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https://www.readbyqxmd.com/read/27911384/analysis-of-scap-n-glycosylation-and-trafficking-in-human-cells
#1
Chunming Cheng, Jeffrey Yunhua Guo, Feng Geng, Xiaoning Wu, Xiang Cheng, Qiyue Li, Deliang Guo
Elevated lipogenesis is a common characteristic of cancer and metabolic diseases. Sterol regulatory element-binding proteins (SREBPs), a family of membrane-bound transcription factors controlling the expression of genes important for the synthesis of cholesterol, fatty acids and phospholipids, are frequently upregulated in these diseases. In the process of SREBP nuclear translocation, SREBP-cleavage activating protein (SCAP) plays a central role in the trafficking of SREBP from the endoplasmic reticulum (ER) to the Golgi and in subsequent proteolysis activation...
November 8, 2016: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/27895089/oxidized-high-density-lipoprotein-induces-macrophage-apoptosis-via-toll-like-receptor-4-dependent-chop-pathway
#2
Shutong Yao, Hua Tian, Li Zhao, Jinguo Li, Libo Yang, Feng Yue, Yanyan Li, Peng Jiao, Nana Yang, Yiwei Wang, Xiangjian Zhang, Shucun Qin
Oxidized high-density lipoprotein (ox-HDL), unlike native HDL that exerts antiatherogenic effects, plays a proatherogenic role. However, the underlying mechanisms are not completely understood. This study was designed to explore the inductive effect of ox-HDL on endoplasmic reticulum (ER) stress-C/EBP homologous protein (CHOP)-mediated macrophage apoptosis and its upstream mechanisms. Our results showed that ox-HDL could be ingested by macrophages, causing intracellular lipid accumulation. Like tunicamycin (an ER stress inducer), ox-HDL induced macrophage apoptosis with concomitant activation of ER stress pathway, including nuclear translocation of activating transcription factor 6, phosphorylation of protein kinase-like ER kinase and eukaryotic translation initiation factor 2α, and upregulation of glucose regulated protein 78 and CHOP, which were inhibited by 4-phenylbutyric acid (PBA, an ER stress inhibitor) and CHOP gene silencing...
November 28, 2016: Journal of Lipid Research
https://www.readbyqxmd.com/read/27889386/protein-disulfide-isomerases-redox-connections-in-and-out-of-the-endoplasmic-reticulum
#3
Ana Iochabel Soares Moretti, Francisco Rafael Martins Laurindo
Protein disulfide isomerases are thiol oxidoreductase chaperones from thioredoxin superfamily. As redox folding catalysts from the endoplasmic reticulum (ER), their roles in ER-related redox homeostasis and signaling is well-studied. PDIA1 exerts thiol oxidation/reduction and isomerization, plus chaperone effects. Also, substantial evidence indicates that PDIs regulate thiol-disulfide switches in other cell locations such as cell surface and possibly cytosol. Subcellular PDI translocation routes remain unclear and seem Golgi-independent...
November 23, 2016: Archives of Biochemistry and Biophysics
https://www.readbyqxmd.com/read/27888218/diverting-cert-mediated-ceramide-transport-to-mitochondria-triggers-bax-dependent-apoptosis
#4
Amrita Jain, Oliver Beutel, Katharina Ebell, Sergey Korneev, Joost C M Holthuis
A deregulation of ceramide biosynthesis in the ER is frequently linked to induction of mitochondrial apoptosis. While in vitro studies suggest that ceramides may initiate cell death by acting directly on mitochondria, their actual contribution to the apoptotic response in living cells is unclear. In here, we analyzed the consequences of targeting the biosynthetic flow of ceramides to mitochondria using a ceramide transfer protein equipped with an outer mitochondrial membrane anchor, mitoCERT. Cells expressing mitoCERT import ceramides into mitochondria and undergo Bax-dependent apoptosis...
