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ADAM metallopeptidase domain 23(ADAM23) is a type I transmembrane glycoprotein encoded by ADAM23 gene, belonging to ADAM family, which has restricted expression characteristics in brain tissue, mainly distributed in mature neurons and glial precursor cells of central nervous system, and located in neuronal cell membrane and synaptic membrane structure. Different from other ADAM family members with typical proteolytic activity, ADAM23's metalloprotease domain is inactivated, but it retains the intact adhesion structure of disintegrin region and cysteine-rich, has no substrate shearing ability, and only specifically regulates the intercellular adhesion process. In the physiological stage of neural development, stably expressed ADAM23 can mediate the homologous adhesion of neurons and support the extension of neurites, the remodeling of dendrites and the formation of immature synaptic structures during brain development. However, in malignant glioma lesions, the silencing of ADAM23 transcription level will release the adhesion between cells and significantly accelerate the migration of tumor cells and the invasion of brain tissue. ADAM23's unique neuron-specific adhesion regulation can't be compensated by other ADAM proteases. Knock-out of this gene will lead to neural circuit assembly defects and increase the susceptibility to epilepsy. Restoring ADAM23's expression can effectively inhibit the invasion phenotype of glioma, making it an indispensable core research target for neural development mechanism and targeted screening of brain tumors.
ADAM23 executes neuron-specific adhesive regulatory function anchored to neuronal lipid bilayers, utilizing intact disintegrin and cysteine-rich extracellular domains to mediate homotypic intercellular neuron crosslinking. Its inactive protease domain clearly separates ADAM23 from catalytic ADAM family members, removing shedding capacity to specialize in cell adhesion control. ADAM23-mediated cell-cell tethering links embryonic neural progenitor differentiation to adult brain circuit stability, balancing neurite growth and tumor invasive potential according to cellular malignant status. ADAM23 participates in cortical neurogenesis, synaptic assembly and high-grade glioma progression control. Loss of functional ADAM23 disrupts ordered neuronal network construction and releases glioma migratory capacity. Therefore, ADAM23 represents a pivotal research target for neural ADAM protein study and anti-glioma therapeutic exploration.
Fig. 1 Schematic of Mendelian randomization causal inference framework: Genetic instrumental variables (G) regulate circulating ADAM/ADAMTS protein exposures (X) to causally affect multi-site bone mineral density outcomes (Y).1
The biological functions of ADAM23 are fully focused on neuron homotypic crosslinking and neurite growth regulation:
Creative Biolabs offers high-quality ADAM23 proteins through optimized mammalian expression systems, including full-length neuronal transmembrane glycoprotein and isolated disintegrin adhesion domain variants. These products retain native homotypic neuronal binding biological activity, suitable for neurite outgrowth and glioma invasion functional screening assays. All ADAM23 proteins undergo strict quality control to ensure consistent performance and reliable application across diverse neuroscience research platforms.
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Creative Biolabs provides custom-engineered ADAM23 stable cell lines, including overexpression and blank empty vector control models. These cell lines are optimized for neuronal ADAM profiling and neurite growth functional analysis. Each cell line undergoes stringent validation to ensure stable expression profiles during long-term continuous cell culture, and can be deployed for anti-glioma migration compound screening tests.
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High-specificity recombinant antibodies targeting ADAM23 are developed via advanced antibody engineering technologies. These antibodies are validated for neuronal and glioma membrane localization detection and brain tissue expression profiling, and can be combined with synaptic marker reagents to analyze ADAM23 adhesion complexes in primary neuron models.
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Beyond catalog products, Creative Biolabs offers specialized custom services for ADAM23 research:
ADAM23 is a catalytically inactive neuronal ADAM glycoprotein that mediates homotypic neuronal adhesion to regulate neurite growth and neural circuit assembly.
ADAM23 is a brain-specific adhesion suppressor whose silencing drives glioma invasion, critical for neurodevelopment and brain tumor research.
No, all ADAM23 products and services are strictly for research use only, not intended for clinical diagnosis or human therapeutic trials.
Offerings include full-length neuronal ADAM23 glycoproteins, isoform-specific detection antibodies and custom stable cell lines for neural tumor research.
ADAM23 proteins are validated via homotypic neuronal cell adhesion functional testing.