Target intelligence / Profile preview

Monooxygenase DBH-like 1 (MOXD1)

Target
MOXD1
Molecular classification
Enzyme, Copper-dependent monooxygenase, Oxidoreductase, Membrane protein
01

Overview

Monooxygenase DBH-like 1 (MOXD1) is a membrane-bound, copper-dependent, ascorbate-requiring enzyme belonging to the type II monooxygenase family. It shares key structural features with dopamine beta-monooxygenase and related enzymes involved in monoamine metabolism, though its preferred natural substrate is unclear. MOXD1 localizes to the endoplasmic reticulum and is tightly membrane-associated, participating in hydroxylation reactions of hydrophobic substrates and post-translational modifications such as glycosylation. In normal physiology, it is linked to neurotransmitter biosynthesis and neural crest development. In cancer biology, elevated MOXD1 expression promotes glioblastoma cell proliferation and migration, while its reduced expression functions as a "tumor suppressor" in neuroblastoma. MOXD1 knockdown induces apoptosis through ER-mitochondrial stress pathways and disrupts cell cycle progression. These findings highlight MOXD1 as a candidate therapeutic target in oncology and a potential biomarker for cancer progression and prognosis[1][2][3][4][5].

Other names
DBH-like monooxygenase protein 1monooxygenase XMOXPRO5780DJ248E1.1UNQ2493/PRO5780dJ248E1.1dopamine-oxygenaseDBH-related proteinMNCb-52033230402N08Rik
02

Mechanism of action

No specific agents documented; in glioblastoma, MOXD1 modulates ER stress and apoptosis, glycosylation pathways, and cancer cell viability and migration—thus, hypothetical agents could inhibit these cancer-related functions[4]

03

Biological functions

Copper ion bindingDopamine beta-monooxygenase activity (predicted)Dopamine catabolismNorepinephrine biosynthetic process (predicted)Octopamine biosynthetic process (predicted)Hydroxylation of hydrophobic substrates (predicted)Regulation of blood pressure (family-related)Post-translational modification/glycosylation (modulation)Regulation of cell proliferationCell cycle controlApoptosis induction via the ER-mitochondrial pathway in cancers[4]Tumor suppressor activity in neuroblastoma[2]
04

Disease associations

Cancer (elevated expression associated with poor prognosis in glioblastoma; tumor suppressor role in neuroblastoma)[4][2]Neurodegenerative disease (family; implicated through catecholamine metabolism)Other: Glandular Tularemia and Oculoglandular Tularemia (association, not direct causation)[5]
05

Safety considerations

Not directly documented; as a copper-dependent enzyme involved in neurotransmitter biosynthesis/metabolism, off-target inhibition could theoretically impact catecholamine pathways or ER homeostasis. Its role in post-translational modifications and cell cycle/apoptosis implies potential for toxicity if targeted without specificity[4]
06

Biomarkers

MOXD1 expression level in glioblastoma (GBM) is associated with patient prognosis; lower expression correlates with better outcomespotential marker in neuroblastoma for tumor suppressor status[4][2]

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