November 25, 2016: Journal of Cell Science
https://www.readbyqxmd.com/read/27880984/diffuse-large-b-cell-lymphoma-with-primary-treatment-failure-ultra-high-risk-features-and-benchmarking-for-experimental-therapies
#5
Luciano J Costa, Kami Maddocks, Narendranath Epperla, Nishitha M Reddy, Reem Karmali, Elvira Umyarova, Veronika Bachanova, Christiana Costa, Martha Glenn, Julio Chavez, Oscar Calzada, Frederick Lansigan, Hossain Nasheed, Stefan Barta, Zheng Zhou, Michael Jaglal, Saurabh Chhabra, Francisco Hernandez-Ilizaliturri, Ana C Xavier, Amitkumar Mehta, Deniz Peker, Andreas Forero-Torres, Zeina Al-Mansour, Andrew M Evens, Jonathon B Cohen, Christopher R Flowers, Timothy S Fenske, Mehdi Hamadani
While a subset of patients with DLBCL relapsing after upfront chemoimmunotherapy can be cured with salvage therapy and autologous hematopoietic cell transplantation (auto-HCT), the outcome of patients with primary treatment failure (PTF) is less clear. For this study we analyzed 331 patients from 15 US institutions with DLBCL and PTF, defined as primary progression while on upfront chemoimmunotherapy (PP), residual disease at the end of upfront therapy (RD) or relapse < 6 months from end of therapy (early relapse; ER)...
November 23, 2016: American Journal of Hematology
https://www.readbyqxmd.com/read/27871932/s100a10-regulates-ulk1-localization-to-er-mitochondria-contact-sites-in-ifn-%C3%AE-triggered-autophagy
#6
Ying-Da Chen, Yi-Ting Fang, Chih-Peng Chang, Chiou-Feng Lin, Li-Jin Hsu, Shang-Rung Wu, Yen-Chi Chiu, Robert Anderson, Yee-Shin Lin
During the process of autophagy, the autophagy-related (ATG) proteins are translocated to autophagosome formation sites. Here, we demonstrate that S100A10 is required for ULK1 localization to autophagosome formation sites. Silencing of S100A10 reduces IFN-γ-induced autophagosome formation. We also determined the role of annexin A2 (ANXA2), a binding partner of S100A10, which has been reported to promote phagophore assembly. Silencing of ANXA2 reduced S100A10 expression. However, overexpression of S100A10 in ANXA2-silenced cells was still able to enhance autophagosome formation, suggesting that ANXA2 regulates IFN-γ-induced autophagy through S100A10...
November 18, 2016: Journal of Molecular Biology
https://www.readbyqxmd.com/read/27865938/pdmp-a-ceramide-analogue-acts-as-an-inhibitor-of-mtorc1-by-inducing-its-translocation-from-lysosome-to-endoplasmic-reticulum
#7
Takashi Ode, Katarzyna A Podyma-Inoue, Kazue Terasawa, Jin-Ichi Inokuchi, Toshihide Kobayashi, Tetsuro Watabe, Yuichi Izumi, Miki Hara-Yokoyama
Mammalian or mechanistic target of rapamycin complex 1 (mTORC1) is a master regulator of cell growth, metabolism, and cell differentiation. Recent studies have revealed that the recruitment of mTORC1 to lysosomes is essential for its activation. The ceramide analogue 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP), a well known glycosphingolipid synthesis inhibitor, also affects the structures and functions of various organelles, including lysosomes and endoplasmic reticulum (ER). We investigated whether PDMP regulates the mTORC1 activity through its effects on organellar behavior...
November 16, 2016: Experimental Cell Research
https://www.readbyqxmd.com/read/27863380/arctigenin-functions-as-a-selective-agonist-of-estrogen-receptor-%C3%AE-to-restrict-mtorc1-activation-and-consequent-th17-differentiation
#8
Xin Wu, Bei Tong, Yan Yang, Jinque Luo, Xusheng Yuan, Zhifeng Wei, Mengfan Yue, Yufeng Xia, Yue Dai
Arctigenin was previously proven to inhibit Th17 cell differentiation and thereby attenuate colitis in mice by down-regulating the activation of mechanistic target of rapamycin complex 1 (mTORC1). The present study was performed to address its underlying mechanism in view of estrogen receptor (ER). The specific antagonist PHTPP or siRNA of ERβ largely diminished the inhibitory effect of arctigenin on the mTORC1 activation in T cell lines and primary CD4+ T cells under Th17-polarization condition, suggesting that arctigenin functioned in an ERβ-dependent manner...
