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Nogo rojo 78 MG is a molecule with an affinity for reticulon 4 receptors, also known as the nogo receptor. In addition to binding to reticulon 4 receptors, MAG also interacts with brain gangliosides, which transduces an inhibitory signal. The co-receptor, NGFR, also binds MAG. The best affinity for MAG is found in GQ1ba, while a fourfold increase is achieved in binding affinity by replacing inner sialic acid with a sulphate.
A series of compounds with low affinities for MAG have been synthesized. The compound seven has been a lead structure for antagonist development because it exhibits excellent correlation with neurite outgrowth. After compound 10, Neu5Ac derivatives were synthesized, each showing a nanomolar affinity. In addition, the affinity data were obtained using different assays. The result is an inhibitory molecule that inhibits the neurotransmitter receptor.
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reticulon 4 receptor
Nogo is a component of myelin in the central nervous system. It inhibits axon outgrowth in adult vertebrate neurons. The nogo receptor encodes a 473 amino acid protein, NogoA. It has been shown that NogoA binds to the cytosolic face of cellular membranes and may contribute to the inhibition of axon regeneration in sites of oligodendrocyte injury.
In adult brains, the ability to regenerate axons is limited. Although neurite outgrowth is possible in principle, this process is inhibited by inhibitor proteins found on residual myelin and astrocytes. There are three major inhibitor proteins known. The inhibitor proteins are reticulon 4, nogo A, and myelin oligodendrocyte glycoprotein (MOG).
Myelin oligodendrocyte glycoprotein (MOG)
The biological function of MOG remains uncertain, but its unique surface topology makes it a potential target for immune responses. The molecular mechanisms that result in the autoimmune attack on MOG are poorly understood, but researchers have discovered that the protein can bind to and stimulate the production of autoantibodies. The molecular pathology of MOG disease is based on the fact that it is a target for both T and B cells, and its immunological properties may contribute to its occurrence in multiple sclerosis.
The incidence of MOG nogo rojo 78 is unknown, but it affects both infants and adults. Males are equally affected, as are women, and most are Caucasian. The clinical presentation of MOGAD is similar to that of neuromyelitis spectrum disorder (NMSD). Associated optic neuritis may be unilateral or bilateral.
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