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The product of MOG is a membrane protein expressed on the oligodendrocyte cell surface and the outermost surface of myelin sheaths. Additionally we are shipping MOG Kits (35) and MOG Proteins (34) and many more products for this protein.
Showing 10 out of 120 products:
Human Monoclonal MOG Primary Antibody for ELISA - ABIN1996577
Hilton, Slavin, Hilton, Bernard: Characterization of cDNA and genomic clones encoding human myelin oligodendrocyte glycoprotein. in Journal of neurochemistry 1995
Show all 2 references for 1996577
Human Polyclonal MOG Primary Antibody for ELISA - ABIN1996579
Johns, Bernard: The structure and function of myelin oligodendrocyte glycoprotein. in Journal of neurochemistry 1999
Show all 2 references for 1996579
Rat (Rattus) Polyclonal MOG Primary Antibody for WB - ABIN1574230
Francosalinas, Cantaert, Nolte, Tak, van Lier, Baeten: Enhanced costimulation by CD70+ B cells aggravates experimental autoimmune encephalomyelitis in autoimmune mice. in Journal of neuroimmunology 2013
Human Polyclonal MOG Primary Antibody for ELISA, WB - ABIN185363
Zai, King, Wigg, Couto, Wong, Honer, Barr, Kennedy: Genetic study of the myelin oligodendrocyte glycoprotein (MOG) gene in schizophrenia. in Genes, brain, and behavior 2005
Identify nerve growth factor as a binding partner for MOG and demonstrate that this interaction is capable of sequestering NGF (show NGFB Antibodies) from TrkA (show NTRK1 Antibodies)-expressing neurons to modulate axon growth and survival.
Data indicate that in mixed chimeras with bone marrow-encoding myelin oligodendrocyte glycoprotein (MOG), the development of MOG-specific B cells was abrogated, resulting in a lack of MOG-specific B cells in all B cell compartments examined.
Identify immunogenic/encephalitogenic T-cell epitopes within MOG capable of inducing experimental autoimmune encephalomyelitis in C57BL/6 mice.
PLP (show C3 Antibodies) significantly suppresses both models of experimental autoimmune encephalitis (EAE)even when there is some evidence of epitope spreading in the myelin oligodendrocyte (MOG)38-50-induced EAE model.
CNTF (show CNTF Antibodies) may play a role in the process of remyelination by inducing the MOG expression.
MOG-specific CD4 (show CD4 Antibodies)-positive T cells accumulate within the chemokine (show CCL1 Antibodies)-expressing draining lymph nodes, rather than within the brain or spinal cord during induction of autoimmune encephalomyelitis.
This study provides valuable information about requirements of anti-myelin oligodendrocyte glycoprotein reactivity for being regarded as a prognostic biomarker in a subtype of MS.
Mice immunized with encephalitogenic myelin oligodendrocyte glycoprotein MOG(35-55) peptide develop significant serum levels of anti-MOG antibodies in parallel with disease progression.
B cell-deficient mice exhibit reduced medullary thymic epithelial cell numbers and reduced MOG mRNA expression.
Cell surface targeting of MOG is not disrupted in the absence of the endoplasmic reticulum chaperones.
Retinal nerve fiber layer may be better preserved in MOG-IgG versus AQP4 (show AQP4 Antibodies)-IgG optic neuritis.
Data show that aquaporin-4 (AQP4 (show AQP4 Antibodies)) and myelin-oligodendrocyte glycoprotein (MOG) autoantibodies double positive neuromyelitis optica spectrum disorder (NMOSD) patients had a multiphase disease course with a high annual relapse rate.
MOG antibody associated optic neuritis tends to involve the anterior optic pathway.
This study demonstrated that increased expression of mRNA of OLIG1 (show OLIG1 Antibodies) in ventral prefrontal white matter in major depressive disorder.
In patients with idiopathic optic neuritis, 27.6% (8/29) were positive for MOG antibodies. Three of the eight MOG-positive patients showed significantly high CSF (show CSF2 Antibodies) levels of myelin basic protein (show MBP Antibodies). Five had optic pain and three had prodromal infection.
Immune modulation by a tolerogenic myelin oligodendrocyte glycoprotein (MOG)10-60 containing fusion protein in the marmoset experimental autoimmune encephalomyelitis model.
These data demonstrate a new role for myelin glycosylation in the control of immune homeostasis in the healthy human brain through the MOG-DC-SIGN (show CD209 Antibodies) homeostatic regulatory axis, which is comprised by inflammatory insults that affect glycosylation.
findings suggest that immune reactions toward MOG and in particular MOG-specific antibodies may play a functional role in multiple sclerosis
Patients with neuromyelitis optica spectrum disorders with MOG antibodies have distinct clinical features, fewer attacks, and better recovery than patients with AQP4 (show AQP4 Antibodies) antibodies or patients seronegative for both antibodies.
Bipolar I disorder and schizophrenia share a number of common genetic risk loci and susceptibility genes including the genes coding for myelin oligodendrocytes glycoprotein (MOG).
The product of this gene is a membrane protein expressed on the oligodendrocyte cell surface and the outermost surface of myelin sheaths. Due to this localization, it is a primary target antigen involved in immune-mediated demyelination. This protein may be involved in completion and maintenance of the myelin sheath and in cell-cell communication. Alternatively spliced transcript variants encoding different isoforms have been identified.
myelin oligodendrocyte glycoprotein
, Myelin-oligodendrocyte glycoprotein
, myelin-oligodendrocyte glycoprotein-like
, MOG alpha-7Cj
, myelin-oligodendrocyte glycoprotein
, MOG Ig-AluB
, MOG alpha-5
, dystonia 2, torsion (autosomal recessive)
, myelin-oligodendrocyte glycoprotein isoform beta1