Affinage

ADAM23

Disintegrin and metalloproteinase domain-containing protein 23 · UniProt O75077

Length
832 aa
Mass
91.9 kDa
Annotated
2026-06-09
46 papers in source corpus 22 papers cited in narrative 22 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ADAM23 is a catalytically inactive, furin-matured transmembrane ADAM-family glycoprotein expressed predominantly in the brain that functions as a cell-surface adhesion receptor and ligand-binding hub (PMID:15505805). Its disintegrin-like domain mediates RGD-independent binding to αvβ3 integrin, promoting adhesion of neural-origin cells while negatively modulating integrin activation; loss of ADAM23 enhances αvβ3 activation, migration, and metastatic colonization, establishing it as a metastasis suppressor (PMID:10749942, PMID:19549921, PMID:26800504). Through its ectodomain, ADAM23 serves as a receptor for the secreted LGI family of proteins (LGI1, LGI3, LGI4), and these interactions underlie its principal neuronal functions (PMID:18974846, PMID:19796686, PMID:38194969). LGI1 binding is required for normal neurite outgrowth and dendritic arborization, and ADAM23-null mice develop spontaneous seizures (PMID:19796686). In axons, ADAM23 acting through LGI2/LGI3 is essential for the accumulation and stability of juxtaparanodal Kv1 potassium channel complexes, co-assembling Kv1 nanoclusters that set the axonal refractory period and support high-frequency firing and short-term synaptic plasticity (PMID:36828548, PMID:38194969). ADAM23 also independently suppresses surface Kv1.1 currents through a clathrin-independent mechanism (PMID:30965109), and undergoes constitutive lipid-raft-dependent endocytosis with recycling to the plasma membrane, conferring high surface stability (PMID:29792904, PMID:33296662). Beyond the nervous system, ADAM23 suppresses cardiac hypertrophy via the FAK-AKT cascade (PMID:30371220) and controls dendritic-cell-driven CD4+ T cell activation through αvβ3 integrin (PMID:27317750). ADAM23 expression is activated by SP1 binding to its proximal promoter (PMID:20851106). A biallelic ADAM23 variant has been linked to lethal neonatal-onset epilepsy and myopathy within the LGI1-ADAM22/23 disease spectrum (PMID:40455867).

Mechanistic history

Synthesis pass · year-by-year structured walk · 21 steps
  1. 2000 High

    Established the molecular basis of ADAM23 adhesive function by showing its disintegrin domain binds a specific integrin partner, addressing how a catalytically inactive ADAM mediates cell adhesion.

    Evidence Recombinant disintegrin-domain adhesion and integrin-binding assays plus full-length transfection across neural cell lines

    PMID:10749942

    Open questions at the time
    • Did not define downstream signaling consequences of αvβ3 engagement
    • Non-RGD binding motif not resolved at residue level
  2. 2004 Medium

    Defined ADAM23 biogenesis, showing maturation depends on furin cleavage and that mature protein localizes to neuronal cell-cell contact sites.

    Evidence Immunoblotting, furin inhibitor experiments and cell fractionation in neurons

    PMID:15505805

    Open questions at the time
    • Identity of the maturation protease not definitively shown to be furin
    • Functional role of contact-site localization untested
  3. 2008 Medium

    Identified ADAM23 as a receptor for secreted LGI-family proteins, expanding its role beyond integrin adhesion to ligand recognition.

    Evidence Cell-ELISA binding assay and co-IP/mass spectrometry for LGI1 and LGI4

    PMID:18974846

    Open questions at the time
    • Binding affinities and stoichiometry not determined
    • Functional consequences of LGI binding not addressed in this study
  4. 2009 High

    Connected ADAM23-LGI1 binding to neuronal morphology and excitability, establishing ADAM23 as a seizure-suppressing receptor in vivo.

    Evidence Unbiased LGI1-binding screen, ADAM23 knockout mouse with neurite/dendrite phenotypes and seizure monitoring

    PMID:19796686

    Open questions at the time
    • Molecular signaling linking LGI1-ADAM23 to neurite outgrowth not resolved
    • Cell-type contribution to seizures not dissected
  5. 2009 High

    Showed ADAM23 functions as a metastasis suppressor by restraining αvβ3 integrin activation, linking its adhesion function to tumor cell behavior.

