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calnexin and channel protein

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https://www.readbyqxmd.com/read/26880754/regulation-of-enac-trafficking-in-rat-kidney
#1
Gustavo Frindt, Diego Gravotta, Lawrence G Palmer
The epithelial Na channel (ENaC) forms a pathway for Na(+) reabsorption in the distal nephron, and regulation of these channels is essential for salt homeostasis. In the rat kidney, ENaC subunits reached the plasma membrane in both immature and fully processed forms, the latter defined by either endoglycosidase H-insensitive glycosylation or proteolytic cleavage. Animals adapted to a low-salt diet have increased ENaC surface expression that is specific for the mature forms of the subunit proteins and is similar (three- to fourfold) for α, β, and γENaC...
March 2016: Journal of General Physiology
https://www.readbyqxmd.com/read/26680228/characterisation-of-arabidopsis-calnexin-1-and-calnexin-2-in-the-endoplasmic-reticulum-and-at-plasmodesmata
#2
Danny Y T Liu, Penelope M C Smith, Deborah A Barton, David A Day, Robyn L Overall
Calnexin (CNX) is a highly conserved endoplasmic reticulum (ER) chaperone protein. Both calnexin and the homologous ER-lumenal protein, calreticulin, bind calcium ions and participate in protein folding. There are two calnexins in Arabidopsis thaliana, CNX1 and CNX2. GUS expression demonstrated that these are expressed in most Arabidopsis tissues throughout development. Calnexin transfer DNA (T-DNA) mutant lines exhibited increased transcript abundances of a number of other ER chaperones, including calreticulins, suggesting a degree of redundancy...
December 17, 2015: Protoplasma
https://www.readbyqxmd.com/read/26303164/high-glucose-represses-herg-k-channel-expression-through-trafficking-inhibition
#3
Yuan-Qi Shi, Meng Yan, Li-Rong Liu, Xiao Zhang, Xue Wang, Huai-Ze Geng, Xin Zhao, Bao-Xin Li
BACKGROUND/AIMS: Abnormal QT prolongation is the most prominent cardiac electrical disturbance in patients with diabetes mellitus (DM). It is well known that the human ether-ago-go-related gene (hERG) controls the rapid delayed rectifier K+ current (IKr) in cardiac cells. The expression of the hERG channel is severely down-regulated in diabetic hearts, and this down-regulation is a critical contributor to the slowing of repolarization and QT prolongation. However, the intracellular mechanisms underlying the diabetes-induced hERG deficiency remain unknown...
2015: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/26168288/l-type-calcium-channel-blockers-enhance-trafficking-and-function-of-epilepsy-associated-%C3%AE-1-d219n-subunits-of-gaba-a-receptors
#4
Dong-Yun Han, Bo-Jhih Guan, Ya-Juan Wang, Maria Hatzoglou, Ting-Wei Mu
Gamma-aminobutyric acid type A (GABAA) receptors are the primary inhibitory ion channels in the mammalian central nervous system and play an essential role in regulating inhibition-excitation balance in neural circuits. The α1 subunit harboring the D219N mutation of GABAA receptors was reported to be retained in the endoplasmic reticulum (ER) and traffic inefficiently to the plasma membrane, leading to a loss of function of α1(D219N) subunits and thus idiopathic generalized epilepsy (IGE). We present the use of small molecule proteostasis regulators to enhance the forward trafficking of α1(D219N) subunits to restore their function...
September 18, 2015: ACS Chemical Biology
https://www.readbyqxmd.com/read/25171176/berberine-induces-herg-channel-deficiency-through-trafficking-inhibition
#5
Kaiping Zhang, Duo Zhi, Ting Huang, Yan Gong, Meng Yan, Chen Liu, Ting Wei, Zengxiang Dong, Baoxin Li, Baofeng Yang
AIMS: The human ether-a-go-go-related gene (hERG) encodes the α subunit of the IKr, which plays an essential role in repolarization of action potentials. hERG channels are targeted by various pro-arrhythmic drugs. Berberine (BBR) was previously found to acutely inhibit hERG currents and prolong action potential duration. The present study aimed to determine long-term effects of BBR on the expression of 135kDa/155kDa hERG and the mechanism. METHODS AND RESULTS: hERG expression was assessed by western blot...
