ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998
The cytoplasmic domain of the large myelin-associated glycoprotein isoform is needed for proper CNS but not peripheral nervous system myelination.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
26 citing papers in PubMed, 81 citations in OpenAlex.
- Article
- Aging differentially alters the transcriptome and landscape of chromatin accessibility in the male and female mouse hippocampus.Frontiers in molecular neuroscience · 2024Article
- Traumatic axonopathy in spinal tracts after impact acceleration head injury: Ultrastructural observations and evidence of SARM1-dependent axonal degeneration.Experimental neurology · 2023Article
- Flexible Players within the Sheaths: The Intrinsically Disordered Proteins of Myelin in Health and Disease.Cells · 2020Review
- Poly(I:C) Challenge Alters Brain Expression of Oligodendroglia-Related Genes of Adult Progeny in a Mouse Model of Maternal Immune Activation.Frontiers in molecular neuroscience · 2020Article
- The Involvement of the Myelin-Associated Inhibitors and Their Receptors in CNS Plasticity and Injury.Molecular neurobiology · 2018Review
- Interferons, signal transduction pathways, and the central nervous system.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014Review
- hnRNP A1 and secondary structure coordinate alternative splicing of Mag.RNA (New York, N.Y.) · 2013Article
- Quaking I controls a unique cytoplasmic pathway that regulates alternative splicing of myelin-associated glycoprotein.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Genetic deletion of paired immunoglobulin-like receptor B does not promote axonal plasticity or functional recovery after traumatic brain injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Deregulated sphingolipid metabolism and membrane organization in neurodegenerative disorders.Molecular neurobiology · 2010Review
- MAG and OMgp synergize with Nogo-A to restrict axonal growth and neurological recovery after spinal cord trauma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Myelin-associated glycoprotein and its axonal receptors.Journal of neuroscience research · 2009Review
- Nur7 is a nonsense mutation in the mouse aspartoacylase gene that causes spongy degeneration of the CNS.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Absence of 2-hydroxylated sphingolipids is compatible with normal neural development but causes late-onset axon and myelin sheath degeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Article
- N-Acetylaspartate in the CNS: from neurodiagnostics to neurobiology.Progress in neurobiology · 2007Review
- Myelin-associated glycoprotein-mediated signaling in central nervous system pathophysiology.Molecular neurobiology · 2006Review
- Extracellular regulators of axonal growth in the adult central nervous system.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2006Review
- Myelin-associated glycoprotein and complementary axonal ligands, gangliosides, mediate axon stability in the CNS and PNS: neuropathology and behavioral deficits in single- and double-null mice.Experimental neurology · 2005Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 3 countries.
Funding
Abstract
The myelin-associated glycoprotein (MAG) is a member of the immunoglobulin gene superfamily and is thought to play a critical role in the interaction of myelinating glial cells with the axon. Myelin from mutant mice incapable of expressing MAG displays various subtle abnormalities in the CNS and degenerates with age in the peripheral nervous system (PNS). Two distinct isoforms, large MAG (L-MAG) and small MAG (S-MAG), are produced through the alternative splicing of the primary MAG transcript. The cytoplasmic domain of L-MAG contains a unique phosphorylation site and has been shown to associate with the fyn tyrosine kinase. Moreover, L-MAG is expressed abundantly early in the myelination process, possibly indicating an important role in the initial stages of myelination. We have adapted the gene-targeting approach in embryonic stem cells to generate mutant mice that express a truncated form of the L-MAG isoform, eliminating the unique portion of its cytoplasmic domain, but that continue to express S-MAG. Similar to the total MAG knockouts, these animals do not express an overt clinical phenotype. CNS myelin of the L-MAG mutant mice displays most of the pathological abnormalities reported for the total MAG knockouts. In contrast to the null MAG mutants, however, PNS axons and myelin of older L-MAG mutant animals do not degenerate, indicating that S-MAG is sufficient to maintain PNS integrity. These observations demonstrate a differential role of the L-MAG isoform in CNS and PNS myelin.
Indexed as
Identifiers
9482783PMC6792935W1634233994What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.