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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

MOG1 Mog1p

MOG1, Mog1p
This gene encodes a protein that has been shown to function as a guanine nucleotide release factor in mouse and to regulate the expression and function of the Nav1.5 cardiac sodium channel in human. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Apr 2010] (from NCBI)
Top mentioned proteins: MOG, SCN5A, RAN, CAN, CD45
Papers on MOG1
Magnetization transfer ratio does not correlate to myelin content in the brain in the MOG-EAE mouse model.
Wergeland et al., Bergen, Norway. In Neurochem Int, Apr 2015
This suggest that MTR measures of brain tissue can give significant differences between control mice and EAE mice not caused by demyelination, inflammation or iron deposition, and may not be useful surrogate markers for demyelination in the MOG1-125 mouse model.
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.
Kerfoot et al., London, Canada. In J Neuroimmunol, Feb 2015
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.
Systemic Escherichia coli infection does not influence clinical symptoms and neurodegeneration in experimental autoimmune encephalomyelitis.
Hein et al., Göttingen, Germany. In Bmc Neurosci, 2014
METHODS: Rats were immunized with myelin oligodendrocyte glycoprotein (MOG1-125) and challenged intraperitoneally with live E. coli K1 in the preclinical or in the clinical phase of the disease.
Multifunctional white-light-emitting metal-organic gels with a sensing ability of nitrobenzene.
Biradha et al., Kharagpur, India. In Acs Appl Mater Interfaces, 2014
The gels MOG-1 and MOG-2 were found to exhibit significant white photoluminescence, whereas the MOG-3 exhbits green emission upon excitation at 325 nm.
Missense mutations in plakophilin-2 cause sodium current deficit and associate with a Brugada syndrome phenotype.
Delmar et al., Pavia, Italy. In Circulation, 2014
METHODS AND RESULTS: We searched for PKP2 variants in the genomic DNA of 200 patients with a BrS diagnosis, no signs of arrhythmogenic cardiomyopathy, and no mutations in BrS-related genes SCN5A, CACNa1c, GPD1L, and MOG1.
Is sudden unexplained nocturnal death syndrome in Southern China a cardiac sodium channel dysfunction disorder?
Cheng et al., Guangzhou, China. In Forensic Sci Int, 2014
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.
Brugada syndrome and p.E61X_RANGRF.
Brugada et al., Girona, Spain. In Cardiol J, 2013
The RANGRF gene has recently been proposed to be associated with Brugada syndrome.
Antigen-specific tolerance by autologous myelin peptide-coupled cells: a phase 1 trial in multiple sclerosis.
Martin et al., Hamburg, Germany. In Sci Transl Med, 2013
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).
MOG1 rescues defective trafficking of Na(v)1.5 mutations in Brugada syndrome and sick sinus syndrome.
Chen et al., Cleveland, United States. In Circ Arrhythm Electrophysiol, 2013
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.
Critical role of activation induced cytidine deaminase in experimental autoimmune encephalomyelitis.
Zarrin et al., San Francisco, United States. In Autoimmunity, 2013
Here, we show that the severity of experimental autoimmune encephalomyelitis (EAE) induced by the extracellular domain of human myelin oligodendrocyte glycoprotein (MOG1-125) is significantly reduced in Aicda deficient mice, which, unlike wild-type mice, lack serum IgG to myelin associated antigens.
Relationship between NMO-antibody and anti-MOG antibody in optic neuritis.
Goto et al., Tokyo, Japan. In J Neuroophthalmol, 2012
At presentation, serum NMO-Ab was measured by immunofluorescence using HEK 293 cells transfected with AQP4-GFP, and anti-MOG1-125 antibody was measured by enzyme-linked immunosorbent assay.
Sodium current and potassium transient outward current genes in Brugada syndrome: screening and bioinformatics.
Tfelt-Hansen et al., Copenhagen, Denmark. In Can J Cardiol, 2012
Previously, the genes SCN1B, SCN3B, MOG1, and KCND3 have been associated with BrS.
Brugada ECG pattern: a physiopathological prospective study based on clinical, electrophysiological, angiographic, and genetic findings.
Hébert et al., Paris, France. In Front Physiol, 2011
MOG1 gene analysis was negative for all patients, as were PKP2, DSP, DSG2, and DSC2 analyzes performed in BrS group III.
A novel nonsense variant in Nav1.5 cofactor MOG1 eliminates its sodium current increasing effect and may increase the risk of arrhythmias.
Svendsen et al., Copenhagen, Denmark. In Can J Cardiol, 2011
Our screening of Nav1.5 cofactor MOG1 uncovered a novel nonsense variant that appeared to be present at a higher frequency among these patients with atrial fibrillation and Brugada syndrome than control subjects.
MOG1: a new susceptibility gene for Brugada syndrome.
Guicheney et al., Paris, France. In Circ Cardiovasc Genet, 2011
Results suggest that dominant-negative mutations in MOG1 can impair the trafficking of Na(v)1.5 to the membrane, leading to I(Na) reduction and clinical manifestation of Brugada syndrome.
Identification of a new co-factor, MOG1, required for the full function of cardiac sodium channel Nav 1.5.
Wang et al., Cleveland, United States. In J Biol Chem, 2008
in cardiomyocytes, MOG1 is mostly localized in the cell membrane and co-localized with Nav1.5, indicating that MOG1 is a critical regulator of sodium channel function in the heart
Role for the Ran binding protein, Mog1p, in Saccharomyces cerevisiae SLN1-SKN7 signal transduction.
Fassler et al., Iowa City, United States. In Eukaryot Cell, 2004
Mog1p may play a role in SLN1-SKN7 signal transduction, Skn7 binding and activation of osmotic response genes
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