    Evidence shRNA knockdown with integrin activation, migration/adhesion assays and in vivo pulmonary arrest model

    PMID:19549921

    Open questions at the time
    • Mechanism by which ADAM23 dampens integrin activation not defined
    • Did not establish whether effect is cell-autonomous in patient tumors
  6. 2009 Medium

    Added cellular prion protein as a direct membrane partner of the ADAM23 disintegrin domain, broadening its neuronal interaction network.

    Evidence Reciprocal co-IP, recombinant pull-down with domain mapping and glycosylation controls

    PMID:19477226

    Open questions at the time
    • Functional consequence of PrPc-ADAM23 interaction unknown
    • Single-lab interaction without in vivo validation
  7. 2010 Medium

    Defined transcriptional control of ADAM23 by identifying an SP1 promoter element regulated by chromatin accessibility.

    Evidence Promoter analysis, EMSA/ChIP for SP1 and RNA Pol II recruitment under serum deprivation

    PMID:20851106

    Open questions at the time
    • Physiological signals driving chromatin opening not identified
    • Relationship to cancer-associated silencing not addressed
  8. 2012 Medium

    Extended LGI-ADAM23 signaling to non-neuronal tissue, showing LGI3 acts through ADAM23 to suppress adipogenesis.

    Evidence Pull-down, co-IP and siRNA rescue of LGI3 anti-adipogenic effect in 3T3-L1 cells

    PMID:22405860

    Open questions at the time
    • Downstream signaling from ADAM23 in adipocytes not mapped
    • In vivo relevance not tested
  9. 2012 Medium

    Linked the ADAM23 disintegrin domain to cell-cycle and differentiation control, showing it suppresses neuronal differentiation via P27KIP1.

    Evidence RNAi knockdown, cell cycle analysis and recombinant disintegrin-domain rescue in P19 cells

    PMID:22973984

    Open questions at the time
    • Receptor mediating the disintegrin effect on differentiation not identified
    • Mechanism linking domain to P27KIP1 induction unclear
  10. 2014 Medium

    Revealed a non-cell-autonomous tumor mechanism whereby ADAM23-negative cells stimulate neighboring ADAM23-positive cells via secreted LGI4 and nitric oxide.

    Evidence Co-culture functional assays with LGI4/NO ablation and in vivo tumor models

    PMID:24662834

    Open questions at the time
    • Receptor/signaling integrating LGI4 and NO not defined
    • Generality across tumor types untested
  11. 2016 Medium

    Demonstrated an immune role for ADAM23, controlling dendritic-cell-driven CD4+ T cell responses through αvβ3 integrin.

    Evidence RNAi knockdown in bone-marrow DCs with T cell proliferation/cytokine readouts and anti-αvβ3 neutralizing phenocopy

    PMID:27317750

    Open questions at the time
    • Molecular signaling from αvβ3 to T cell outcomes not mapped
    • In vivo immune consequences not established
  12. 2016 Medium

    Confirmed the disintegrin-αvβ3 axis as the basis of ADAM23 tumor suppression in lung cancer using domain-specific antagonists.

    Evidence Gain/loss-of-function with anti-ADAM23, anti-αvβ3 and disintegrin peptide blockade plus in vivo metastasis model

    PMID:26800504

    Open questions at the time
    • Did not resolve intracellular signaling downstream of integrin modulation
    • Clinical correlation limited
  13. 2016 Medium

    Linked disease-causing LGI1 missense mutations to loss of ADAM22/ADAM23 binding, defining a binding-deficient mechanism of epilepsy distinct from secretion failure.

    Evidence Co-IP, immunofluorescence and surface-binding assays of ADLTE mutants with structural modeling

    PMID:27760137

    Open questions at the time
    • Relative contribution of ADAM23 versus ADAM22 binding not separated
    • Structural model not experimentally determined
  14. 2018 High

    Defined a cardiac function for ADAM23, showing it suppresses hypertrophy through the FAK-AKT cascade.

    Evidence Cardiac-specific knockout, transgenic overexpression, aortic banding and pharmacologic FAK inhibition rescue

    PMID:30371220

    Open questions at the time
    • Upstream receptor/ligand triggering FAK-AKT regulation in cardiomyocytes not identified
    • Whether integrin or LGI ligands mediate this is unknown
  15. 2018 Medium

    Placed ADAM23 in lipid-raft microdomains and showed its mature form partitions between raft and non-raft domains, providing membrane-organization context.

