Affinage

ADAM23

Disintegrin and metalloproteinase domain-containing protein 23 · UniProt O75077

Length
832 aa
Mass
91.9 kDa
Annotated
2026-04-28
45 papers in source corpus 23 papers cited in narrative 23 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ADAM23 is a catalytically inactive member of the ADAM transmembrane protein family that functions as a cell-surface adhesion molecule and receptor, with principal roles in CNS development, axonal excitability, and integrin regulation. Its disrupted metalloprotease domain renders it protease-dead, but its disintegrin domain mediates RGD-independent binding to αvβ3 integrin, negatively modulating integrin activation and thereby suppressing cell migration and metastatic behaviors (PMID:10749942, PMID:19549921). ADAM23 serves as a neuronal receptor for secreted LGI family proteins (LGI1–LGI4), and through LGI2/LGI3 interactions organizes juxtaparanodal Kv1 potassium channel complexes that control the refractory period, high-frequency burst firing, and short-term synaptic plasticity, while also promoting LGI1 trafficking to the axon initial segment and supporting dendritic arborization (PMID:36828548, PMID:38194969, PMID:19796686, PMID:30598502). Biallelic loss-of-function variants in ADAM23 cause lethal neonatal-onset epilepsy and myopathy in humans (PMID:40455867).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1998 High

    Sequence analysis established that ADAM23 belongs to a subfamily of catalytically inactive ADAMs, resolving whether it could act as a sheddase and redirecting attention to its disintegrin domain as the functional module.

    Evidence Deduced amino acid sequence showing disrupted zinc-binding motif in the metalloprotease domain

    PMID:9693107

    Open questions at the time
    • No direct experimental demonstration of protease inactivity via enzyme assay
    • Functional significance of the intact disintegrin domain was untested
  2. 2000 High

    The disintegrin domain was shown to mediate direct, RGD-independent binding to αvβ3 integrin, establishing ADAM23 as a cell-adhesion molecule rather than a protease.

    Evidence Recombinant protein binding assays with integrin-blocking reagents, HeLa transfection with full-length ADAM23

    PMID:10749942

    Open questions at the time
    • Physiological cell type and tissue context of the integrin interaction were unknown
    • Whether ADAM23 regulated integrin signaling directionally was untested
  3. 2004 Medium

    Biochemical characterization revealed that ADAM23 undergoes furin-dependent maturation and localizes to intercellular contacts on CNS neurons, placing it at a position consistent with adhesive function.

    Evidence Western blot with domain-specific antibody, furin inhibitor experiments, immunostaining of cerebellar granule neurons

    PMID:15505805

    Open questions at the time
    • Whether furin cleavage is required for adhesive or receptor functions was not tested
    • The identity of cell-surface binding partners at neuronal contacts was unknown
  4. 2008 High

    Identification of LGI1 and LGI4 as secreted ligands for ADAM23 established that ADAM23 functions as a receptor in trans-synaptic and intercellular signaling, expanding its role beyond integrin-mediated adhesion.

    Evidence Co-immunoprecipitation from brain lysates, mass spectrometry, quantitative cell-ELISA binding assay

    PMID:18974846

    Open questions at the time
    • Downstream signaling consequences of LGI binding to ADAM23 were unknown
    • Whether different LGI family members signal through ADAM23 in distinct tissues was untested
  5. 2009 High

    Three parallel studies revealed that ADAM23 negatively modulates αvβ3 integrin activation (suppressing migration and metastasis), mediates LGI1-dependent dendritic arborization and neurite outgrowth, and interacts with cellular prion protein at the neuronal surface, diversifying ADAM23's known functional repertoire.

    Evidence shRNA knockdown with integrin activation assays and in vivo pulmonary arrest model; ADAM23 KO mouse with seizures and reduced dendritic arbors plus neurite outgrowth assays; Co-IP and pull-down identifying PrPc interaction via disintegrin domain

    PMID:19477226 PMID:19549921 PMID:19796686

    Open questions at the time
    • Whether integrin-modulation and LGI-receptor functions operate independently or coordinately was unknown
    • Functional consequence of PrPc interaction was not determined
    • Mechanism linking ADAM23 loss to seizures was unclear
  6. 2012 Medium

    ADAM23 was found to participate in non-neural signaling: it mediates LGI3-dependent suppression of adipogenesis and regulates neuronal differentiation through P27KIP1 and cell-cycle control, indicating context-dependent functions.

