keyword
MENU ▼
Read by QxMD icon Read
search

MOG1

keyword
https://www.readbyqxmd.com/read/29141529/experimental-autoimmune-encephalomyelitis-eae-model-of-cynomolgus-macaques-induced-by-recombinant-human-mog1-125-rhmog1-125-protein-and-mog34-56-peptide
#1
Zhen Peng, Libiao Zhang, Huaqian Wang, Xiangyang He, Xingwen Peng, Qin Zhang, Hui Liu, Junhua Rao, Haifeng Wang, Jie Wu, Yunxiao Sun
BACKGROUND: Experimental autoimmune encephalomyelitis (EAE) induced by self-myelin antigen is a widely used in multiple sclerosis (MS) model for preclinical studies of new therapeutics and potential pathogenesis. By comparison with rodent EAE models, EAE models in primates are more similar to MS. Some groups have developed EAE models in primates by using common marmoset (Callithrix jacchus). However, this model has some limitations. EAE in cynomolgus monkey (Macaque fasciculrais) could overcome these limitations...
February 8, 2018: Protein and Peptide Letters
https://www.readbyqxmd.com/read/29040603/mitosis-specific-acetylation-tunes-ran-effector-binding-for-chromosome-segregation
#2
Xiaoling Bao, Heng Liu, Xing Liu, Ke Ruan, Yonghui Zhang, Zhiyong Zhang, Qi Hu, Ying Liu, Saima Akram, Jiahai Zhang, Qingguo Gong, Wenwen Wang, Xiao Yuan, Jian Li, Lingli Zhao, Zhen Dou, Ruijun Tian, Xuebiao Yao, Jihui Wu, Yunyu Shi
Stable transmission of genetic information during cell division requires faithful mitotic spindle assembly and chromosome segregation. The Ran GTPase plays a key role in mitotic spindle assembly. However, how the generation of a chemical gradient of Ran-GTP at the spindle is coupled to mitotic post-translational modifications has never been characterized. Here, we solved the complex structure of Ran with the nucleotide release factor Mog1 and delineated a novel mitosis-specific acetylation-regulated Ran-Mog1 interaction during chromosome segregation...
February 1, 2018: Journal of Molecular Cell Biology
https://www.readbyqxmd.com/read/28837624/rare-variants-in-genes-encoding-the-cardiac-sodium-channel-and-associated-compounds-and-their-impact-on-outcome-of-catheter-ablation-of-atrial-fibrillation
#3
Daniela Husser, Laura Ueberham, Gerhard Hindricks, Petra Büttner, Christie Ingram, Peter Weeke, M Benjamin Shoemaker, Volker Adams, Arash Arya, Philipp Sommer, Dawood Darbar, Dan M Roden, Andreas Bollmann
AIM: Rare variants of genes encoding the cardiac sodium channel and associated compounds have been linked with atrial fibrillation (AF). Nevertheless, current expert consensus does not support genetic testing in AF, which is in part based on the fact that "there is no therapeutic impact derived from AF genetic test results". However, there are no studies available supporting this recommendation. Consequently, this study analyzed the impact of rare variants affecting the cardiac sodium channel on rhythm outcome of AF catheter ablation...
2017: PloS One
https://www.readbyqxmd.com/read/28796037/functional-prediction-of-mir-3144-5p-in-human-cardiac-myocytes-based-on-transcriptome-sequencing-and-bioinformatics
#4
Lei Ruan, Yi Yang, Yi Huang, Ling Ding, Cuntai Zhang, Xiaofen Wu
BACKGROUND: RAN guanine nucleotide release factor (RANGRF) encoding protein MOG1 plays an important role in cardiac arrhythmia, so we intended to investigate the regulatory miRNA of RANGRF and explore its potential regulatory mechanism in arrhythmogenesis. METHODS: Based on bioinformatic analysis, miR-3144-5p was predicted to be a regulatory miRNA of RANGRF, which were then validated through a dual-luciferase reporter plasmid assay. Subsequently, the expression level of miR-3144-5p in human cardiac myocytes (HCMs) was detected, followed by cell transfection with miR-3144-5p mimics...
