ArticleScientific reports2017
Ectodomain shedding of Limbic System-Associated Membrane Protein (LSAMP) by ADAM Metallopeptidases promotes neurite outgrowth in DRG neurons.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
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- Behavioral Phenotyping of Bbs6 and Bbs8 Knockout Mice Reveals Major Alterations in Communication and Anxiety.International journal of molecular sciences · 2022Article
- Tissue Inhibitor of Metalloproteases 3 (TIMP-3): In Vivo Analysis Underpins Its Role as a Master Regulator of Ectodomain Shedding.Membranes · 2022Review
- Interactions between maternal fluoxetine exposure, the maternal gut microbiome and fetal neurodevelopment in mice.Behavioural brain research · 2021Article
- Utilizing an Animal Model to Identify Brain Neurodegeneration-Related Biomarkers in Aging.International journal of molecular sciences · 2021Article
- Depression-Associated GeneCells · 2020Article
- NrCAM is a marker for substrate-selective activation of ADAM10 in Alzheimer's disease.EMBO molecular medicine · 2019Article
- MT3-MMP Promotes Excitatory Synapse Formation by Promoting Nogo-66 Receptor Ectodomain Shedding.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Molecular Evolution and Functional Divergence of the IgLON Family.Evolutionary bioinformatics online · 2018Article
- Neuronal Growth and Behavioral Alterations in Mice Deficient for the Psychiatric Disease-AssociatedFrontiers in molecular neuroscience · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
IgLONs are members of the immunoglobulin superfamily of cell adhesion proteins implicated in the process of neuronal outgrowth, cell adhesion and subdomain target recognition. IgLONs form homophilic and heterophilic complexes on the cell surface that repress or promote growth depending on the neuronal population, the developmental stage and surface repertoire of IgLON family members. In the present study, we identified a metalloproteinase-dependent mechanism necessary to promote growth in embryonic dorsal root ganglion cells (DRGs). Treatment of embryonic DRG neurons with pan-metalloproteinase inhibitors, tissue inhibitor of metalloproteinase-3, or an inhibitor of ADAM Metallopeptidase Domain 10 (ADAM10) reduces outgrowth from DRG neurons indicating that metalloproteinase activity is important for outgrowth. The IgLON family members Neurotrimin (NTM) and Limbic System-Associated Membrane Protein (LSAMP) were identified as ADAM10 substrates that are shed from the cell surface of DRG neurons. Overexpression of LSAMP and NTM suppresses outgrowth from DRG neurons. Furthermore, LSAMP loss of function decreases the outgrowth sensitivity to an ADAM10 inhibitor. Together our findings support a role for ADAM-dependent shedding of cell surface LSAMP in promoting outgrowth from DRG neurons.
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