2014: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/25107562/the-rescuable-function-and-mechanism-of-resveratrol-on-as%C3%A2-o%C3%A2-induced-herg-k%C3%A2-%C2%BA-channel-deficiency
#6
Xin Zhao, Kai-Ping Zhang, Ting Huang, Cai-Chuan Yan, Li-Rong Liu, Qi-Lei Zhu, Feng-Feng Guo, Chen Liu, Bao-Xin Li
Arsenic trioxide (As2O3) is used to treat acute promyelocytic leukemia. However, the cardiotoxicity of long QT syndrome restricts its clinical application. Previous studies showed that As2O3 can damage the human ether-a-go-go-related gene (hERG) current via disturbing its trafficking to cellular membrane. This study aimed to investigate whether the As2O3-insulted hERG channel can be rescued by resveratrol, a recognized cardioprotective agent. The whole-cell patch clamp technique was used to record the hERG current and action potential duration...
November 2014: Naunyn-Schmiedeberg's Archives of Pharmacology
https://www.readbyqxmd.com/read/25065395/roscovitine-is-a-proteostasis-regulator-that-corrects-the-trafficking-defect-of-f508del-cftr-by-a-cdk-independent-mechanism
#7
C Norez, C Vandebrouck, J Bertrand, S Noel, E Durieu, N Oumata, H Galons, F Antigny, A Chatelier, P Bois, L Meijer, F Becq
BACKGROUND AND PURPOSE: The most common mutation in cystic fibrosis (CF), F508del, causes defects in trafficking, channel gating and endocytosis of the CF transmembrane conductance regulator (CFTR) protein. Because CF is an orphan disease, therapeutic strategies aimed at improving mutant CFTR functions are needed to target the root cause of CF. EXPERIMENTAL APPROACH: Human CF airway epithelial cells were treated with roscovitine 100 μM for 2 h before CFTR maturation, expression and activity were examined...
November 2014: British Journal of Pharmacology
https://www.readbyqxmd.com/read/24220678/blockage-of-trpm7-channel-induces-hepatic-stellate-cell-death-through-endoplasmic-reticulum-stress-mediated-apoptosis
#8
Yongjun Zhu, Ruoting Men, Maoyao Wen, Xiaolin Hu, Xiaojing Liu, Li Yang
AIMS: Proliferation is a 'multiplier' for extracellular matrix production and contraction of activated hepatic stellate cells (HSC) in fibrotic liver. Transient receptor potential melastatin-like 7 channels (TRPM7) are implicated in the survival and proliferation of several kinds of cells. This study was aimed to investigate the effect of TRPM7 blocker 2-APB on survival and proliferation of HSC and the underlying mechanisms. MAIN METHODS: Rat HSC were stimulated by 2-APB for 24 h and then collected for further use...
January 14, 2014: Life Sciences
https://www.readbyqxmd.com/read/24211135/saha-enhances-proteostasis-of-epilepsy-associated-%C3%AE-1-a322d-%C3%AE-2%C3%AE-2-gaba-a-receptors
#9
Xiao-Jing Di, Dong-Yun Han, Ya-Juan Wang, Mark R Chance, Ting-Wei Mu
GABA(A) receptors are the primary inhibitory ion channels in the mammalian central nervous system. The A322D mutation in the α1 subunit of GABA(A) receptors is known to result in its degradation and reduce its cell surface expression, leading to loss of GABAA receptor function in autosomal dominant juvenile myoclonic epilepsy. Here, we show that SAHA, a FDA-approved drug, increases the transcription of the α1(A322D) subunit, enhances its folding and trafficking posttranslationally, increases its cell surface level, and restores the GABA-induced maximal current in HEK293 cells expressing α1(A322D)β2γ2 receptors to 10% of that for wild-type receptors...
December 19, 2013: Chemistry & Biology
https://www.readbyqxmd.com/read/24142691/-ca2-i-elevation-and-oxidative-stress-induce-kcnq1-protein-translocation-from-the-cytosol-to-the-cell-surface-and-increase-slow-delayed-rectifier-iks-in-cardiac-myocytes
#10
Yuhong Wang, Dimitar P Zankov, Min Jiang, Mei Zhang, Scott C Henderson, Gea-Ny Tseng
Our goals are to simultaneously determine the three-dimensional distribution patterns of KCNQ1 and KCNE1 in cardiac myocytes and to study the mechanism and functional implications for variations in KCNQ1/KCNE1 colocalization in myocytes. We monitored the distribution patterns of KCNQ1, KCNE1, and markers for subcellular compartments/organelles using immunofluorescence/confocal microscopy and confirmed the findings in ventricular myocytes by directly observing fluorescently tagged KCNQ1-GFP and KCNE1-dsRed expressed in these cells...