November 14, 2016: Oncotarget
https://www.readbyqxmd.com/read/27843443/rna-interference-mediated-simultaneous-suppression-of-seed-storage-proteins-in-rice-grains
#9
Kyoungwon Cho, Hye-Jung Lee, Yeong-Min Jo, Sun-Hyung Lim, Randeep Rakwal, Jong-Yeol Lee, Young-Mi Kim
Seed storage proteins (SSPs) such as glutelin, prolamin, and globulin are abundant components in some of the most widely consumed food cereals in the world. Synthesized in the rough endoplasmic reticulum (ER), SSPs are translocated to the protein bodies. Prolamins are located at the spherical protein body I derived from the ER, whereas, glutelins and globulin are accumulated in the irregularly shaped protein bodies derived from vacuoles. Our previous studies have shown that the individual suppression of glutelins, 13-kDa prolamins and globulin caused the compensative accumulation of other SSPs...
2016: Frontiers in Plant Science
https://www.readbyqxmd.com/read/27826237/the-effect-of-chronic-ozone-exposure-on-the-activation-of-endoplasmic-reticulum-stress-and-apoptosis-in-rat-hippocampus
#10
Erika Rodríguez-Martínez, Concepcion Nava-Ruiz, Elsa Escamilla-Chimal, Gabino Borgonio-Perez, Selva Rivas-Arancibia
The chronic exposure to low doses of ozone, like in environmental pollution, leads to a state of oxidative stress, which has been proposed to contribute to neurodegenerative disorders, including Alzheimer's disease (AD). It induces an increase of calcium in the endoplasmic reticulum (ER), which produces ER stress. On the other hand, different studies show that, in diseases such as Alzheimer's, there exist disturbances in protein folding where ER plays an important role. The objective of this study was to evaluate the state of chronic oxidative stress on ER stress and its relationship with apoptotic death in the hippocampus of rats exposed to low doses of ozone...
2016: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/27825129/late-stage-inhibition-of-autophagy-enhances-calreticulin-surface-exposure
#11
Dan-Dan Li, Bo Xie, Xiao-Jun Wu, Jing-Jing Li, Ya Ding, Xi-Zhi Wen, Xing Zhang, Shu-Guang Zhu, Wei Liu, Xiao-Shi Zhang, Rui-Qing Peng
Calreticulin (CRT) exposure on the cell surface is essential for inducing immunogenic cell death by chemotherapy. Recent studies have shown conflicting effects of chemotherapy-induced autophagy on CRT exposure in cancer cells. Our data revealed that surface-exposed CRT (Ecto-CRT) emission was attenuated by inhibition of autophagy at early stages; however, inhibition of autophagy at late stages resulted in increased Ecto-CRT. Furthermore, neither autophagy activation nor endoplasmic reticulum (ER) stress induction alone was sufficient for CRT surface exposure...
November 4, 2016: Oncotarget
https://www.readbyqxmd.com/read/27815895/image-cytofluorometry-for-the-quantification-of-ploidy-and-endoplasmic-reticulum-stress-in-cancer-cells
#12
Laura Senovilla, Yohann Demont, Juliette Humeau, Norma Bloy, Guido Kroemer
One of the mechanisms of cancer-associated genomic instability involves a transient phase of polyploidization, in most cases tetraploidization, followed by asymmetric divisions and chromosome loss. Increases in ploidy are consistently accompanied by the activation of an endoplasmic reticulum (ER) stress response, resulting in the translocation of calreticulin to the outer surface of the plasma membrane where it stimulates anticancer immune responses. Conversely, immunoselection leads to a coordinated reduction in ploidy, ER stress, and calreticulin exposure...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/27795429/host-cellular-protein-trappc6a%C3%AE-interacts-with-influenza-a-virus-m2-protein-and-regulates-viral-propagation-by-modulating-m2-trafficking
#13
Pengyang Zhu, Libin Liang, Xinyuan Shao, Weiyu Luo, Shuitao Jiang, Qingqing Zhao, Nan Sun, Yuhui Zhao, Junping Li, Jinguang Wang, Yuan Zhou, Jie Zhang, Guangwen Wang, Li Jiang, Hualan Chen, Chengjun Li
: Influenza A virus (IAV) matrix protein 2 (M2) plays multiple roles in the early and late phases of viral infection. Once synthesized, M2 is translocated to the endoplasmic reticulum (ER), travels to the Golgi apparatus, and is sorted at the trans-Golgi network (TGN) for transport to the apical plasma membrane, where it functions in virus budding. We hypothesized that M2 trafficking along with its secretory pathway must be finely regulated, and host factors could be involved in this process...