August 2017: Medicine (Baltimore)
https://www.readbyqxmd.com/read/26903377/cardiac-sodium-channel-regulator-mog1-regulates-cardiac-morphogenesis-and-rhythm
#5
Juan Zhou, Longfei Wang, Mengxia Zuo, Xiaojing Wang, Abu Shufian Ishtiaq Ahmed, Qiuyun Chen, Qing K Wang
MOG1 was initially identified as a protein that interacts with the small GTPase Ran involved in transport of macromolecules into and out of the nucleus. In addition, we have established that MOG1 interacts with the cardiac sodium channel Nav1.5 and regulates cell surface trafficking of Nav1.5. Here we used zebrafish as a model system to study the in vivo physiological role of MOG1. Knockdown of mog1 expression in zebrafish embryos significantly decreased the heart rate (HR). Consistently, the HR increases in embryos with over-expression of human MOG1...
February 23, 2016: Scientific Reports
https://www.readbyqxmd.com/read/26088203/systemic-escherichia-coli-infection-does-not-influence-clinical-symptoms-and-neurodegeneration-in-experimental-autoimmune-encephalomyelitis
#6
Prateek Kumar, Katharina Friebe, Rieka Schallhorn, Zahra Moinfar, Roland Nau, Mathias Bähr, Sandra Schütze, Katharina Hein
BACKGROUND: Systemic infections can influence the course of multiple sclerosis (MS), especially by driving recurrent acute episodes. The question whether the infection enhances tissue damage is of great clinical importance and cannot easily be assessed in clinical trials. Here, we investigated the effects of a systemic infection with Escherichia coli, a Gram-negative bacterium frequently causing urinary tract infections, on the clinical course as well as on neurodegeneration in experimental autoimmune encephalomyelitis (EAE), an animal model of MS...
2015: BMC Neuroscience
https://www.readbyqxmd.com/read/25744931/magnetization-transfer-ratio-does-not-correlate-to-myelin-content-in-the-brain-in-the-mog-eae-mouse-model
#7
Sveinung Fjær, Lars Bø, Kjell-Morten Myhr, Øivind Torkildsen, Stig Wergeland
Magnetization transfer ratio (MTR) is a magnetic resonance imaging (MRI) method which may detect demyelination not detected by conventional MRI in the central nervous system of patients with multiple sclerosis (MS). A decrease in MTR value has previously been shown to correlate to myelin loss in the mouse cuprizone model for demyelination. In this study, we investigated the sensitivity of MTR for demyelination in the myelin oligodendrocyte (MOG) 1-125 induced experimental autoimmune encephalomyelitis (EAE) mouse model...
April 2015: Neurochemistry International
https://www.readbyqxmd.com/read/25595255/b-cell-recognition-of-myelin-oligodendrocyte-glycoprotein-autoantigen-depends-on-immunization-with-protein-rather-than-short-peptide-while-b-cell-invasion-of-the-cns-in-autoimmunity-does-not
#8
Amy K Dang, Rajiv W Jain, Heather C Craig, Steven M Kerfoot
We develop a new fusion protein reagent (MOGtag), based on the extracellular domain of mouse myelin oligodendrocyte glycoprotein (MOG1-125), designed to induce autoimmune responses in mice that incorporates both T and B cell recognition of antigen. Reports of similar reagents, primarily based on foreign MOG proteins, rely largely on disease incidence and severity, with little analysis of the underlying immune response or pathology. We characterize the immune response and central nervous system autoimmune disease elicited by MOGtag in mice and find that it results in the formation of a T cell-dependent germinal center B cell response...
January 15, 2015: Journal of Neuroimmunology
https://www.readbyqxmd.com/read/24529773/is-sudden-unexplained-nocturnal-death-syndrome-in-southern-china-a-cardiac-sodium-channel-dysfunction-disorder
#9
Chao Liu, David J Tester, Yiding Hou, Wen Wang, Guoli Lv, Michael J Ackerman, Jonathan C Makielski, Jianding Cheng
Sudden unexplained nocturnal death syndrome (SUNDS) remains an enigma to both forensic pathologists and physicians. Previous epidemiological, clinical, and pilot genetic studies have implicated that SUNDS is most likely a disease allelic to Brugada syndrome (BrS). We have performed postmortem genetic testing to address the spectrum and role of genetic abnormalities in the SCN5A-encoded cardiac sodium channel and its several associated proteins in SUNDS victims from Southern China. Genomic DNA extracted from the blood samples of 123 medico-legal autopsy-negative SUNDS cases and 104 sex-, age- and ethnic-matched controls from Southern China underwent comprehensive amino acid coding region mutational analysis for the BrS associated genes SCN5A, SCN1B, SCN2B, SCN3B, SCN4B, MOG1, and GPD1-L using PCR and direct sequencing...