    Evidence Co-IP and siRNA rescue in 3T3-L1 adipogenesis assays; RNAi knockdown in P19 cells with cell-cycle analysis and recombinant disintegrin domain rescue

    PMID:22405860 PMID:22973984

    Open questions at the time
    • Signaling intermediates downstream of ADAM23 in adipocytes were not identified
    • P27KIP1 regulation mechanism by ADAM23 was not elucidated
  7. 2016 Medium

    Studies demonstrated that ADAM23 functions in immune cells—governing dendritic cell-mediated T cell activation via αvβ3 integrin—and that ADLTE-causing LGI1 mutations specifically disrupt LGI1 binding to ADAM22/ADAM23 receptors, linking ADAM23 to human epilepsy pathogenesis.

    Evidence RNAi in BMDCs with T cell assays and anti-αvβ3 phenocopy; Co-IP of secretion-competent ADLTE LGI1 mutants showing impaired ADAM22/23 binding

    PMID:27317750 PMID:27760137

    Open questions at the time
    • Whether ADAM23 on DCs signals bidirectionally with T cells was unknown
    • Whether ADAM23-specific LGI1-binding loss versus ADAM22 loss differentially contributes to epilepsy was not resolved
  8. 2018 High

    ADAM23 was shown to exert anti-hypertrophic effects in cardiomyocytes by inhibiting FAK-AKT signaling, and the mature form was found to partition into lipid raft membrane domains, suggesting signaling-competent microdomains.

    Evidence Cardiac-specific KO and transgenic overexpression mice with pressure-overload model and FAK inhibitor rescue; detergent-resistant membrane fractionation in brain and primary neurons

    PMID:29792904 PMID:30371220

    Open questions at the time
    • How ADAM23 inhibits FAK at the molecular level (direct vs. indirect) was not resolved
    • Whether lipid raft partitioning is functionally required for signaling or adhesion was untested
  9. 2019 High

    ADAM23 was established as a co-transporter of LGI1 to the axon initial segment and a negative regulator of Kv1.1 surface expression and currents, defining its role in organizing the molecular architecture of axonal excitability.

    Evidence Live-cell axonal transport imaging in rat hippocampal neurons; whole-cell patch-clamp electrophysiology and Kv1.1 surface quantification in transfected cells

    PMID:30598502 PMID:30965109

    Open questions at the time
    • Whether ADAM23-mediated Kv1.1 downregulation occurs in vivo at native nodes was unknown
    • Mechanism of Kv1.1 surface-expression reduction (retention, degradation, or redistribution) was not determined
  10. 2020 Medium

    ADAM23 was found to undergo constitutive lipid-raft-dependent endocytosis and recycling, with higher surface stability than other ADAMs, providing a trafficking framework for its sustained adhesive and receptor functions.

    Evidence Endocytosis, recycling, and half-life assays with lipid raft disruption

    PMID:33296662

    Open questions at the time
    • Whether endocytic cycling is regulated by LGI binding or neuronal activity was not tested
    • Recycling pathway components were not identified
  11. 2023 High

    In vivo ADAM23 knockout and LGI3 knockout studies demonstrated that axonal ADAM23 is essential for juxtaparanodal Kv1 channel clustering through LGI2/LGI3 interactions, controlling the refractory period, high-frequency firing, and short-term synaptic plasticity—resolving the functional consequence of ADAM23 at myelinated axons.

    Evidence ADAM23 KO and Lgi3 KO mice with Kv1 clustering quantification, electrophysiological refractory period measurement, short-term plasticity assays, oligodendrocyte-derived LGI3 proteomics

    PMID:36828548 PMID:38194969

    Open questions at the time
    • Whether ADAM23 organizes other juxtaparanodal components beyond Kv1 channels is unknown
    • Structural basis of the ADAM23–LGI2/LGI3–Kv1 complex has not been determined
  12. 2025 Medium

    Human genetics established that biallelic ADAM23 loss-of-function variants cause lethal neonatal epilepsy and myopathy, confirming ADAM23 as an essential gene in the LGI1–ADAM22/23 excitatory synapse pathway in humans.

