Myelin oligodendrocyte glycoprotein

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Available structures
PDBOrtholog search: PDBe RCSB
AliasesMOG, BTN6, BTNL11, MOGIG2, NRCLP7, myelin oligodendrocyte glycoprotein
External IDsOMIM: 159465 MGI: 97435 HomoloGene: 111009 GeneCards: MOG
Gene location (Human)
Chromosome 6 (human)
Chr.Chromosome 6 (human)[1]
Chromosome 6 (human)
Genomic location for MOG
Genomic location for MOG
Band6p22.1Start29,657,002 bp[1]
End29,672,372 bp[1]
RefSeq (mRNA)


RefSeq (protein)


Location (UCSC)Chr 6: 29.66 – 29.67 MbChr 17: 37.01 – 37.02 Mb
PubMed search[3][4]
View/Edit HumanView/Edit Mouse

Myelin oligodendrocyte glycoprotein (MOG) is a glycoprotein believed to be important in the myelination of nerves in the central nervous system (CNS). In humans this protein is encoded by the MOG gene,[5][6][7] it is speculated to serve as a necessary "adhesion molecule" to provide structural integrity to the myelin sheath and is known to develop late on the oligodendrocyte.[8]

Molecular function[edit]

While the primary molecular function of MOG is not yet known, its likely role with the myelin sheath is either in sheath "completion and/or maintenance".[7] More specifically, MOG is speculated to be "necessary" as an "adhesion molecule" on the myelin sheath of the CNS to provide the structural integrity of the myelin sheath.[8]"

MOG's cDNA coding region in humans have been shown to be "highly homologous"[9] to rats, mice, and bovine, and hence highly conserved; this suggests "an important biological role for this protein".[7]


The gene for MOG, found on chromosome 6 p21.3-p22,[10] was first sequenced in 1995.[3] It is a transmembrane protein expressed on the surface of oligodendrocyte cell and on the outermost surface of myelin sheaths. "MOG is a quantitatively minor type I transmembrane protein,[11] and is found exclusively in the CNS. "A single Ig-domain is exposed to the extracellular space"[11] and consequently allows autoantibodies easy access. and therefore easily accessible for autoantibodies.[7][11] The MOG "primary nuclear transcript … is 15,561 nucleotides in length"[7] and, for humans, it has eight exons which are "separated by seven introns";[7] the introns "contain numerous reptitive [sic] DNA[7]" sequences, among which is "14 Alu sequences within 3 introns",[7] and have a range varying from 242 to 6484 bp.


Because of alternatively spliced from human mRNA of MOG gene forming at least nine isoforms.[12]

The crystal structure of myelin oligodendrocyte glycoprotein was determined by x-ray diffraction at a resolution of 1.45 Angstrom, using protein from the Norway rat. This protein is 139 residues long, and is a member of the immunoglobulin superfamily;[13] the dssp secondary structure of the protein is 6% helical and 43% beta sheet: there are three short helical segments and ten beta strands.[14] The beta strands are within two antiparallel beta sheets that form an immunoglobulin-like beta-sandwich fold.[15] Several features of the protein structure suggest MOG has a role as an "adhesin in the completion and/or compaction of the myelin sheath." There is a "significant strip" of electronegative charge beginning near the N-terminus and running about half the length of the molecule. Also, MOG was shown to dimerize in solution, and the shape complementarity index is high at the dimer interface, suggesting a "biologically relevant MOG dimer."[16]


Developmentally, MOG is formed "very late on oligodendrocytes and the myelin sheath".[8]

Role in disease[edit]

Non-inflammatory demyelinating diseases[edit]

Interest in MOG has centered on its role in demyelinating diseases; some of them are not-inflammatory, such as adrenoleukodystrophy, vanishing white matter disease, and Rubella induced mental retardation.[17]

Anti-MOG associated inflammatory demyelinating diseases[edit]

MOG has received much of its laboratory attention in studies dealing with MS. Several studies have shown a role for antibodies against MOG in the pathogenesis of MS,[8][18] though most of them were written before the discovery of NMO-IgG and the NMO spectrum of diseases.

Anti-MOG status is different depending whether it is measured by ELISA or by microarray (CBA); the proper way to identify it is by microarray, reacting patient serum with living cells, and detecting the binding IgG via a fluorescent-labeled secondary antibody.[19]

In animal models[edit]

Animal models of MS, EAE, have shown that "MOG-specific EAE models (of different animal strains) display/mirror human multiple sclerosis",[8] but basically explains the part involved in the optic neuritis[20] These models with anti-MOG antibodies have been investigated extensively and are considered the only antibodies with demyelinating capacity[8] but again, EAE pathology is closer to NMO and ADEM than to the confluent demyelination observed in MS.

Anti-MOG mediated demyelination was shown to behave similar to NMO in animal models,[20] and currently it is considered even a biomarker against the MS diagnosis[21][22]

In seronegative neuromyelitis optica[edit]

Anti-MOG autoimmunity has been found to be involved in the seronegative NMO[23][24] and also in optic neuritis and some fulminant forms of ADEM[25] MOG antibodies in NMOSD are variable depending on the seropositivity status[26]

In other conditions[edit]

The presence of anti-MOG autoantibodies has been associated with the following conditions[27]


  1. ^ a b c ENSG00000232641, ENSG00000137345, ENSG00000230885, ENSG00000236561, ENSG00000237834, ENSG00000204655, ENSG00000234623 GRCh38: Ensembl release 89: ENSG00000234096, ENSG00000232641, ENSG00000137345, ENSG00000230885, ENSG00000236561, ENSG00000237834, ENSG00000204655, ENSG00000234623 - Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000076439 - Ensembl, May 2017
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  19. ^ Ichiro Nakashima, Anti-myelin oligodendrocyte glycoprotein antibody in demyelinating diseases [1]
  20. ^ a b Kezuka T, Usui Y, Yamakawa N, Matsunaga Y, Matsuda R, Masuda M, Utsumi H, Tanaka K, Goto H (June 2012). "Relationship between NMO-antibody and anti-MOG antibody in optic neuritis". Journal of Neuro-Ophthalmology. 32 (2): 107–10. doi:10.1097/WNO.0b013e31823c9b6c. PMID 22157536.
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  28. ^ Spadaro M, Gerdes LA, Mayer MC, Ertl-Wagner B, Laurent S, Krumbholz M, Breithaupt C, Högen T, Straube A, Giese A, Hohlfeld R, Lassmann H, Meinl E, Kümpfel T (March 2015). "Histopathology and clinical course of MOG-antibody-associated encephalomyelitis". Annals of Clinical and Translational Neurology. 2 (3): 295–301. doi:10.1002/acn3.164. PMC 4369279. PMID 25815356.
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External links[edit]