Target intelligence / Profile preview

Disintegrin and metalloproteinase domain-containing protein 11 (ADAM11)

Target
ADAM11
Molecular classification
Enzyme (specifically a metalloendopeptidase/metalloproteinase, although ADAM11 is classified as non-proteolytic), Membrane-anchored protein
01

Overview

Disintegrin and metalloproteinase domain-containing protein 11 (ADAM11) is a member of the ADAM (a disintegrin and metalloprotease) family, encoded by the ADAM11 gene. Unlike many ADAMs, ADAM11 lacks proteolytic activity (non-catalytic) and functions primarily in protein-protein interactions and cell signaling regulation. ADAM11 is membrane-anchored and implicated in cell adhesion, migration, neural development, spatial learning, motor coordination, and nociceptive pain response[4]. It has an established role as a regulator of Wnt and BMP4 signaling pathways, impacting embryonic neural crest development and proliferation[2]. ADAM11 is considered a tumor suppressor candidate in breast cancer due to its genomic location and observed expression patterns[3][4]. Decreased ADAM11 expression is found in many solid tumors, correlating with upregulation of Wnt signaling and proliferation markers (CyclinD1); in neuroblastoma, increased ADAM11 expression correlates with stem cell marker profiles[2]. There are currently no known drugs that directly target ADAM11, and its modulation presents significant safety concerns due to its role in neural development and tissue homeostasis.

Other names
Disintegrin and metalloproteinase domain-containing protein 11ADAM11MDCADAM 11Metalloproteinase-like, disintegrin-like, and cysteine-rich proteinMDC protein
02

Biological functions

Cell-cell and cell-matrix interactionRegulation of signaling pathways (Wnt and BMP4)Spatial learning and motor coordinationNociceptive pain responseInfluences neural crest cell migration and differentiation
03

Disease associations

Cancer (notably breast cancer; candidate tumor suppressor)Neurodevelopmental disordersEpilepsy (Familial temporal lobe epilepsy)Neuroblastoma
04

Safety considerations

Therapeutic modulation could disrupt neural development or stem cell homeostasisFine control of ADAM11 appears necessary for normal development; both increased and decreased expression may contribute to pathology
05

Biomarkers

Altered expression in solid tumors (reduced expression correlates with increased Wnt signaling and Cyclin D1)High in neuroblastoma (correlates with increased Smad1/5 and decreased Sox3)

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