March 2014: Forensic Science International
https://www.readbyqxmd.com/read/24352520/missense-mutations-in-plakophilin-2-cause-sodium-current-deficit-and-associate-with-a-brugada-syndrome-phenotype
#10
Marina Cerrone, Xianming Lin, Mingliang Zhang, Esperanza Agullo-Pascual, Anna Pfenniger, Halina Chkourko Gusky, Valeria Novelli, Changsung Kim, Tiara Tirasawadichai, Daniel P Judge, Eli Rothenberg, Huei-Sheng Vincent Chen, Carlo Napolitano, Silvia G Priori, Mario Delmar
BACKGROUND: Brugada syndrome (BrS) primarily associates with the loss of sodium channel function. Previous studies showed features consistent with sodium current (INa) deficit in patients carrying desmosomal mutations, diagnosed with arrhythmogenic cardiomyopathy (or arrhythmogenic right ventricular cardiomyopathy). Experimental models showed correlation between the loss of expression of desmosomal protein plakophilin-2 (PKP2) and reduced INa. We hypothesized that PKP2 variants that reduce INa could yield a BrS phenotype, even without overt structural features characteristic of arrhythmogenic right ventricular cardiomyopathy...
March 11, 2014: Circulation
https://www.readbyqxmd.com/read/24142675/brugada-syndrome-and-p-e61x_rangrf
#11
Oscar Campuzano, Paola Berne, Elisabeth Selga, Catarina Allegue, Anna Iglesias, Josep Brugada, Ramon Brugada
BACKGROUND: Brugada syndrome is an inherited cardiac condition transmitted with an autosomal dominant pattern which can lead to sudden cardiac death from malignant ventricular arrhythmias. The RANGRF gene has recently been proposed to be associated with Brugada syndrome. This gene encodes the MOG1 protein, a co-factor required for the full functioning of the cardiac sodium channel Nav1.5. The nonsense p.E61X genetic variation in the RANGRF gene has been postulated as responsible for Brugada syndrome although no clear association has been established...
2014: Cardiology Journal
https://www.readbyqxmd.com/read/23740901/antigen-specific-tolerance-by-autologous-myelin-peptide-coupled-cells-a-phase-1-trial-in-multiple-sclerosis
#12
Andreas Lutterotti, Sara Yousef, Andreas Sputtek, Klarissa H Stürner, Jan-Patrick Stellmann, Petra Breiden, Stefanie Reinhardt, Christian Schulze, Maxim Bester, Christoph Heesen, Sven Schippling, Stephen D Miller, Mireia Sospedra, Roland Martin
Multiple sclerosis (MS) is a devastating inflammatory disease of the brain and spinal cord that is thought to result from an autoimmune attack directed against antigens in the central nervous system. The aim of this first-in-man trial was to assess the feasibility, safety, and tolerability of a tolerization regimen in MS patients that uses a single infusion of autologous peripheral blood mononuclear cells chemically coupled with seven myelin peptides (MOG1-20, MOG35-55, MBP13-32, MBP83-99, MBP111-129, MBP146-170, and PLP139-154)...
June 5, 2013: Science Translational Medicine
https://www.readbyqxmd.com/read/23420830/mog1-rescues-defective-trafficking-of-na-v-1-5-mutations-in-brugada-syndrome-and-sick-sinus-syndrome
#13
COMPARATIVE STUDY
Susmita Chakrabarti, Xiaofen Wu, Zhaogang Yang, Ling Wu, Sandro L Yong, Cuntai Zhang, Keli Hu, Qing K Wang, Qiuyun Chen
BACKGROUND: Loss-of-function mutations in Na(v)1.5 cause sodium channelopathies, including Brugada syndrome, dilated cardiomyopathy, and sick sinus syndrome; however, no effective therapy exists. MOG1 increases plasma membrane (PM) expression of Na(v)1.5 and sodium current (I(Na)) density, thus we hypothesize that MOG1 can serve as a therapeutic target for sodium channelopathies. METHODS AND RESULTS: Knockdown of MOG1 expression using small interfering RNAs reduced Na(v)1...
