The Nogo-66 receptor (NgR) plays a pivotal role in the inhibition of neuroregeneration as the receptor for multiple neurite outgrowth inhibitors such as Nogo-A. We have previously shown that NgR undergoes zinc metalloproteinase-mediated ectodomain shedding in neuroblastoma cells. Here, we demonstrate that the NgR-related protein NgR homologue-1 is released from neuroblastoma cells as a full-length ectodomain (NgRH1-ecto) and an N-terminal fragment (NTF-NgRH1) containing the leucine-rich repeat region of the protein. Inhibitors of the major protease classes failed to block the release of NgRH1-ecto, suggesting that this occurs via a protease-independent mechanism, presumably by a phospholipase-like enzyme. The release of NTF-NgRH1 was blocked by a hydroxamate-based zinc metalloproteinase inhibitor and tissue inhibitor of metalloproteinases-2 and -3, but not -1, implicating the involvement of membrane-type matrix metalloproteinases in this process. Our findings thus highlight the parallels between the ectodomain shedding of NgRH1 and that previously described for NgR.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.bbrc.2004.12.001 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
What are the levels and interactions of neuroligin-1, neuroligin-3, and inflammatory cytokines (IL-6, IL-8) in children diagnosed with autism spectrum disorder?
Prog Neuropsychopharmacol Biol Psychiatry
January 2025
Department of Child and Adolescent Psychiatry, Selcuk University Faculty of Medicine Hospital, 42130 Konya, Turkey.
Autism spectrum disorder (ASD) is characterized by deficits in social interaction, restricted interests, and repetitive behaviors. Several genes, including synaptic proteins and environmental risk factors, play a role in the etiology of autism. We aimed to evaluate the relationship between neuroligin-1 (NLGN-1) and neuroligin-3 (NLGN-3) levels, which are neuronal cell adhesion molecules (CAMs), and inflammatory cytokine (IL-6, IL-8) levels with disease severity and symptom clusters and with each other in children with ASD.
View Article and Find Full Text PDFPrion Protein Endoproteolysis: Cleavage Sites, Mechanisms and Connections to Prion Disease.
J Neurochem
January 2025
Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Canada.
Highly abundant in neurons, the cellular prion protein (PrP) is an obligatory precursor to the disease-associated misfolded isoform denoted PrP that accumulates in the rare neurodegenerative disorders referred to either as transmissible spongiform encephalopathies (TSEs) or as prion diseases. The ability of PrP to serve as a substrate for this template-mediated conversion process depends on several criteria but importantly includes the presence or absence of certain endoproteolytic events performed at the cell surface or in acidic endolysosomal compartments. The major endoproteolytic events affecting PrP are referred to as α- and β-cleavages, and in this review we outline the sites within PrP at which the cleavages occur, the mechanisms potentially responsible and their relevance to pathology.
View Article and Find Full Text PDFDecoding the MMP14 Integrin Link: Key Player in the Secretome Landscape.
Matrix Biol
January 2025
Institute of Physiological Chemistry and Pathobiochemistry, University of Münster, Münster, Germany. Electronic address:
Rapid progress has been made in the exciting field of secretome research in health and disease. The tumor secretome, which is a significant proportion of the tumor proteome, is secreted into the extracellular space to promote intercellular communication and thus tumor progression. Among the many molecules of the secretome, integrins and matrix metalloproteinase 14 (MMP14) stand out as the interplay of adhesion and proteolysis drives invasion.
View Article and Find Full Text PDFUpdates on Inflammatory Molecular Pathways Mediated by ADAM17 in Autoimmunity.
Cells
December 2024
Department of Translational Biomedicine and Neuroscience (DiBraiN), Section of Human Anatomy and Histology, University of Bari "Aldo Moro", Piazza Giulio Cesare 1, I-70124 Bari, Italy.
ADAM17 is a member of the disintegrin and metalloproteinase (ADAM) family of transmembrane proteases with immunoregulatory activity in multiple signaling pathways. The functional ADAM17 is involved in the shedding of the ectodomain characterizing many substrates belonging to growth factors, cytokines, receptors, and adhesion molecules. The ADAM17-dependent pathways are known to be crucial in tumor development and progression and in the modulation of many pathological and physiological processes.
View Article and Find Full Text PDFWooden breast myopathy is characterized by satellite cell dysfunction and syndecan-4 shedding.
Front Physiol
December 2024
Raw Materials and Optimalization, Nofima AS, Ås, Norway.
Introduction: Skeletal muscle satellite cells (MuSCs or stem cells) play a crucial role in muscle development, maintenance, and regeneration, supporting both hypertrophy and regenerative myogenesis. Syndecans (SDCs) act as communication bridges within the muscle microenvironment, regulating interactions with extracellular matrix components and contributing significantly to tissue repair and inflammation. Specifically, syndecan-4 (SDC4) is involved in muscle regeneration at multiple stages.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!