ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Adam22 is a major neuronal receptor for Lgi4-mediated Schwann cell signaling.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 100 citations in OpenAlex.
- Lgi3-4 proteins modulate the KV1.5 channelosome and are potential therapeutic targets for atrial fibrillation.Cardiovascular research · 2026Article
- Multi-dimensional plasma proteomic profiling elucidates molecular mechanisms and pathophysiological networks in pediatric severe traumatic brain injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Spatially Contextualized Integrative Genomics Highlights Neuronal and Glial Regulatory Programs in Low Back Pain.Journal of pain research · 2026Article
- Propofol inhibits glioma growth by blocking the formation of the NF-κB/LGI4 feedback loop to activate TP53 self-transcription.Translational oncology · 2025Article
- Clinical Spectrum, Pathology, and Mechanisms of Anti-LGI4 Antibody-Positive Autoimmune Nodopathy.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- The Role of tRNA Fragments on Neurogenesis Alteration by H₂O₂-induced Oxidative Stress.Journal of molecular neuroscience : MN · 2025Article
- Schwann Cell Development and Myelination.Cold Spring Harbor perspectives in biology · 2024Review
- Oligodendrocyte-derived LGI3 and its receptor ADAM23 organize juxtaparanodal Kv1 channel clustering for short-term synaptic plasticity.Cell reports · 2024Article
- Morvan Syndrome Associated With Anti-LGI1 Antibodies and Thymoma.Journal of clinical neurology (Seoul, Korea) · 2024Article
- The construction and validation of ECM-related prognosis model in laryngeal squamous cell carcinoma.Heliyon · 2023Article
- LGI3/2-ADAM23 interactions cluster Kv1 channels in myelinated axons to regulate refractory period.The Journal of cell biology · 2023Article
- Anti-LGI4 Antibody Is a Novel Juxtaparanodal Autoantibody for Chronic Inflammatory Demyelinating Polyneuropathy.Neurology(R) neuroimmunology & neuroinflammation · 2023Article
- Article
- Pathology of Initial Axon Segments in Chronic Inflammatory Demyelinating Polyradiculoneuropathy and Related Disorders.International journal of molecular sciences · 2022Review
- Oral Cancer Cells Release Vesicles that Cause Pain.Advanced biology · 2022Article
- A reverse genetics and genomics approach to gene paralog function and disease: Myokymia and the juxtaparanode.American journal of human genetics · 2022Article
- Biallelic ADAM22 pathogenic variants cause progressive encephalopathy and infantile-onset refractory epilepsy.Brain : a journal of neurology · 2022Article
- Beyond Wrapping: Canonical and Noncanonical Functions of Schwann Cells.Annual review of neuroscience · 2022Review
- Effect of Interleukin-1β on Gene Expression Signatures in Schwann Cells Associated with Neuropathic Pain.Neurochemical research · 2021Article
- Myelin Biology.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
The segregation and myelination of axons in the developing PNS, results from a complex series of cellular and molecular interactions between Schwann cells and axons. Previously we identified the Lgi4 gene (leucine-rich glioma-inactivated4) as an important regulator of myelination in the PNS, and its dysfunction results in arthrogryposis as observed in claw paw mice. Lgi4 is a secreted protein and a member of a small family of proteins that are predominantly expressed in the nervous system. Their mechanism of action is unknown but may involve binding to members of the Adam (A disintegrin and metalloprotease) family of transmembrane proteins, in particular Adam22. We found that Lgi4 and Adam22 are both expressed in Schwann cells as well as in sensory neurons and that Lgi4 binds directly to Adam22 without a requirement for additional membrane associated factors. To determine whether Lgi4-Adam22 function involves a paracrine and/or an autocrine mechanism of action we performed heterotypic Schwann cell sensory neuron cultures and cell type-specific ablation of Lgi4 and Adam22 in mice. We show that Schwann cells are the principal cellular source of Lgi4 in the developing nerve and that Adam22 is required on axons. Our results thus reveal a novel paracrine signaling axis in peripheral nerve myelination in which Schwann cell secreted Lgi4 functions through binding of axonal Adam22 to drive the differentiation of Schwann cells.
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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.