December 6, 2013: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/24037923/calnexin-silencing-in-mouse-neonatal-cardiomyocytes-induces-ca2-cycling-defects-er-stress-and-apoptosis
#11
Nicolas Bousette, Cynthia Abbasi, Roxana Chis, Anthony O Gramolini
Calnexin (CNX) is an endoplasmic reticulum (ER) quality control chaperone that has been implicated in ER stress. ER stress is a prominent pathological feature of various pathologic conditions, including cardiovascular diseases. However, the role of CNX and ER stress has not been studied in the heart. In the present study, we aimed to characterize the role of CNX in cardiomyocyte physiology with respect to ER stress, apoptosis, and cardiomyocyte Ca(2+) cycling. We demonstrated significantly decreased CNX mRNA and protein levels by LentiVector mediated transduction of targeting shRNAs...
March 2014: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/23501103/tespa1-is-a-novel-component-of-mitochondria-associated-endoplasmic-reticulum-membranes-and-affects-mitochondrial-calcium-flux
#12
Hiroshi Matsuzaki, Takahiro Fujimoto, Masatoshi Tanaka, Senji Shirasawa
Regulation of intracellular Ca(2+) concentration is critical in numerous biological processes. Inositol 1,4,5-trisphosphate receptor (IP3R) functions as the Ca(2+) release channel on endoplasmic reticulum (ER) membranes. Much attention has been dedicated to mitochondrial Ca(2+) uptake via mitochondria-associated ER membranes (MAM) which is involved in intracellular Ca(2+) homeostasis; however, the molecular mechanisms that link the MAM to mitochondria still remain elusive. We previously reported that Tespa1 (thymocyte-expressed, positive selection-associated gene 1) expressed in lymphocytes physically interacts with IP3R...
April 12, 2013: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/23385635/alteration-of-proteomic-profiles-in-pbmc-isolated-from-patients-with-fabry-disease-preliminary-findings
#13
Diego Cigna, Claudia D'Anna, Carmela Zizzo, Daniele Francofonte, Iacopo Sorrentino, Paolo Colomba, Giuseppe Albeggiani, Alessandro Armini, Laura Bianchi, Luca Bini, Giovanni Duro
Fabry disease (FD) is an X-linked progressive multisystem disease due to mutations in the gene encoding the lysosomal enzyme α-galactosidase A (α-GalA). The deficiency in α-GalA activity leads to an intra-lysosomal accumulation of neutral glycosphingolipids, mainly globotriaosylceramide (Gb3), in various organs and systems. Enzyme replacement therapy is available and alternative therapeutic approaches are being explored. No diagnostic test, other than sequencing of the α-galactosidase A gene, is available, no biomarker has been proven useful to screen for and predict the disease, and underlying mechanisms are still elusive...
June 2013: Molecular BioSystems
https://www.readbyqxmd.com/read/22526458/regulation-of-enac-biogenesis-by-the-stress-response-protein-serp1
#14
Diana Faria, Nicolas Lentze, Joana Almaça, Simão Luz, Luisa Alessio, Yuemin Tian, José Paulo Martins, Pedro Cruz, Rainer Schreiber, Mandana Rezwan, Carlos Miguel Farinha, Daniel Auerbach, Margarida D Amaral, Karl Kunzelmann
Cystic fibrosis lung disease is caused by reduced Cl(-) secretion along with enhanced Na(+) absorption, leading to reduced airway surface liquid and compromised mucociliary clearance. Therapeutic strategies have been developed to activate cystic fibrosis transmembrane conductance regulator (CFTR) or to overcome enhanced Na(+) absorption by the epithelial Na(+) channel (ENaC). In a split-ubiquitin-based two-hybrid screening, we identified stress-associated ER protein 1 (SERP1)/ribosome-associated membrane protein 4 as a novel interacting partner for the ENaC β-subunit...
June 2012: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/22505584/ryanodine-receptor-antagonists-adapt-npc1-proteostasis-to-ameliorate-lipid-storage-in-niemann-pick-type-c-disease-fibroblasts
#15
Ting Yu, Chan Chung, Dongbiao Shen, Haoxing Xu, Andrew P Lieberman
Niemann-Pick type C disease is a lysosomal storage disorder most often caused by loss-of-function mutations in the NPC1 gene. The encoded multipass transmembrane protein is required for cholesterol efflux from late endosomes and lysosomes. Numerous missense mutations in the NPC1 gene cause disease, including the prevalent I1061T mutation that leads to protein misfolding and degradation. Here, we sought to modulate the cellular proteostasis machinery to achieve functional recovery in primary patient fibroblasts...