    Evidence International patient cohort with biallelic ADAM23 variants, functional validation of LGI1 variant secretion and ADAM22 binding, Lgi1 KO hippocampal electrophysiology

    PMID:40455867

    Open questions at the time
    • Number of families is limited; broader phenotypic spectrum is undefined
    • Whether ADAM23 loss causes disease through Kv1 channel, LGI1-trafficking, or integrin-dependent mechanisms is unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • The structural basis of the ADAM23–LGI–Kv1 supramolecular complex, the mechanism by which ADAM23 inhibits FAK, and whether integrin-modulating and LGI-receptor functions are coordinated or independent remain unresolved.
  • No cryo-EM or crystal structure of any ADAM23 complex exists
  • Relative contributions of ADAM23's integrin-binding versus LGI-receptor functions to seizure phenotypes are unknown
  • Whether ADAM23 functions at the juxtaparanode also regulate synaptic transmission at central synapses is untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0098631 cell adhesion mediator activity 3 GO:0098772 molecular function regulator activity 3
Localization
GO:0005886 plasma membrane 5 GO:0005768 endosome 1 GO:0005856 cytoskeleton 1
Pathway
R-HSA-112316 Neuronal System 5 R-HSA-1500931 Cell-Cell communication 3 R-HSA-1266738 Developmental Biology 2 R-HSA-162582 Signal Transduction 2 R-HSA-168256 Immune System 1
Partners
ADAM22ITGAVITGB3LGI1LGI2LGI3LGI4PRNP
Complex memberships
LGI1-ADAM22/ADAM23 complexLGI2/LGI3-ADAM23-Kv1 juxtaparanodal complex

