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FLASH GENE
Symbol ADAM23 contributors: npt/mct - updated : 16-11-2022
HGNC name ADAM metallopeptidase domain 23
HGNC id 202
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • domains similar to hemorrhagic snake venom proteins (HSVP)
  • a disrupted Zn-binding site metalloproteinase
  • a zinc metalloprotease domain
  • a disintegrin domain that may serve as an integrin ligand, able to interact directly with PRNP
  • a cysteine-rich domain
  • an EGF-like repeat
  • a transmembrane domain and a cytoplasmic tail
  • conjugated GlycoP , MetalloP
    HOMOLOGY
    Homologene
    FAMILY
  • ADAM (a disintegrin and metalloprotease domain) family
  • CATEGORY adhesion
    SUBCELLULAR LOCALIZATION extracellular
        plasma membrane
    basic FUNCTION
  • a disintegrin and metalloprotease, cell surface adhesion protein
  • may play roles in the development and maintenance of neural function
  • may serves to mediate cell-cell interactions within the CNS
  • functional role during metastatic progression by negatively modulating alpha(5)beta(3) integrin activation
  • is important for the development of CNS (central nervous system)
  • ADAM23 regulates likely neuronal differentiation by triggering specific signaling pathways during human neural progenitor cells (hNPCs) differentiation
  • is recycled from intracellular compartments back to the plasma membrane and thus has longer half-life and higher cell surface stability compared with other ADAMs
  • CELLULAR PROCESS protein, degradation
    cell organization/biogenesis
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule metal binding,
  • Zn2+
  • protein
  • binding to integrin alphavbeta 3
  • with ADAM22 and ADAM11, binds LGI1 and LGI4 (LGI-ADAM system seems to be regulated not only by the affinity but also by the cell-type-specific expression of each protein) (Sagane 2008)
  • LGI1 binding to ADAM23 is necessary to correctly pattern neuronal morphology and altered anatomical patterning contributes to partial epilepsy with auditory features
  • physical interaction between ADAM23 and both recombinant and endogenous PRNP
  • ADAM23 is a negative regulator of cardiac hypertrophy through inhibiting focal adhesion kinase-protein kinase B signaling pathway
  • ADAM22 and ADAM23 modulate the trafficking of LGI1, and promote its ER export and expression at the overall neuronal cell surface
  • cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral     --low  
    silenced in gastric cancer by homozygous deletion or aberrant promoter hypermethylation
    tumoral     --low  
    by aberrant promoter hypermethylation during the progression of colorectal cancer
    tumoral     --low  
    low expression levels of LGI3, ADAM22 and ADAM23 were significantly associated with poor prognosis of glioma
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    cancer  
    regulation of ADAM23 endocytosis/stability could be exploited therapeutically in diseases in which ADAM23 is directly involved, such as cancer progression
    neurologyepilepsy 
    regulation of ADAM23 endocytosis/stability could be exploited therapeutically in diseases in which ADAM23 is directly involved, such as epilepsy
    cardiovascularaquiredheart failure
    regulation of ADAM23 endocytosis/stability could be exploited therapeutically in diseases in which ADAM23 is directly involved, such as cardiac hypertrophy
    ANIMAL & CELL MODELS