    Evidence Lipid raft fractionation and immunoblotting across brain regions and primary neurons

    PMID:29792904

    Open questions at the time
    • Functional importance of raft partitioning not directly tested here
    • Raft residency relationship to ligand binding unknown
  16. 2019 Medium

    Showed ADAM22/ADAM23 chaperone LGI1 trafficking, promoting ER export and axonal co-transport to the axon initial segment.

    Evidence Live-cell imaging and co-transport tracking in hippocampal neurons with disease-mutant analysis

    PMID:30598502

    Open questions at the time
    • Relative roles of ADAM22 versus ADAM23 in trafficking not fully separated
    • Structural basis of co-transport vesicle loading unknown
  17. 2019 Medium

    Demonstrated direct ADAM23 regulation of Kv1.1 surface expression and current through a clathrin-independent, LGI1-independent mechanism.

    Evidence Whole-cell patch-clamp and surface Kv1.1 immunostaining in transfected cells

    PMID:30965109

    Open questions at the time
    • Molecular pathway of clathrin-independent Kv1.1 internalization unresolved
    • Reconciliation with juxtaparanodal clustering role not addressed
  18. 2023 High

    Established axonal ADAM23 as essential for juxtaparanodal Kv1 channel clustering through LGI2/LGI3, defining its role in setting the refractory period and burst firing.

    Evidence ADAM23 knockout mouse with juxtaparanodal immunofluorescence, electrophysiology and LGI2/LGI3 genetic epistasis

    PMID:36828548

    Open questions at the time
    • Molecular bridge between ADAM23 and Kv1 channel scaffolding not defined
    • Reconciliation with ADAM23's negative Kv1.1 regulation unresolved
  19. 2023 Medium

    Identified a γ-secretase-dependent invasion mechanism unleashed by ADAM23 loss in astrocytoma, linking ADAM23 deficiency to Aβ and NICD-driven infiltration.

    Evidence In vitro/in vivo functional assays, RNA-seq, γ-secretase activity assay and pharmacologic inhibition

    PMID:38024245

    Open questions at the time
    • Mechanism by which ADAM23 restrains γ-secretase activity unknown
    • Clinical translatability of GS inhibition untested
  20. 2024 High

    Defined oligodendrocyte-derived LGI3 as a juxtaparanodal ligand that uses ADAM23 to co-assemble Kv1 nanoclusters and support short-term synaptic plasticity.

    Evidence Epitope-tagged Lgi3 knockin proteomics, Lgi3 knockout immunofluorescence and electrophysiology

    PMID:38194969

    Open questions at the time
    • Stoichiometry of the LGI3-ADAM23-Kv1 assembly not resolved
    • Glia-axon directionality of complex assembly not fully mapped
  21. 2025 Medium

    Genetically linked ADAM23 to human disease, associating a biallelic variant with lethal neonatal-onset epilepsy and myopathy within the LGI1-ADAM22/23 spectrum.

    Evidence Functional variant assays plus Lgi1-/- and ADAM22-DEE mouse models

    PMID:40455867

    Open questions at the time
    • ADAM23 finding rests on a single variant report
    • Functional consequence of the ADAM23 variant not directly characterized

Open questions

Synthesis pass · forward-looking unresolved questions
  • The molecular scaffold linking ADAM23 to Kv1 channels and reconciling its dual roles as a Kv1.1 negative regulator and a juxtaparanodal Kv1-clustering factor remains undefined.
  • No structural model of the ADAM23-LGI-Kv1 complex
  • Downstream signaling from αvβ3 integrin modulation in different tissues not unified
  • Direct functional characterization of disease-associated ADAM23 variants lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0001618 virus receptor activity 4 GO:0098772 molecular function regulator activity 3 GO:0060089 molecular transducer activity 2 GO:0098631 cell adhesion mediator activity 2
Localization
GO:0005886 plasma membrane 4 GO:0005768 endosome 1 GO:0031410 cytoplasmic vesicle 1
Pathway
R-HSA-112316 Neuronal System 3 R-HSA-162582 Signal Transduction 2 R-HSA-1643685 Disease 2 R-HSA-168256 Immune System 1
Partners
ITGAVITGB3LGI1LGI2LGI3LGI4PRNP
Complex memberships
juxtaparanodal Kv1 channel complex

