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FLASH GENE

Symbol

ADAM23

contributors: npt/mct - updated : 16-11-2022

HGNC name	ADAM metallopeptidase domain 23
HGNC id	202

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

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)

Type Gene Modification Chromosome rearrangement Protein expression Protein 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
	System Type Disorder Pubmed cancer     regulation of ADAM23 endocytosis/stability could be exploited therapeutically in diseases in which ADAM23 is directly involved, such as cancer progression neurology epilepsy   regulation of ADAM23 endocytosis/stability could be exploited therapeutically in diseases in which ADAM23 is directly involved, such as epilepsy cardiovascular aquired heart 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