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 The disintegrin-like domain of ADAM23 promotes cell adhesion through a specific interaction with αvβ3 integrin via an RGD-independent mechanism; the short amino acid sequence in the disintegrin loop mediates this binding, and full-length ADAM23-transfected HeLa cells also support αvβ3-mediated adhesion. Recombinant protein binding assays, integrin-specific blocking experiments, HeLa cell transfection with full-length cDNA Molecular biology of the cell High 10749942
1998 ADAM23 (MDC3) has a disrupted zinc-binding motif in its metalloprotease-like domain, indicating it lacks catalytic protease activity, while retaining a disintegrin-like domain capable of integrin ligand interactions. Sequence analysis of deduced amino acid sequence; identification of disrupted zinc-binding motif The Biochemical journal High 9693107
2008 ADAM23 binds LGI1 and LGI4; LGI1 and LGI4 interact with ADAM22, ADAM23, and ADAM11 with significant but differential binding affinities, establishing ADAM23 as a receptor for LGI family ligands. Immunoprecipitation of brain lysates, mass spectrometric identification, quantitative cell-ELISA binding assay International journal of biological sciences High 18974846
2009 LGI1 binding to ADAM23 is required for normal neuronal morphology: ADAM23 knockout neurons show reduced dendritic arborization, LGI1 promotes neurite outgrowth in wild-type but not ADAM23-/- neurons, and ADAM23-/- mice exhibit spontaneous seizures. Unbiased brain binding screen, 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-mediated knockdown of ADAM23 in MDA-MB-435 cells enhanced αvβ3 integrin activation by 2-4 fold, increased cell migration, adhesion to αvβ3 ligands, and pulmonary tumor cell arrest in vivo. shRNA knockdown, integrin activation assays, migration/adhesion assays, in vivo mouse pulmonary arrest model Cancer research High 19549921
2004 ADAM23 is synthesized as a ~100 kDa glycosylated precursor whose maturation requires cleavage by furin or a related enzyme, and the mature protein is expressed primarily at the cell surface localized to sites of intercellular contact in CNS neurons. Western blotting, antibody raised against disintegrin domain, furin inhibitor experiments, immunostaining of cerebellar granule cells Journal of neuroscience research Medium 15505805
2009 ADAM23 physically interacts with cellular prion protein (PrPc) at the plasma membrane of hippocampal neurons; the disintegrin domain of ADAM23 mediates this interaction, which is glycosylation-independent. Co-immunoprecipitation, pull-down assays with recombinant and endogenous proteins, co-localization immunofluorescence, in vitro binding with bacterially expressed proteins Neuroscience letters Medium 19477226
2012 LGI3 associates with ADAM23 in adipose tissue and 3T3-L1 cells; LGI3 suppresses adipogenesis through ADAM23, as LGI3 treatment attenuates adipogenesis and this effect is reversed by siRNA knockdown of ADAM23. Pull-down, co-immunoprecipitation, immunocytochemistry, siRNA knockdown, adipogenesis assays Biochimica et biophysica acta Medium 22405860
2014 In intratumoral heterogeneous environments, ADAM23-negative cells promote proliferation and invasion of ADAM23-positive cells through secretion of LGI4 and nitric oxide; ablation of LGI4 and NO in ADAM23-negative cells attenuates ADAM23-positive cell proliferation and invasion. In vitro co-culture functional assays, LGI4 and NO ablation experiments, in vivo tumor models Oncogene Medium 24662834
2016 Four secretion-positive ADLTE-causing LGI1 mutations (T380A, R407C, S473L, R474Q) impair LGI1 interaction with ADAM22 and ADAM23 receptors at the cell surface without affecting protein folding or secretion, revealing a second loss-of-function mechanism. Co-immunoprecipitation, immunofluorescence, 3D protein modelling, cell-surface binding assays PLoS genetics Medium 27760137
2016 ADAM23 expression on dendritic cells governs CD4+ T cell activation, proliferation, and cytokine production via αvβ3 integrin; ADAM23 knockdown in BMDCs impairs cognate T cell responses, and anti-αvβ3 neutralizing antibodies phenocopy ADAM23 knockdown. RNAi knockdown in BMDCs, T cell proliferation and cytokine assays, αvβ3 neutralizing antibody experiments Journal of leukocyte biology Medium 27317750
2016 ADAM23 suppresses lung cancer cell colony formation, adhesion, and migration through its interaction with αvβ3 integrin; these effects are blocked by neutralizing anti-ADAM23 antibody, anti-αvβ3 antibody, or ADAM23 disintegrin peptide. ADAM23 expression negatively regulates lung metastasis in vivo. Overexpression and shRNA knockdown, colony formation assays, adhesion and migration assays, neutralizing antibodies, in vivo metastasis model Cancer science Medium 26800504
2018 ADAM23 exerts anti-hypertrophic effects in cardiomyocytes by specifically inhibiting the FAK-AKT signaling cascade; cardiac-specific ADAM23 knockout exacerbates hypertrophy and dysfunction while ADAM23 transgenic overexpression is protective, and FAK inhibition reverses the detrimental effects of ADAM23 knockout. Cardiac-specific conditional KO mice, ADAM23 transgenic overexpression mice, aortic banding pressure overload model, FAK inhibitor (PF-562271) rescue, AngII-induced neonatal cardiomyocyte hypertrophy Journal of the American Heart Association High 30371220
2019 ADAM22 and ADAM23 modulate LGI1 trafficking: they promote LGI1 ER export and expression at the neuronal cell surface, and LGI1 is co-transported in axonal vesicles with ADAM22 and ADAM23 to the axon initial segment where it colocalizes with Kv1 channels. ADLTE missense mutations in LGI1 prevent its association with ADAM22 and enrichment at the AIS. Live-cell imaging, immunofluorescence in rat hippocampal neurons, dominant-negative and overexpression approaches, co-transport analysis Journal of cell science High 30598502
2019 ADAM23 is a negative regulator of Kv1.1 currents: ADAM23 expression causes decreased surface expression of Kv1.1 subunits and reduced voltage-gated potassium currents, independent of clathrin-mediated endocytosis. This effect is not reversed by LGI1-conditioned media, contrasting with ADAM22 which potentiates Kv1.1 currents in the presence of LGI1. Whole-cell patch-clamp electrophysiology, immunostaining of Kv1.1, surface expression quantification in transfected cells, LGI1-conditioned media treatment Neuroscience letters Medium 30965109
2020 ADAM23 undergoes constitutive internalization from the plasma membrane via a lipid raft-dependent mechanism, is redistributed to early and recycling endosomes, recycled back to the plasma membrane, and has a longer half-life and higher cell surface stability compared to other ADAMs. Endocytosis assays, lipid raft disruption, subcellular fractionation, recycling assays, half-life determination Experimental cell research Medium 33296662
2018 ADAM23 mature protein (70 kDa) partitions between lipid raft and non-raft membrane domains, while the pro-protein form (100 kDa) is mainly in non-raft domains; this localization was confirmed in brain region homogenates and primary cultured neurons. Detergent-resistant membrane fractionation, monoclonal antibody (DL11C8) against cysteine-rich domain, immunoblotting of brain regions and cultured neurons Neuroscience Medium 29792904
2023 Axonal ADAM23 is essential for accumulation and stability of juxtaparanodal Kv1 channel complexes, functioning critically through interaction with its extracellular ligands LGI2 and LGI3; juxtaparanodal Kv1 complexes affect the refractory period and enable high-frequency burst firing. ADAM23 knockout mouse analysis, Kv1 channel clustering quantification, electrophysiological refractory period measurement, LGI2/LGI3 interaction studies The Journal of cell biology High 36828548
2024 LGI3 is secreted from oligodendrocytes and uses ADAM23 as a receptor to organize juxtaparanodal Kv1 channel clustering; loss of LGI3 disrupts juxtaparanodal clustering of ADAM23 and Kv1 channels and suppresses Kv1-channel-mediated short-term synaptic plasticity. Epitope-tagged Lgi3 knockin mice, proteomic analysis, Lgi3 knockout mouse analysis, electrophysiology for short-term synaptic plasticity, immunofluorescence Cell reports High 38194969
2010 SP1 binds a site at -202/-190 of the ADAM23 proximal promoter; serum deprivation enhances chromatin accessibility at this site, promoting SP1 binding and RNA polymerase II recruitment, resulting in upregulation of ADAM23 expression. Promoter reporter assays, chromatin accessibility assays, SP1 binding site mutagenesis, ChIP for RNA polymerase II Biochemical and biophysical research communications Medium 20851106
2012 ADAM23 knockdown in P19 cells promotes neuronal differentiation through upregulation of P27KIP1, causing G1 arrest; recombinant GST-ADAM23 disintegrin domain protein inhibits neuronal differentiation, indicating the disintegrin domain mediates suppression of differentiation. RNAi knockdown, cell cycle analysis, P27KIP1 expression analysis, recombinant disintegrin domain protein rescue experiment Cell biology international Medium 22973984
2023 ADAM23 deficiency in astrocytomas induces γ-secretase complex activity, contributing to production and deposition of amyloid-β and release of NICD, promoting cell invasion; γ-secretase ablation in ADAM23-low astrocytomas inhibits invasive programs. In vitro and in vivo functional assays, RNA sequencing, γ-secretase activity assays, pharmacological inhibition Neuro-oncology advances Medium 38024245
2025 Biallelic ADAM23 variants cause lethal neonatal-onset epilepsy and myopathy, placing ADAM23 within the LGI1-ADAM22/23 pathway that regulates excitatory synaptic transmission; functional analyses of LGI1 variants showed reduced secretion and ADAM22-binding, and hippocampal epileptic discharges were observed in Lgi1-/- knockout mice. Human genetics (international data sharing), functional analyses of LGI1 secretion and ADAM22-binding, isolated whole-hippocampus electrophysiology in Lgi1-/- mice Brain : a journal of neurology Medium 40455867

