ArticleScientific reports2019
L1cam-mediated developmental processes of the nervous system are differentially regulated by proteolytic processing.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.
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Who cites it
39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 55 citations in OpenAlex.
- Identification of Key Genes and Regulatory Pathways in Multiple Sclerosis Brain Samples: A Meta-Analysis of Micro-Array Datasets.International journal of molecular sciences · 2023Pooled it
- Pooled it
- Loss of L1CAM from gastric epithelial cells and extracellular vesicles promotes Helicobacter pylori-driven cancer progression and invasiveness.Cell communication and signaling : CCS · 2026Article
- Alzheimer's Disease Risk Factor APOE4 Exerts Dimorphic Effects on Female Bone.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Investigating and correcting a rare pathogenic mutation in GDF11.HGG advances · 2026Article
- Pbx1 and Pbx3 cooperatively regulate intermediate progenitor genesis and corticogenesis in the mouse neocortex.Frontiers in cell and developmental biology · 2026Article
- Bridging the anatomical gap: evolutionary conservation of genetic mechanisms in corpus callosum disorders across human, mouse, and zebrafish.Frontiers in molecular neuroscience · 2026Review
- Surface Problem: Unveiling Extracellular Vesicles Surface Markers and Their Implications for Central Nervous System Diseases' Diagnosis and Treatment.Molecular neurobiology · 2025Review
- Circulating Neuronal Exosome Cargo as Biomarkers of Neuroplasticity in Cushing's Syndrome.Molecular neurobiology · 2025Article
- Identification and functional characteristics of a novel splice site variant inFrontiers in genetics · 2025Article
- Advancing Hydrocephalus Management: Pathogenesis Insights, Therapeutic Innovations, and Emerging Challenges.Aging and disease · 2024Review
- Molecular signatures of normal pressure hydrocephalus: a large-scale proteomic analysis of cerebrospinal fluid.Fluids and barriers of the CNS · 2024Article
- Single-extracellular vesicle (EV) analyses validate the use of L1 Cell Adhesion Molecule (L1CAM) as a reliable biomarker of neuron-derived EVs.Journal of extracellular vesicles · 2024Article
- Mice Mutated in the First Fibronectin Domain of Adhesion Molecule L1 Show Brain Malformations and Behavioral Abnormalities.Biomolecules · 2024Article
- Emergence of Extracellular Vesicles as "Liquid Biopsy" for Neurological Disorders: Boom or Bust.Pharmacological reviews · 2024Review
- Genetic and molecular mechanisms of hydrocephalus.Frontiers in molecular neuroscience · 2024Review
- Diving deep: zebrafish models in motor neuron degeneration research.Frontiers in neuroscience · 2024Review
- Mice Mutated in the Third Fibronectin Domain of L1 Show Enhanced Hippocampal Neuronal Cell Death, Astrogliosis and Alterations in Behavior.Biomolecules · 2023Article
- Discovery of Biomarkers for Amyotrophic Lateral Sclerosis from Human Cerebrospinal Fluid Using Mass-Spectrometry-Based Proteomics.Biomedicines · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Normal brain development depends on tight temporal and spatial regulation of connections between cells. Mutations in L1cam, a member of the immunoglobulin (Ig) superfamily that mediate cell-cell contacts through homo- and heterophilic interactions, are associated with several developmental abnormalities of the nervous system, including mental retardation, limb spasticity, hydrocephalus, and corpus callosum aplasia. L1cam has been reported to be shed from the cell surface, but the significance of this during different phases of brain development is unknown. We here show that ADAM10-mediated shedding of L1cam is regulated by its fibronectin type III (FNIII) domains. Specifically, the third FNIII domain is important for maintaining a conformation where access to a membrane proximal cleavage site is restricted. To define the role of ADAM10/17/BACE1-mediated shedding of L1cam during brain development, we used a zebrafish model system. Knockdown of the zebrafish, l1camb, caused hydrocephalus, defects in axonal outgrowth, and myelination abnormalities. Rescue experiments with proteinase-resistant and soluble L1cam variants showed that proteolytic cleavage is not required for normal axonal outgrowth and development of the ventricular system. In contrast, metalloproteinase-mediated shedding is required for efficient myelination, and only specific fragments are able to mediate this stimulatory function of the shedded L1cam.
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