins accumulate in the corneal endothelium in FECD and if they are involved in triggering cell death. Methods: Descemet's membranes with corneal endothelial cells (CECs) were obtained during keratoplasty, and expression of aggresomes, type 1 collagen, fibronectin, and agrin was evaluated...
July 1, 2017: Investigative Ophthalmology & Visual Science
https://www.readbyqxmd.com/read/28725179/fine-tuning-er-stress-signal-transducers-to-treat-amyotrophic-lateral-sclerosis
#13
Danilo B Medinas, Jose V González, Paulina Falcon, Claudio Hetz
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the progressive loss of motoneurons and paralysis. The mechanisms underlying neuronal degeneration in ALS are starting to be elucidated, highlighting disturbances in motoneuron proteostasis. Endoplasmic reticulum (ER) stress has emerged as an early pathogenic event underlying motoneuron vulnerability and denervation in ALS. Maintenance of ER proteostasis is controlled by a dynamic signaling network known as the unfolded protein response (UPR)...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28723893/in-vivo-crispr-screening-identifies-ptpn2-as-a-cancer-immunotherapy-target
#14
Robert T Manguso, Hans W Pope, Margaret D Zimmer, Flavian D Brown, Kathleen B Yates, Brian C Miller, Natalie B Collins, Kevin Bi, Martin W LaFleur, Vikram R Juneja, Sarah A Weiss, Jennifer Lo, David E Fisher, Diana Miao, Eliezer Van Allen, David E Root, Arlene H Sharpe, John G Doench, W Nicholas Haining
Immunotherapy with PD-1 checkpoint blockade is effective in only a minority of patients with cancer, suggesting that additional treatment strategies are needed. Here we use a pooled in vivo genetic screening approach using CRISPR-Cas9 genome editing in transplantable tumours in mice treated with immunotherapy to discover previously undescribed immunotherapy targets. We tested 2,368 genes expressed by melanoma cells to identify those that synergize with or cause resistance to checkpoint blockade. We recovered the known immune evasion molecules PD-L1 and CD47, and confirmed that defects in interferon-γ signalling caused resistance to immunotherapy...
July 27, 2017: Nature
https://www.readbyqxmd.com/read/28719799/mesencephalic-astrocyte-derived-neurotrophic-factor-manf-a-new-player-in-endoplasmic-reticulum-diseases-structure-biology-and-therapeutic-roles
#15
REVIEW
Yeawon Kim, Sun-Ji Park, Ying Maggie Chen
Mesencephalic astrocyte-derived neurotrophic factor (MANF), a newly identified 18-kDa soluble protein, localizes to the luminal endoplasmic reticulum (ER), whose stress can stimulate MANF expression and secretion. In Drosophila and zebrafish, MANF regulates dopaminergic neuron development. In contrast, in mice, MANF deficiency leads to diabetes and activation of the unfolded protein response. Recent studies in rodent models have demonstrated that MANF mitigates diabetes, exerts neurotrophic function in neurodegenerative disease, protects cardiomyocytes and neurons in myocardial infarction and cerebral ischemia, respectively, and promotes immune cell phenotype switch from proinflammatory macrophages to prorepair anti-inflammatory macrophages...
June 29, 2017: Translational Research: the Journal of Laboratory and Clinical Medicine
https://www.readbyqxmd.com/read/28718404/emerging-role-of-the-unfolded-protein-response-in-tumor-immunosurveillance
#16
REVIEW
Hélène Vanacker, Jessica Vetters, Lyvia Moudombi, Christophe Caux, Sophie Janssens, Marie-Cécile Michallet
Disruption of endoplasmic reticulum (ER) homeostasis results in ER stress and activation of the unfolded protein response (UPR). This response alleviates cell stress, and is activated in both tumor cells and tumor infiltrating immune cells. The UPR plays a dual function in cancer biology, acting as a barrier to tumorigenesis at the premalignant stage, while fostering cancer maintenance in established tumors. In infiltrating immune cells, the UPR has been involved in both immunosurveillance and immunosuppressive functions...
July 2017: Trends in Cancer
https://www.readbyqxmd.com/read/28718225/proteostasis-and-ageing-insights-from-long-lived-mutant-mice
#17
William A Sands, Melissa M Page, Colin Selman
The global increase in life expectancy is creating significant medical, social and economic challenges to current and future generations. Consequently, there is a need to identify the fundamental mechanisms underlying the ageing process. This knowledge should help develop realistic interventions capable of combatting age-related disease, and thus improving late-life health and vitality. While several mechanisms have been proposed as conserved lifespan determinants, the loss of proteostasis- where proteostasis is defined here as the maintenance of the proteome- appears highly relevant to both ageing and disease...
July 17, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28713984/downregulation-of-microrna%C3%A2-199a%C3%A2-5p-protects-cardiomyocytes-in-cyanotic-congenital-heart-disease-by-attenuating-endoplasmic-reticulum-stress
#18
Yang Zhou, Wei-Kun Jia, Zhao Jian, Liang Zhao, Chen-Cheng Liu, Yong Wang, Ying-Bin Xiao
Chronic hypoxia is a key pathological change in patients with cyanotic congenital heart defect (CCHD). It has been demonstrated that enhanced myocardial unfolded protein response (UPR) increases the capacity to buffer endoplasmic reticulum (ER) stress and to avoid subsequent apoptosis caused by the hypoxia that underlies CCHD. The present study was performed to determine the regulatory role of microRNAs (miRNAs) in this cytoprotective UPR process. The results revealed that miR‑199a‑5p was markedly downregulated in the cardiac tissue of patients with CCHD and in human myocardial cells cultured in hypoxic conditions...
September 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28712094/different-mutations-of-gap-junction-connexin-47-lead-to-discrepant-activation-of-unfolded-protein-response-pathway-in-pelizaeus-merzbacher-like-disease
#19
Na Chen, Jingmin Wang, Yuwu Jiang, Ye Wu, Hongjun Hao, Taoyun Ji
No abstract text is available yet for this article.
July 16, 2017: Neuropediatrics
https://www.readbyqxmd.com/read/28710693/driving-cancer-tumorigenesis-and-metastasis-through-upr-signaling
#20
Alexandra Papaioannou, Eric Chevet
In the tumor microenvironment, cancer cells encounter both external and internal factors that can lead to the accumulation of improperly folded proteins in the Endoplasmic Reticulum (ER) lumen, thus causing ER stress. When this happens, an adaptive mechanism named the Unfolded Protein Response (UPR) is triggered to help the cell cope with this change and restore protein homeostasis in the ER. Sequentially, one would expect that the activation of the three UPR branches, driven namely by IRE1, PERK, and ATF6, are crucial for the adaptation of cancer cells to the changing environment and thus for their survival and further propagation...
July 15, 2017: Current Topics in Microbiology and Immunology
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