April 2013: Circulation. Arrhythmia and Electrophysiology
https://www.readbyqxmd.com/read/23293604/brugada-ecg-pattern-a-physiopathological-prospective-study-based-on-clinical-electrophysiological-angiographic-and-genetic-findings
#14
Guillaume Duthoit, Véronique Fressart, Françoise Hidden-Lucet, Françoise Simon, Darouna Kattygnarath, Philippe Charron, Caroline Himbert, Philip Aouate, Pascale Guicheney, Yves Lecarpentier, Robert Frank, Jean-Louis Hébert
INTRODUCTION: Brugada syndrome (BrS) is considered a primary electrical disease. However, morphological abnormalities have been reported and localized arrhythmogenic right ventricular (RV) dysplasia/cardiomyopathy (ARVD/C) may mimic its phenotype, raising the question of an overlap between these two conditions and making difficult the therapeutic management of patients with borderline forms. The main objective of this study was to assess prospectively the prevalence of BrS and ARVD/C on the basis of international criteria, in patients with BrS-ECG and normal echocardiography, looking for a potential overlap between the two pathologies...
2012: Frontiers in Physiology
https://www.readbyqxmd.com/read/23167594/critical-role-of-activation-induced-cytidine-deaminase-in-experimental-autoimmune-encephalomyelitis
#15
Yonglian Sun, Ivan Peng, Kate Senger, Kajal Hamidzadeh, Mike Reichelt, Miriam Baca, Ronald Yeh, Maria N Lorenzo, Andrew Sebrell, Christopher Dela Cruz, Lucinda Tam, Racquel Corpuz, Jiansheng Wu, Tao Sai, Merone Roose-Girma, Søren Warming, Mercedesz Balazs, Lino C Gonzalez, Patrick Caplazi, Flavius Martin, Jason Devoss, Ali A Zarrin
Multiple Sclerosis (MS) is a neurodegenerative autoimmune disorder caused by chronic inflammation and demyelination within the central nervous system (CNS). Clinical studies in MS patients have demonstrated efficacy with B cell targeted therapies such as anti-CD20. However, the exact role that B cells play in the disease process is unclear. Activation Induced cytidine deaminase (AID) is an essential enzyme for the processes of antibody affinity maturation and isotype switching. To evaluate the impact of affinity maturation and isotype switching, we have interrogated the effect of AID-deficiency in an animal model of MS...
March 2013: Autoimmunity
https://www.readbyqxmd.com/read/22284586/sodium-current-and-potassium-transient-outward-current-genes-in-brugada-syndrome-screening-and-bioinformatics
#16
Anders G Holst, Siamak Saber, Massoud Houshmand, Elena V Zaklyazminskaya, Yinman Wang, Henrik Kjærulf Jensen, Lena Refsgaard, Stig Haunsø, Jesper Hastrup Svendsen, Morten S Olesen, Jacob Tfelt-Hansen
BACKGROUND: Brugada syndrome (BrS) is a primary arrhythmia syndrome characterized by the occurrence of malignant ventricular arrhythmias. Previously, the genes SCN1B, SCN3B, MOG1, and KCND3 have been associated with BrS. Recent data from exome screening efforts permit better discrimination between low-frequency genetic variants and true monogenetic disease-causing variants. We aimed to screen the genes SCN1B through SCN4B, MOG1, CAV3, and KCND3 for variations in a population of SCN5A negative Danish and Iranian BrS patients, as well as research prior associations using newly released exome data...
