Ligand for NRCAM and NFASC/neurofascin that plays a role in the formation and maintenance of the nodes of Ranvier on myelinated axons. Mediates interaction between Schwann cell microvilli and axons via its interactions with NRCAM and NFASC (PubMed:20188654). Nodes of Ranvier contain clustered sodium channels that are crucial for the saltatory propagation of action potentials along myelinated axons. During development, nodes of Ranvier are formed by the fusion of two heminodes. Required for normal clustering of sodium channels at heminodes; not required for the formation of mature nodes with normal sodium channel clusters (PubMed:20188654). Required, together with NRCAM, for maintaining NFASC and sodium channel clusters at mature nodes of Ranvier (PubMed:24719088). Homotrimer (via collagen-like domains) (PubMed:17293346). Interacts with NRCAM and NFASC/neurofascin (PubMed:16039564, PubMed:20188654). Interaction with glial NRCAM enhances interaction with axonal NFASC (PubMed:20188654). Interacts with MYOC (PubMed:23897819). Localizes to the nodes of Ranvier (PubMed:17293346, PubMed:20188654). Detected at immature heminodes (By similarity). Proteolytic processing gives rise to a soluble extracellular domain that is secreted (PubMed:17293346). The gliomedin shedded ectodomain localizes to the nodes of Ranvier (By similarity). Detected in sciatic nerve (at protein level) (PubMed:17293346, PubMed:20188654, PubMed:24719088). Widely expressed with higher expression in testis and skeletal muscle (PubMed:12642876). The olfactomedin-like domain mediates NFASC/neurofascin and NRCAM binding. N-glycosylated. Proteolytic proccessing by a furin-like protease causes shedding of the ectodomain. Further cleavage by BMP1 releases the olfactomedin-like domain. Mutant mice present no obvious neurological phenotype and have normal nerve conduction. Nerves from their peripheral nervous system have myelin sheets that are indistinguishable from wild-type. In contrast, they present impaired and disorganized attachment of Schwann cell microvilli to the axolemma at nodes of Ranvier. Mature nodes are formed by the fusion of two heminodes. During development, mutant mice present defective clustering of sodium channels at heminodes, but display normal sodium channel clustering at mature nodes (PubMed:20188654). Mice lacking both Gldn and Nrcam are born at the expected Mendelian rate, but are smaller than control littermates and display important neurological impairments, in spite of seemingly normal nerve myelination. Motor abnormalities vary between individuals, ranging from ataxia, uncoordinated movements and premature death to weakness of the hind limbs, hypomotility, strongly impaired ability to hang from a horizontal bar with their forelimbs and a tendency to stumble. The motor defects correlate with decreased velocity of nerve conduction and slower propagation of action potentials. Most mice die within 60 days after birth, and none are fertile. Mutant mice display delayed formation of mature nodes of Ranvier; 15 days after birth about 20% of the nodes lack detectable sodium channel clusters. Sodium channel clustering and nerve conduction appear normal 60 and 75 days after birth, but subsequently a gradual disintegration of the nodal protein complexes is seen. About 70% of the mutant nodes present high-density sodium channel clustering at 120 days after birth, as opposed to nearly 100% for wild-type. Contrary to wild-type, in adult nodes of Ranvier the sodium channels are often clustered near the paranode border with an empty gap in the middle. At nodes of Ranvier, Schwann cell microvilli are sparse or absent and show defects in their orientation, resulting in various structural abnormalities at the node and the paranode border (PubMed:24719088).