October 19, 2016: Journal of Virology
https://www.readbyqxmd.com/read/27771715/er-stress-via-chop-pathway-is-involved-in-fk506-induced-apoptosis-in-rat-fibroblasts
#14
Jian Tang, Yingbin Ge, Lei Yang, Xinyu Xu, Tao Sui, Dawei Ge, Jun Que, Xiaojian Cao
BACKGROUND/AIMS: Hypertrophic scars (HS) formation results from reduced apoptosis and increased proliferation of fibroblasts. Therefore, apoptosis of fibroblasts is a key target for the development of novel therapeutic strategies for HS. Previous reports demonstrated that FK506 could attenuate scar formation in vivo and FK506 could also induce endoplasmic reticulum stress (ER stress). However, the effects of FK506 on ER stress-mediated apoptosis in fibroblasts remain unclear. METHODS: Rat skin fibroblasts were used in the study...
October 24, 2016: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/27766462/sugar-modified-poly-propylene-imine-dendrimers-stimulate-the-nf-%C3%AE%C2%BAb-pathway-in-a-myeloid-cell-line
#15
Izabela Jatczak-Pawlik, Michal Gorzkiewicz, Maciej Studzian, Dietmar Appelhans, Brigitte Voit, Lukasz Pulaski, Barbara Klajnert-Maculewicz
PURPOSE: Fourth-generation poly(propylene imine) dendrimers fully surface-modified by maltose (dense shell, PPI-m DS) were shown to be biocompatible in cellular models, which is important for their application in drug delivery. We decided to verify also their inherent bioactivity, including immunomodulatory activity, for potential clinical applications. We tested their effects on the THP-1 monocytic cell line model of innate immunity effectors. METHODS: To estimate the cytotoxicity of dendrimers the reasazurin assay was performed...
October 20, 2016: Pharmaceutical Research
https://www.readbyqxmd.com/read/27749824/translocon-component-sec62-acts-in-endoplasmic-reticulum-turnover-during-stress-recovery
#16
Fiorenza Fumagalli, Julia Noack, Timothy J Bergmann, Eduardo Cebollero, Giorgia Brambilla Pisoni, Elisa Fasana, Ilaria Fregno, Carmela Galli, Marisa Loi, Tatiana Soldà, Rocco D'Antuono, Andrea Raimondi, Martin Jung, Armin Melnyk, Stefan Schorr, Anne Schreiber, Luca Simonelli, Luca Varani, Caroline Wilson-Zbinden, Oliver Zerbe, Kay Hofmann, Matthias Peter, Manfredo Quadroni, Richard Zimmermann, Maurizio Molinari
The endoplasmic reticulum (ER) is a site of protein biogenesis in eukaryotic cells. Perturbing ER homeostasis activates stress programs collectively called the unfolded protein response (UPR). The UPR enhances production of ER-resident chaperones and enzymes to reduce the burden of misfolded proteins. On resolution of ER stress, ill-defined, selective autophagic programs remove excess ER components. Here we identify Sec62, a constituent of the translocon complex regulating protein import in the mammalian ER, as an ER-resident autophagy receptor...
