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Description |
Axon regeneration is arrested in the injured CNS (Central Nervous System) by
axon growth-inhibitory ligands expressed in oligodendrocytes/myelin and reactive
astrocytes in the lesion and by fibroblasts in scar tissue. Growth cone
receptors bind inhibitory ligands, activating a Rho-family GTPase intracellular
signaling pathway that disrupts the actin cytoskeleton inducing growth cone
collapse/repulsion. The known inhibitory ligands include Eph (Ephrins) expressed
on astrocyte/fibroblast membranes; the myelin/oligodendrocyte-derived growth
inhibitors Nogo, MAG
(Myelin-Associated Glycoprotein), and OMGP
(Oligodendrocyte Myelin Glycoprotein); and
membrane-bound Sema (Semaphorins) produced by meningeal fibroblasts invading the
scar (Ref.1).
The ligand-binding receptor for all the myelin inhibitors
is NgR
(Nogo Receptor) and requires p75(NTR) (p75 Neurotrophin
Receptor) for transmembrane signaling. NgR
is a GPI
(Glycosyl Phosphatidylinositol)-linked LRR (Leucine-Rich
Repeat) protein expressed in [...] |
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References:
1. Oligodendrocyte myelin glycoprotein (OMgp): evolution, structure and function.Vourc'h P, Andres C.Brain Res Brain Res Rev. 2004 May; 45(2):115-24. Review.2. Regulation of Nogo and Nogo receptor during the development of the entorhino-hippocampal pathway and after adult hippocampal lesions.Mingorance A, Fontana X, Sole M, Burgaya F, Urena JM, Teng FY, Tang BL, Hunt D, Anderson PN, Bethea JR, Schwab ME, Soriano E, del Rio JA.Mol Cell Neurosci. 2004 May; 26(1):34-49.
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