Normal function · from ai-gene-review (O14672, commit e7236877cf14) · AI-generated, not KB evidence

ADAM10 encodes a single-pass type I transmembrane zinc metalloprotease of the ADAM family. The mature enzyme acts mainly at the cell surface, Golgi-derived vesicles, synaptic membranes, adherens junctions, and tetraspanin-enriched membrane domains, where it cleaves extracellular juxtamembrane regions of many membrane proteins. Its core roles are membrane-protein ectodomain shedding and alpha-secretase processing, including non-amyloidogenic cleavage of APP, S2 cleavage of Notch receptors, and processing of adhesion molecules, growth-factor and cytokine precursors, immune receptors, and other signaling substrates. ADAM10 localization, maturation, endocytosis, and substrate selectivity are regulated by tetraspanins, clathrin/AP2-dependent trafficking, and substrate-specific adaptor contexts.

ADAM10 is a zinc-dependent type I membrane metalloendopeptidase that performs ectodomain shedding and alpha-secretase cleavage of transmembrane substrates at the cell surface and regulated membrane compartments.
In the knowledge base · computed from kb/ at build time

Disorders

Relationship is the entry's genetic[].relationship_type. untyped means the entry has a genetic record for the gene but does not type it; its free-text association is shown instead.

DisorderRelationshipWhere the gene appears
Alzheimer Disease risk factor
mechanism: Amyloid Plaque Formation
scoped to subtype: Late-Onset Alzheimer's Disease
Reticulate Acropigmentation Of Kitamura causative germline loss of function
mechanism: ADAM10 Loss of Function

Identity from HGNC (snapshot 2026-10-24). Page layers are described in the gene pages documentation.