November 2016: Nature Cell Biology
https://www.readbyqxmd.com/read/27737648/interplay-of-n-cadherin-and-matrix-metalloproteinase-9-enhances-human-nasopharyngeal-carcinoma-cell-invasion
#17
Chih-Chin Hsu, Shiang-Fu Huang, Jong-Shyan Wang, Wing-Keung Chu, Ju-En Nien, Wei-Shan Chen, Shu-Er Chow
BACKGROUND: N-cadherin is a trans-membrane adhesion molecule associated with advanced carcinoma progression and poor prognosis. The effect of N-cadherin on matrix metalloproteinase 9 (MMP-9) regulation is implicated in human nasopharyngeal carcinoma (NPC) cell invasion. METHODS AND RESULTS: Exposure of NPC cells to phorbol-12-myristate-13-acetate (PMA) or macrophage conditioned media (CM) upregulated MMP-9 and N-cadherin cleavage, which resulted in NPC cell invasion...
October 13, 2016: BMC Cancer
https://www.readbyqxmd.com/read/27735945/liver-ubiquitome-uncovers-nutrient-stress-mediated-trafficking-and-secretion-of-complement-c3
#18
Helena de Fatima Magliarelli, Mariette Matondo, Gergő Mészáros, Alexander Goginashvili, Eric Erbs, Zhirong Zhang, Michael Mihlan, Christian Wolfrum, Ruedi Aebersold, Izabela Sumara, Romeo Ricci
Adaptation to changes in nutrient availability is crucial for cells and organisms. Posttranslational modifications of signaling proteins are very dynamic and are therefore key to promptly respond to nutrient deprivation or overload. Herein we screened for ubiquitylation of proteins in the livers of fasted and refed mice using a comprehensive systemic proteomic approach. Among 1641 identified proteins, 117 were differentially ubiquitylated upon fasting or refeeding. Endoplasmic reticulum (ER) and secretory proteins were enriched in the livers of refed mice in part owing to an ER-stress-mediated response engaging retro-translocation and ubiquitylation of proteins from the ER...
October 13, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27728894/madecassic-acid-protects-against-hypoxia-induced-oxidative-stress-in-retinal-microvascular-endothelial-cells-via-ros-mediated-endoplasmic-reticulum-stress
#19
Boyu Yang, Yue Xu, Yaguang Hu, Yiwen Luo, Xi Lu, Ching Kit Tsui, Lin Lu, Xiaoling Liang
Madecassic acid (MA) is an abundant triterpenoid in Centella asiatica (L.) Urban. (Apiaceae) that has been used as a wound-healing, anti-inflammatory and anti-cancer agent. Up to now, the effects of MA against oxidative stress remain unclear. In this study, we investigated the effect of MA and its mechanisms on hypoxia-induced human Retinal Microvascular Endothelial Cells (hRMECs). hRMECs were pre-treated with different concentrations of MA (0-50μM) for 30min before being incubated under hypoxia condition (37°C, 5% CO2 and 95% N2)...
October 8, 2016: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/27721408/cytoplasmic-gper-translocation-in-cancer-associated-fibroblasts-mediates-camp-pka-creb-glycolytic-axis-to-confer-tumor-cells-with-multidrug-resistance
#20
T Yu, G Yang, Y Hou, X Tang, C Wu, X-A Wu, L Guo, Q Zhu, H Luo, Y-E Du, S Wen, L Xu, J Yin, G Tu, M Liu
Multiple drug resistance is a challenging issue in the clinic. There is growing evidence that the G-protein-coupled estrogen receptor (GPER) is a novel mediator in the development of multidrug resistance in both estrogen receptor (ER)-positive and -negative breast cancers, and that cancer-associated fibroblasts (CAFs) in the tumor microenvironment may be a new agent that promotes drug resistance in tumor cells. However, the role of cytoplasmic GPER of CAFs on tumor therapy remains unclear. Here we first show that the breast tumor cell-activated PI3K/AKT (phosphoinositide 3-kinase/AKT) signaling pathway induces the cytoplasmic GPER translocation of CAFs in a CRM1-dependent pattern, and leads to the activation of a novel estrogen/GPER/cAMP/PKA/CREB signaling axis that triggers the aerobic glycolysis switch in CAFs...
October 10, 2016: Oncogene
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