March 2012: Canadian Journal of Cardiology
https://www.readbyqxmd.com/read/22157536/relationship-between-nmo-antibody-and-anti-mog-antibody-in-optic-neuritis
#17
COMPARATIVE STUDY
Takeshi Kezuka, Yoshihiko Usui, Naoyuki Yamakawa, Yoshimichi Matsunaga, Ryusaku Matsuda, Masayuki Masuda, Hiroya Utsumi, Keiko Tanaka, Hiroshi Goto
BACKGROUND: Damage to astrocytes by anti-aquaporin-4 antibody (AQP4-Ab), also known as NMO antibody, has been implicated as the cause of neuromyelitis optica. Myelin oligodendrocyte glycoprotein (MOG) is well known as the causative protein of multiple sclerosis (MS). MOG antigen is currently considered as a cause of optic neuritis (ON) associated with MS because immunization with MOG antigen derived from oligodendrocytes induces murine ON with myelitis. We investigated the relationship between NMO antibody (NMO-Ab) and anti-MOG antibody (MOG-Ab) and potential in patients with ON for recovery of vision...
June 2012: Journal of Neuro-ophthalmology: the Official Journal of the North American Neuro-Ophthalmology Society
https://www.readbyqxmd.com/read/21621375/a-novel-nonsense-variant-in-nav1-5-cofactor-mog1-eliminates-its-sodium-current-increasing-effect-and-may-increase-the-risk-of-arrhythmias
#18
Morten S Olesen, Niels F Jensen, Anders G Holst, Jonas B Nielsen, Jacob Tfelt-Hansen, Thomas Jespersen, Ahmad Sajadieh, Stig Haunsø, Jens T Lund, Kirstine Calloe, Nicole Schmitt, Jesper Hastrup Svendsen
BACKGROUND: The protein MOG1 is a cofactor of the cardiac sodium channel, Nav1.5. Overexpression of MOG1 in Nav1.5-expressing cells increases sodium current markedly. Mutations in the genes encoding Nav1.5 and its accessory proteins have been associated with cardiac arrhythmias of significant clinical impact. We sought to investigate whether MOG1 is implicated in cardiac arrhythmias. METHODS: We performed a genetic screening of the MOG1-encoding gene (gene symbol RANGRF, alias MOG1) in 220 Danish patients with cardiac arrhythmia...
July 2011: Canadian Journal of Cardiology
https://www.readbyqxmd.com/read/21447824/mog1-a-new-susceptibility-gene-for-brugada-syndrome
#19
Darouna Kattygnarath, Svetlana Maugenre, Nathalie Neyroud, Elise Balse, Carole Ichai, Isabelle Denjoy, Gilles Dilanian, Raphaël P Martins, Véronique Fressart, Myriam Berthet, Jean Jacques Schott, Antoine Leenhardt, Vincent Probst, Hervé Le Marec, Bernard Hainque, Alain Coulombe, Stéphane N Hatem, Pascale Guicheney
BACKGROUND: Brugada syndrome (BrS) is caused mainly by mutations in the SCN5A gene, which encodes the α-subunit of the cardiac sodium channel Na(v)1.5. However, ≈ 20% of probands have SCN5A mutations, suggesting the implication of other genes. MOG1 recently was described as a new partner of Na(v)1.5, playing a potential role in the regulation of its expression and trafficking. We investigated whether mutations in MOG1 could cause BrS. METHODS AND RESULTS: MOG1 was screened by direct sequencing in patients with BrS and idiopathic ventricular fibrillation...
June 2011: Circulation. Cardiovascular Genetics
https://www.readbyqxmd.com/read/18184654/identification-of-a-new-co-factor-mog1-required-for-the-full-function-of-cardiac-sodium-channel-nav-1-5
#20
Ling Wu, Sandro L Yong, Chun Fan, Ying Ni, Shin Yoo, Teng Zhang, Xianqin Zhang, Carlos A Obejero-Paz, Hyun-Jin Rho, Tie Ke, Przemyslaw Szafranski, Stephen W Jones, Qiuyun Chen, Qing Kenneth Wang
The cardiac sodium channel Nav 1.5 is essential for the physiological function of the heart and contributes to lethal cardiac arrhythmias and sudden death when mutated. Here, we report that MOG1, a small protein that is highly conserved from yeast to humans, is a central component of the channel complex and modulates the physiological function of Nav 1.5. The yeast two-hybrid screen identified MOG1 as a new protein that interacts with the cytoplasmic loop II (between transmembrane domains DII and DIII) of Nav 1...
March 14, 2008: Journal of Biological Chemistry
keyword
keyword
165259
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"