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 The disintegrin-like domain of ADAM23 directly binds αvβ3 integrin via a non-RGD sequence in its putative disintegrin loop, promoting cell adhesion of neural-origin cells (neuroblastoma, astrocytoma, HeLa) in an RGD-independent manner. Recombinant protein adhesion assay, integrin-binding assay with recombinant disintegrin domain, full-length cDNA transfection in HeLa cells Molecular biology of the cell High 10749942
2008 ADAM23 binds both LGI1 and LGI4 via its ectodomain, establishing it as a receptor for LGI-family secreted proteins alongside ADAM22 and ADAM11. Quantitative cell-ELISA binding assay, immunoprecipitation and mass spectrometry International journal of biological sciences Medium 18974846
2009 LGI1 binding to ADAM23 is required for correct neuronal morphology: LGI1 promotes neurite outgrowth from wild-type but not ADAM23-/- neurons, and ADAM23-/- hippocampal CA1 pyramidal neurons show reduced dendritic arborization. ADAM23-/- mice exhibit spontaneous seizures and ADAM23+/- mice have reduced seizure thresholds. Unbiased LGI1-binding screen (identified ADAM23 as the primary interactor), ADAM23 knockout mouse analysis, neurite outgrowth assay, in vivo seizure monitoring Molecular and cellular neurosciences High 19796686
2009 ADAM23 negatively modulates αvβ3 integrin activation: shRNA knockdown of ADAM23 in MDA-MB-435 cells enhances αvβ3 integrin activation by 2–4-fold, increases migration and adhesion to αvβ3 ligands, and enhances pulmonary tumor cell arrest in mice. shRNA knockdown, integrin activation assay, cell migration and adhesion assay, in vivo pulmonary arrest model Cancer research High 19549921
2009 ADAM23 physically interacts with cellular prion protein (PrPc) at the plasma membrane of hippocampal neurons and neuroblastoma cells; the disintegrin domain of ADAM23 is sufficient for this interaction, and the interaction is glycosylation-independent. Co-immunoprecipitation, pull-down assay with recombinant proteins (bacterial and eukaryotic), co-localization by immunofluorescence, in vitro binding with tunicamycin-treated cells Neuroscience letters Medium 19477226
2004 ADAM23 is synthesized as a ~100 kDa glycosylated precursor whose maturation to a lower molecular weight form depends on cleavage by furin or a related enzyme; mature ADAM23 is expressed primarily as a cell-surface protein localized to sites of intercellular contact in neurons. Immunoblotting with anti-ADAM23 disintegrin-domain antibody, furin inhibitor experiments, cell fractionation, tissue distribution analysis Journal of neuroscience research Medium 15505805
2012 LGI3 physically associates with ADAM23 in adipose tissue and 3T3-L1 cells; LGI3 suppresses adipogenesis through ADAM23, as the anti-adipogenic effect of exogenous LGI3 protein is abolished by ADAM23 siRNA knockdown. Pull-down, co-immunoprecipitation, immunocytochemistry, siRNA knockdown, adipogenesis assay Biochimica et biophysica acta Medium 22405860
2014 In ADAM23-heterotypic tumor environments, ADAM23-negative cells promote proliferation and invasion of adjacent ADAM23-positive cells through secretion of LGI4 and nitric oxide (NO); ablation of LGI4 and NO in ADAM23-negative cells significantly attenuates ADAM23-positive cell proliferation and invasion. In vitro co-culture functional assays, LGI4 and NO pathway ablation, in vivo tumor growth/metastasis assays Oncogene Medium 24662834
2016 ADAM23 expression on dendritic cells (DCs) governs CD4+ T cell activation, proliferation, and cytokine production (IL-2, IFN-γ, IL-4, IL-17) through the αvβ3 integrin receptor; this is independent of DC maturation profile, and neutralizing anti-αvβ3 antibodies phenocopy ADAM23 knockdown. RNAi knockdown in bone marrow-derived DCs, T cell proliferation assay, cytokine measurement, neutralizing antibody experiments Journal of leukocyte biology Medium 27317750
2016 ADAM23 suppresses lung cancer cell colony formation, adhesion, and migration through interaction with αvβ3 integrin via its disintegrin domain; these effects are abolished by anti-ADAM23, anti-αvβ3 antibodies, or ADAM23 disintegrin peptide. ADAM23 expression levels negatively regulate lung metastasis in vivo. Overexpression and shRNA knockdown, neutralizing antibody/peptide assays, in vivo lung metastasis model Cancer science Medium 26800504
2016 Four secretion-positive ADLTE-causing LGI1 missense mutations (T380A, R407C, S473L, R474Q) significantly impair LGI1 interaction with both ADAM22 and ADAM23 on the cell surface, defining a second loss-of-function mechanism distinct from impaired secretion. Co-immunoprecipitation, immunofluorescence, cell-surface binding assay, 3D protein modelling PLoS genetics Medium 27760137
