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FLASH GENE

Symbol

ADAM10

contributors: mct - updated : 14-10-2018

HGNC name	ADAM metallopeptidase domain 10
HGNC id	188

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

ASSOCIATED DISORDERS

corresponding disease(s)

RAK

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function constitutional     --over   in atrial fibrillation constitutional     --low   in platelet of Alzheimer disease tumoral       gain of function by RAR and acitretin, resulting in an increase of the ratio between alpha- and beta-secretase activity in neuroblastoma cells constitutional       gain of function constitutive activation of ADAM10 contributes to the growth of mantle cell lymphoma constitutional     --other   in FRA X fibroblasts, a dual dysregulation of APP and ADAM10 leads to the production of an excess of soluble APPalpha and to synaptic and behavioral deficits

Susceptibility

Variant & Polymorphism

Candidate gene	participating in signaling intrinsic to NOTCH1 mutations associated with leukemia
	candidate gene for Alzeihmer's disease with two potentially pathogenic mutations (Q170H, R181G) with incomplete penetrance
Marker
Therapy target
	System Type Disorder Pubmed neurology neurodegenerative alzheimer pharmacological activation of alpha-secretase (ADAM10) may be a therapeutic approach to Alzheimer disease cancer digestive liver antidrug cancer can modulate expression of ADAM10, epirubicin therapy may have an effect on antitumor immunity in hepatocellular carcinoma patients neurology neurodegenerative alzheimer activation of ADAM10 by epigallocatechin-3-gallate (EGCG), and promotion of non-amyloidogenic APP processing is warranted to support the use of this compound as a safe alternative to estrogen replacement therapy in the prevention and treatment of Alzheime cancer hemopathy   may be a useful strategy to enhance the response of mantle cell lymphoma to other therapeutic agents mental retardation fragile X   downregulation of ADAM10 activity at synapses may be an effective strategy for ameliorating Fragile X phenotypes neurology neurodegenerative alzheimer increasing ADAM10 activity is suggested as a therapy to prevent the production of the neurotoxic APP peptide in Alzheimer disease

ANIMAL & CELL MODELS

ADAM10-null mice display no obvious alteration of myelination