Source papers

Stage 0 corpus · 45 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 94 18974846
2009 LGI1-associated epilepsy through altered ADAM23-dependent neuronal morphology. Molecular and cellular neurosciences 77 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
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 ADAM23 is downregulated in side population and suppresses lung metastasis of lung carcinoma cells. Cancer science 25 26800504
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 24 27317750
2018 ADAM23 in Cardiomyocyte Inhibits Cardiac Hypertrophy by Targeting FAK - AKT Signaling. Journal of the American Heart Association 21 30371220
2015 Identification of a common risk haplotype for canine idiopathic epilepsy in the ADAM23 gene. BMC genomics 21 26084559
2017 ADAM23 is a common risk gene for canine idiopathic epilepsy. BMC genetics 20 28143391
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
2005 ADAM23 methylation and expression analysis in brain tumors. Neuroscience letters 16 15862898
2017 ADAM23 promotes neuronal differentiation of human neural progenitor cells. Cellular & molecular biology letters 15 28828010
2023 LGI3/2-ADAM23 interactions cluster Kv1 channels in myelinated axons to regulate refractory period. The Journal of cell biology 14 36828548
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 7 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
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
2025 Case Report: Anti-ADAM23 antibody: an overlooked autoantibody against VGKC-complex in autoimmune encephalitis. Frontiers in immunology 0 40519920
2025 ADAM23 haploinsufficiency as a putative oligogenic contributor in an individual with focal epilepsy. Seizure 0 40865352