July 15, 2012: Human Molecular Genetics
https://www.readbyqxmd.com/read/22242185/trafficking-deficient-g572r-herg-and-e637k-herg-activate-stress-and-clearance-pathways-in-endoplasmic-reticulum
#16
Ying Wang, Xiaoyan Huang, Jianqing Zhou, Xi Yang, Di Li, Haiyan Mao, Huan Huan Sun, Ningsheng Liu, Jiangfang Lian
BACKGROUND: Long QT syndrome type 2 (LQT2) is the second most common type of all long QT syndromes. It is well-known that trafficking deficient mutant human ether-a-go-go-related gene (hERG) proteins are often involved in LQT2. Cells respond to misfolded and trafficking-deficient proteins by eliciting the unfolded protein response (UPR) and Activating Transcription Factor (ATF6) has been identified as a key regulator of the mammalian UPR. In this study, we investigated the role of ER chaperone proteins (Calnexin and Calreticulin) in the processing of G572R-hERG and E637K-hERG mutant proteins...
2012: PloS One
https://www.readbyqxmd.com/read/22016385/selenoprotein-k-binds-multiprotein-complexes-and-is-involved-in-the-regulation-of-endoplasmic-reticulum-homeostasis
#17
Valentina A Shchedrina, Robert A Everley, Yan Zhang, Steven P Gygi, Dolph L Hatfield, Vadim N Gladyshev
Selenoprotein K (SelK) is an 11-kDa endoplasmic reticulum (ER) protein of unknown function. Herein, we defined a new eukaryotic protein family that includes SelK, selenoprotein S (SelS), and distantly related proteins. Comparative genomics analyses indicate that this family is the most widespread eukaryotic selenoprotein family. A biochemical search for proteins that interact with SelK revealed ER-associated degradation (ERAD) components (p97 ATPase, Derlins, and SelS). In this complex, SelK showed higher affinity for Derlin-1, whereas SelS had higher affinity for Derlin-2, suggesting that these selenoproteins could determine the nature of the substrate translocated through the Derlin channel...
December 16, 2011: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/21646389/severity-of-diabetes-governs-vascular-lipoprotein-lipase-by-affecting-enzyme-dimerization-and-disassembly
#18
Ying Wang, Prasanth Puthanveetil, Fang Wang, Min Suk Kim, Ashraf Abrahani, Brian Rodrigues
OBJECTIVE: In diabetes, when glucose consumption is restricted, the heart adapts to use fatty acid (FA) exclusively. The majority of FA provided to the heart comes from the breakdown of circulating triglyceride (TG), a process catalyzed by lipoprotein lipase (LPL) located at the vascular lumen. The objective of the current study was to determine the mechanisms behind LPL processing and breakdown after moderate and severe diabetes. RESEARCH DESIGN AND METHODS: To induce acute hyperglycemia, diazoxide, a selective, ATP-sensitive K(+) channel opener was used...
August 2011: Diabetes
https://www.readbyqxmd.com/read/21490315/trafficking-deficient-herg-k%C3%A2-%C2%BA-channels-linked-to-long-qt-syndrome-are-regulated-by-a-microtubule-dependent-quality-control-compartment-in-the-er
#19
Jennifer L Smith, Christie M McBride, Parvathi S Nataraj, Daniel C Bartos, Craig T January, Brian P Delisle
The human ether-a-go-go related gene (hERG) encodes the voltage-gated K(+) channel that underlies the rapidly activating delayed-rectifier current in cardiac myocytes. hERG is synthesized in the endoplasmic reticulum (ER) as an "immature" N-linked glycoprotein and is terminally glycosylated in the Golgi apparatus. Most hERG missense mutations linked to long QT syndrome type 2 (LQT2) reduce the terminal glycosylation and functional expression. We tested the hypothesis that a distinct pre-Golgi compartment negatively regulates the trafficking of some LQT2 mutations to the Golgi apparatus...
July 2011: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/21329881/structural-basis-of-an-erad-pathway-mediated-by-the-er-resident-protein-disulfide-reductase-erdj5
#20
Masatoshi Hagiwara, Ken-Ichi Maegawa, Mamoru Suzuki, Ryo Ushioda, Kazutaka Araki, Yushi Matsumoto, Jun Hoseki, Kazuhiro Nagata, Kenji Inaba
ER-associated degradation (ERAD) is an ER quality-control process that eliminates terminally misfolded proteins. ERdj5 was recently discovered to be a key ER-resident PDI family member protein that accelerates ERAD by reducing incorrect disulfide bonds in misfolded glycoproteins recognized by EDEM1. We here solved the crystal structure of full-length ERdj5, thereby revealing that ERdj5 contains the N-terminal J domain and six tandem thioredoxin domains that can be divided into the N- and C-terminal clusters...
February 18, 2011: Molecular Cell
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