Myelin oligodendrocyte glycoprotein (MOG), a member of the immunoglobulin (Ig) superfamily, is myelin protein expressed at outermost lamellae sheaths and oligodendrocytes (OGD) memb...

basic research on the autoimmune disease multiple sclerosis has been performed mainly on its animal model namely experimental allergic encephalomyelitis. there are many different approaches established to get this model. despite the existence of many references in literature in this regard, we have been faced with many difficulties generating the model suitable for studying different therapies....

Myelin oligodendrocyte glycoprotein antibody associated disease (MOGAD) is an inflammatory demyelinating disorder caused by the development of immunoglobulin G autoantibody targeting MOG, which expressed exclusively on outer surface myelin sheath and plasma membrane oligodendrocyte. MOGAD can present in different clinical spectrum including acute disseminated encephalomyelitis (ADEM), optic neu...

Myelin-Oligodendrocyte Glycoprotein (MOG) is an adhesive molecule responsible for myelin sheath structural integrity and maintenance. Patients with spectrum of inflammatory demyelinating disease particularly in central nervous system are reported to have antibodies against this protein. Diseases such as multiple sclerosis, clinically isolated syndrome, neuro-myelitis optica (NMO) spectrum disor...

The oligodendrocyte-myelin glycoprotein is a ligand of the neuronal Nogo receptor and a potent inhibitor of neurite outgrowth, but its physiological function remains to be elucidated. The oligodendrocyte-myelin glycoprotein is anchored solely in the outer leaflet of the plasma membrane via its glycosylphosphatidylinositol anchor, and through its leucine-rich repeat domain, it likely interacts w...

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an increasingly recognized disorder, particularly in children. Acute disseminated encephalomyelitis (ADEM) the most common presentation of paediatric MOGAD. Children with ADEM should always be evaluated for MOGAD, as appropriate and timely treatment may help improve long-term outcomes.

A pair of photomicrographs showing the multiple sclerosis histological immunopathology pattern I. The image on left is stained for myelin oligodendrocyte glycoprotein (MOG) and shows demyelination side lesion. right an adjacent section through same plaque, with KiM1P antibody macrophages microglia, demonstrating infiltration into demyelinated area. See paper by Metz colleagues (pp. 440–454) in ...

Prior studies support a role for mammalian target of rapamycin (mTOR) signaling in oligodendrocyte differentiation and myelination. Here we use Cre-recombinase driven by the CNP promoter to generate a mouse line with oligodendrocyte-specific knockdown of mTOR (mTOR cKO) in the CNS. We provide evidence that mTOR is necessary for proper oligodendrocyte differentiation and myelination in the spina...

Although myelin oligodendrocyte glycoprotein is a candidate autoantigen in multiple sclerosis, its function remains unknown. In humans, mRNA expressed by the myelin oligodendrocyte glycoprotein gene is alternatively spliced resulting in at least nine unique protein isoforms. In this study, we investigated the sub-cellular localisation and membrane trafficking of six isoforms by cloning them int...

Growth inhibition in the central nervous system (CNS) is a major barrier to axon regeneration. Recent findings indicate that three distinct myelin proteins, myelin-associated glycoprotein (MAG), Nogo, and oligodendrocyte-myelin glycoprotein (OMgp), inhibit axon growth by binding a common receptor, the Nogo66 receptor (NgR), and likely converge on a common signaling cascade.