2018 ADAM23 in cardiomyocytes inhibits cardiac hypertrophy by specifically targeting the FAK-AKT signaling cascade; cardiac-specific ADAM23 knockout exacerbates hypertrophy/fibrosis and ADAM23 transgenic overexpression reduces it; FAK inhibitor (PF-562271) reverses the detrimental effects of ADAM23 knockout. Cardiac-specific conditional knockout, transgenic overexpression, aortic banding model, pharmacologic FAK inhibition, signaling pathway analysis Journal of the American Heart Association High 30371220
2018 ADAM23 is present in lipid raft membrane microdomains of neuronal cells; the mature 70 kDa form partitions between raft and non-raft domains, while the pro-protein 100 kDa form is mainly in non-raft domains. Lipid raft fractionation, immunoblotting with monoclonal antibody DL11C8 (targeting cysteine-rich domain), brain region homogenates and primary cultured neurons Neuroscience Medium 29792904
2019 ADAM22 and ADAM23 modulate trafficking of LGI1: they promote its ER export and expression at the neuronal cell surface, and co-transport LGI1 in axonal vesicles to the axon initial segment (AIS). ADLTE-causing LGI1 mutations (S473L, R474Q) prevent association with ADAM22 and enrichment at the AIS. Live-cell imaging in rat hippocampal neurons, immunofluorescence co-localization, co-transport tracking, LGI1 mutant analysis Journal of cell science Medium 30598502
2019 ADAM23 negatively regulates Kv1.1 potassium currents and decreases surface expression of Kv1.1 subunits via a clathrin-independent mechanism; this regulation is not reversed by LGI1. Whole-cell patch-clamp electrophysiology, immunostaining of surface Kv1.1, transfected cultured cells, LGI1-conditioned media treatment Neuroscience letters Medium 30965109
2020 ADAM23 undergoes constitutive internalization from the plasma membrane via lipid raft-dependent endocytosis and is recycled back to the plasma membrane through early and recycling endosomes; ADAM23 has longer half-life and higher cell surface stability compared to other ADAMs. Endocytosis assays, lipid raft disruption, subcellular fractionation, pulse-chase/half-life measurement, immunofluorescence Experimental cell research Medium 33296662
2023 Axonal ADAM23 is essential for the accumulation and stability of juxtaparanodal Kv1 channel complexes; this function critically depends on ADAM23 interaction with its extracellular ligands LGI2 and LGI3. Juxtaparanodal Kv1 complexes organized via ADAM23 affect the refractory period and enable high-frequency burst firing. ADAM23 knockout mouse, immunofluorescence at juxtaparanodes, electrophysiology (refractory period measurement), genetic epistasis with LGI2/LGI3 The Journal of cell biology High 36828548
2023 ADAM23 deficiency in astrocytomas induces γ-secretase (GS) complex activity, leading to increased Amyloid-β production/deposition and NICD release, which drives increased cell infiltration; GS inhibition in ADAM23-low astrocytomas reduces invasion. In vitro and in vivo functional assays, RNA sequencing, GS activity assay, pharmacological GS inhibition Neuro-oncology advances Medium 38024245
2024 LGI3 is secreted from oligodendrocytes, enriched at juxtaparanodes, and uses ADAM23 as a receptor (shown by proteomic analysis with epitope-tagged Lgi3 knockin); the LGI3-ADAM23 interaction co-assembles Kv1 channels into juxtaparanodal nanoclusters, and loss of Lgi3 disrupts juxtaparanodal clustering of ADAM23 and Kv1 channels and suppresses Kv1-mediated short-term synaptic plasticity. Epitope-tagged knockin mouse proteomics, immunofluorescence, Lgi3 knockout mouse, electrophysiology (short-term synaptic plasticity) Cell reports High 38194969
2010 SP1 binds a specific site (-202/-190) in the proximal ADAM23 promoter; serum deprivation enhances chromatin accessibility at this site, allowing SP1 binding to recruit RNA polymerase II and upregulate ADAM23 expression. Promoter analysis, chromatin accessibility assay, electrophoretic mobility shift assay/ChIP (SP1 binding), RNA polymerase II recruitment assay Biochemical and biophysical research communications Medium 20851106
2012 ADAM23 knockdown in P19 cells promotes G1 arrest and neuronal differentiation (without RA) by upregulating P27KIP1 (and P57KIP2); recombinant GST-ADAM23 disintegrin domain inhibits this differentiation, placing the disintegrin domain as the functional suppressor of differentiation. RNAi knockdown, cell cycle analysis, recombinant domain rescue, P27KIP1 overexpression Cell biology international Medium 22973984
2025 Biallelic loss-of-function LGI1 variants result in reduced LGI1 secretion and impaired ADAM22 binding; residual LGI1 function levels correlate with clinical severity. An ADAM23 variant is associated with lethal neonatal-onset epilepsy and myopathy, genetically linking ADAM23 to the LGI1-ADAM22/23 pathway-related disease spectrum. Functional secretion assays, ADAM22-binding assays for LGI1 mutants, Lgi1-/- knockout mouse electrophysiology (isolated whole hippocampus), ADAM22-DEE mouse model behavioral analysis Brain : a journal of neurology Medium 40455867

