Adhesion molecule that mediates interactions between myelinating cells and neurons by binding to neuronal sialic acid-containing gangliosides and to the glycoproteins RTN4R and RTN4RL2 (PubMed:7533044, PubMed:12089450, PubMed:27922006). Not required for initial myelination, but seems to play a role in the maintenance of normal axon myelination (PubMed:7516497, PubMed:9262180, PubMed:9482781, PubMed:9482783, PubMed:9469574, PubMed:10625334). Protects motoneurons against apoptosis, also after injury; protection against apoptosis is probably mediated via interaction with neuronal RTN4R and RTN4RL2 (PubMed:26335717). Required to prevent degeneration of myelinated axons in adults; this probably depends on binding to gangliosides on the axon cell membrane (PubMed:15953602, PubMed:19158290). Negative regulator of neurite outgrowth that inhibits axon longitudinal growth (PubMed:19158290, PubMed:27922006, PubMed:12089450). Negative regulator of neurite outgrowth; in dorsal root ganglion neurons the inhibition is mediated primarily via binding to neuronal RTN4R or RTN4RL2 and to a lesser degree via binding to neuronal gangliosides (PubMed:17640868). In cerebellar granule cells the inhibition is mediated via binding to neuronal gangliosides (PubMed:17640868). In sensory neurons, inhibition of neurite extension depends only partially on RTN4R, RTN4RL2 and gangliosides (By similarity). Inhibits axon outgrowth by binding to RTN4R (PubMed:12089450). Preferentially binds to alpha-2,3-linked sialic acid (PubMed:7533044, PubMed:27922006). Binds ganglioside Gt1b (PubMed:27922006). Monomer and homodimer (PubMed:27922006). Interacts (via the first three N-terminal Ig-like domains) with RTN4R and RTN4RL2 (PubMed:12089450, PubMed:26335717). Interacts with isoform 2 of BSG (PubMed:12558975). Detected in the myelin tract in brain, especially in the corpus callosum and in peripheral nerve (PubMed:7516497, PubMed:9482783, PubMed:24191038). Expressed by myelinating glial cells in the central and peripheral nervous system (PubMed:10625334). Detected in oligodendrocyte processes before formation of compact myelin (PubMed:2474006, PubMed:10625334). Restricted to the periaxonal space after myelination (PubMed:10625334). Isoform S-MAG is the predominant isoform in CNS and PNS of the adult (at protein level) (PubMed:1716323). In CNS isoform L-MAG is the major form synthesized early in development, and it persists as a significant proportion of the MAG present in the adult. In the PNS isoform L-MAG is expressed at modest levels during development; it is absent in the adult. The C-terminal cytoplasmic region found only in isoform L-MAG is required for normal myelination in the central nervous system (CNS), but is apparently not required for normal myelination in the peripheral nervous system (PNS). The extracellular domain is required to protect against axon degeneration (PubMed:19158290, PubMed:26335717). The first three Ig-like domains mediate interaction with RTN4R and RTN4RL2, but are not sufficient to inhibit neurite outgrowth (By similarity). The two C-terminal extracellular Ig-like C2-type domains are required for inhibition of axon longitudinal growth. Besides, the two C-terminal extracellular Ig-like C2-type domains are required for protection against apoptosis after nerve injury (PubMed:26335717). N-glycosylated. Phosphorylated on tyrosine residues. Ubiquitinated, leading to proteasomal degradation. Mutant mice appear normal, excepting subtle defects in motor coordination and a slight intention tremor (PubMed:7516497). They have similar numbers of motoneurons as wild-type at birth, but display an important loss of motoneurons during the first week after birth (PubMed:26335717).Five month old mutant mice display a decreased ability to remain on a rotating cylinder (PubMed:15953602). Contrary to wild-type, about 40% of mutant mice have severe episodes of whole-body tremor, both during movement and when resting (PubMed:15953602). The myelination in brain and around peripheral nerves appears grossly normal in young animals, but the periaxonal cytoplasmic collar is often missing in optic nerve (PubMed:7516497, PubMed:9262180, PubMed:9482781, PubMed:9469574). When present, the cytoplasm of the periaxonal collar has generally a disorganized aspect (PubMed:7516497). Mutant mice have an increased percentage of unmyelinated axons in optic nerve (PubMed:9262180, PubMed:9469574). Besides, a small proportion of nerves from mutant mice display redundant myelination, and also rare cases of multiple myelination, where axons are surrounded by two or more compact myelin sheets (PubMed:9469574). Sciatic nerves from over three month old mutant mice show signs of Wallerian degeneration, with redundant myelin, degeneration of myelinated fibers, and an apparent decrease in the diameter of myelinated axons (PubMed:9482781, PubMed:15953602). The distances between neurofilaments in myelinated axons from over 3 month old mice are shorter than normal (PubMed:9482781, PubMed:15953602). With increasing age, mutant mice display progressive axon degeneration in the spinal cord and sciatic nerve, resulting in a decrease of 28% in the number of spinal cord axons after 15 months (PubMed:19158290). Mutant mice display increased motoneuron apoptosis after injury (PubMed:26335717). Likewise, they display strongly increased axon degeneration after treatment with the neurotoxin acrylamide (PubMed:19158290). Mutant mice display much more severe axon loss in response to experimental autoimmune encephalitis (PubMed:19158290). Belongs to the immunoglobulin superfamily. SIGLEC (sialic acid binding Ig-like lectin) family. Siglec-4 Siglec-4a [3 Fc Domains]