Source papers

Stage 0 corpus · 46 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2000 ADAM 23/MDC3, a human disintegrin that promotes cell adhesion via interaction with the alphavbeta3 integrin through an RGD-independent mechanism. Molecular biology of the cell 106 10749942
2008 LGI1 and LGI4 bind to ADAM22, ADAM23 and ADAM11. International journal of biological sciences 95 18974846
2009 LGI1-associated epilepsy through altered ADAM23-dependent neuronal morphology. Molecular and cellular neurosciences 78 19796686
1998 Metalloproteinase-like, disintegrin-like, cysteine-rich proteins MDC2 and MDC3: novel human cellular disintegrins highly expressed in the brain. The Biochemical journal 74 9693107
2007 Methylation profile of genes CDKN2A (p14 and p16), DAPK1, CDH1, and ADAM23 in head and neck cancer. Cancer genetics and cytogenetics 70 17284367
2005 ADAM23, a possible tumor suppressor gene, is frequently silenced in gastric cancers by homozygous deletion or aberrant promoter hypermethylation. Oncogene 59 16103878
1999 Cloning and chromosomal mapping of mouse ADAM11, ADAM22 and ADAM23. Gene 55 10433968
2004 Epigenetic silencing of the adhesion molecule ADAM23 is highly frequent in breast tumors. Oncogene 51 14661055
2009 ADAM23 negatively modulates alpha(v)beta(3) integrin activation during metastasis. Cancer research 47 19549921
2019 ADAM22 and ADAM23 modulate the targeting of the Kv1 channel-associated protein LGI1 to the axon initial segment. Journal of cell science 37 30598502
2004 ADAM23 is a cell-surface glycoprotein expressed by central nervous system neurons. Journal of neuroscience research 34 15505805
2015 CXCL12 and ADAM23 hypermethylation are associated with advanced breast cancers. Translational research : the journal of laboratory and clinical medicine 30 25620615
2012 Leucine-rich glioma inactivated 3 regulates adipogenesis through ADAM23. Biochimica et biophysica acta 29 22405860
2009 Promoter hypermethylation of the ADAM23 gene in colorectal cancer cell lines and cancer tissues. International journal of cancer 27 19089928
2016 ADAM23 is downregulated in side population and suppresses lung metastasis of lung carcinoma cells. Cancer science 26 26800504
2021 Mechanism and Role of the Neuropeptide LGI1 Receptor ADAM23 in Regulating Biomarkers of Ferroptosis and Progression of Esophageal Cancer. Disease markers 25 35003396
2016 Dendritic cell expression of ADAM23 governs T cell proliferation and cytokine production through the α(v)β(3) integrin receptor. Journal of leukocyte biology 25 27317750
2018 ADAM23 in Cardiomyocyte Inhibits Cardiac Hypertrophy by Targeting FAK - AKT Signaling. Journal of the American Heart Association 23 30371220
2017 ADAM23 is a common risk gene for canine idiopathic epilepsy. BMC genetics 21 28143391
2015 Identification of a common risk haplotype for canine idiopathic epilepsy in the ADAM23 gene. BMC genomics 21 26084559
2016 Secretion-Positive LGI1 Mutations Linked to Lateral Temporal Epilepsy Impair Binding to ADAM22 and ADAM23 Receptors. PLoS genetics 19 27760137
2014 Intratumoral heterogeneity of ADAM23 promotes tumor growth and metastasis through LGI4 and nitric oxide signals. Oncogene 19 24662834
2023 LGI3/2-ADAM23 interactions cluster Kv1 channels in myelinated axons to regulate refractory period. The Journal of cell biology 16 36828548
2017 ADAM23 promotes neuronal differentiation of human neural progenitor cells. Cellular & molecular biology letters 16 28828010
2005 ADAM23 methylation and expression analysis in brain tumors. Neuroscience letters 16 15862898
2007 ADAM23 plays multiple roles in neuronal differentiation of P19 embryonal carcinoma cells. Neurochemical research 14 17333391
2019 ADAM23 is a negative regulator of Kv1.1/Kv1.4 potassium currents. Neuroscience letters 13 30965109
2018 Decreased methylation in the SNAI2 and ADAM23 genes associated with de-differentiation and haematogenous dissemination in breast cancers. BMC cancer 13 30189837
2011 The expression of ADAM23 and its correlation with promoter methylation in non-small-cell lung carcinoma. International journal of experimental pathology 12 21429053
2009 Characterization of a specific interaction between ADAM23 and cellular prion protein. Neuroscience letters 11 19477226
2024 Oligodendrocyte-derived LGI3 and its receptor ADAM23 organize juxtaparanodal Kv1 channel clustering for short-term synaptic plasticity. Cell reports 10 38194969
2023 Identification of ADAM23 as a Potential Signature for Psoriasis Using Integrative Machine-Learning and Experimental Verification. International journal of general medicine 8 38148887
2015 Differential Expression of ADAM23, CDKN2A (P16), MMP14 and VIM Associated with Giant Cell Tumor of Bone. Journal of Cancer 7 26078788
2004 Two novel isoforms of Adam23 expressed in the developmental process of mouse and human brains. Gene 7 14697522
2012 ADAM23 knockdown promotes neuronal differentiation of P19 embryonal carcinoma cells by up-regulating P27KIP1 expression. Cell biology international 6 22973984
2010 SP1 acts as a key factor, contributes to upregulation of ADAM23 expression under serum deprivation. Biochemical and biophysical research communications 4 20851106
2020 Endocytosis of the non-catalytic ADAM23: Recycling and long half-life properties. Experimental cell research 3 33296662
2010 ADAM23, a Gene Related to LGI1, Is Not Linked to Autosomal Dominant Lateral Temporal Epilepsy. Epilepsy research and treatment 3 22937229
2018 Monoclonal Antibody DL11C8 Identifies ADAM23 as a Component of Lipid Raft Microdomains. Neuroscience 2 29792904
2025 Biallelic LGI1 and ADAM23 variants cause hippocampal epileptic encephalopathy via the LGI1-ADAM22/23 pathway. Brain : a journal of neurology 1 40455867
2025 ADAM23 haploinsufficiency as a putative oligogenic contributor in an individual with focal epilepsy. Seizure 1 40865352
2023 A novel program of infiltrative control in astrocytomas: ADAM23 depletion promotes cell invasion by activating γ-secretase complex. Neuro-oncology advances 1 38024245
2026 Species-Specific Parent-Of-Origin Expression of Adam23 in the Mammalian Brain. Genes to cells : devoted to molecular & cellular mechanisms 0 41568889
2026 Epitranscriptomic Regulation of Platinum Resistance via the METTL3-ADAM23 Axis in Ovarian Cancer. Cells 0 41677656
2026 Gene burden meta-analysis of 748 879 individuals identifies LGI1-ADAM23 protein complex association with epilepsy. Epilepsia 0 42216960
2025 Case Report: Anti-ADAM23 antibody: an overlooked autoantibody against VGKC-complex in autoimmune encephalitis. Frontiers in immunology 0 40519920

Missed literature

Know a paper Affinage missed for ADAM23? Flag it for the maintainers and the community.

No submissions yet.