HomeAboutRankingsData Sources
Β© 2026 GeneE
🧬
GeneE
10 sources retrieved Β· Most recent: April 2026 Β· Index updated 15 days ago
β“˜GeneE is for informational purposes only. It is not a substitute for professional medical advice, diagnosis, or treatment.
DUOXA2
dual oxidase maturation factor 2
Chromosome 15 Β· 15q21.1
NCBI Gene: 405753Ensembl: ENSG00000140274.15HGNC: HGNC:32698UniProt: Q1HG44
24PubMed Papers
21Diseases
0Drugs
27Pathogenic Variants
FUNCTIONAL ROLE
Transporter
CLINICAL
OMIM Disease Gene
DATA QUALITY
βœ“ Experimental GO Evidenceβœ“ Swiss-Prot Reviewed
cytosolenzyme bindingintracellular protein localizationpositive regulation of hydrogen peroxide biosynthetic processfamilial thyroid dyshormonogenesiscongenital hypothyroidismgenetic disordertransient congenital hypothyroidism
✦AI Summary

DUOXA2 (dual oxidase maturation factor 2) is essential for thyroid hormone synthesis by enabling DUOX2 protein maturation and trafficking. DUOXA2 recruits DUOX2 from the endoplasmic reticulum to the apical plasma membrane 12, where the DUOX2-DUOXA2 complex catalyzes hydrogen peroxide (H2O2) production critical for thyroid peroxidase function 3. DUOXA2 mutations cause thyroid dyshormonogenesis, a major form of congenital hypothyroidism (CH) characterized by impaired thyroid hormone synthesis despite normal gland morphology 45. In Chinese populations, DUOXA2 variants occur in approximately 6.7% of CH patients and are particularly prevalent in thyroid dysgenesis cases (18.75%) 67. Mutations disrupting DUOXA2 function impair DUOX2 enzyme activity and H2O2 generation, leading to inherited CH typically following autosomal recessive inheritance 47. Clinically, DUOXA2-mutated patients tend to present milder disease with normal thyroid size compared to other genetic forms of CH 7. DUOXA2 gene screening enhances diagnostic accuracy when combined with screening of other dyshormonogenesis-related genes, supporting early intervention and personalized treatment planning in affected children 3.

Sources cited
1
DUOXA2 is required for DUOX2 maturation and transport from endoplasmic reticulum to plasma membrane
PMID: 16651268
2
DUOXA2 recruits DUOX2 to the apical cell membrane
PMID: 39126279
3
DUOXA2 and DUOX2 form a complex that promotes H2O2 generation in thyroid hormone synthesis; DUOXA2 mutations disrupt this process leading to CH
PMID: 39673194
4
DUOXA2 mutations cause thyroid dyshormonogenesis with autosomal recessive inheritance; DUOXA2 is among the causative genes for CH
PMID: 29650690
5
DUOXA2 variants contribute to the high mutation rate in DUOX system genes in CH patients; DUOX system gene mutations are associated with transient CH and goiter presentation
PMID: 33631011
6
DUOXA2 variants are prominent in thyroid dysgenesis cases (18.75%); p.Y246X is the most common DUOXA2 variant hotspot
PMID: 32425884
7
DUOXA2 variants occur in 6.7% of CH patients; mutations disrupt DUOX2 enzyme activity and H2O2 production; DUOXA2-mutated patients present milder disease with normal thyroid size
PMID: 40510014
Disease Associationsβ“˜21
familial thyroid dyshormonogenesisOpen Targets
0.65Moderate
congenital hypothyroidismOpen Targets
0.42Moderate
genetic disorderOpen Targets
0.41Moderate
transient congenital hypothyroidismOpen Targets
0.37Weak
Iron deficiency anemiaOpen Targets
0.20Weak
ulcerative colitisOpen Targets
0.07Suggestive
parasitic infectionOpen Targets
0.06Suggestive
Crohn's diseaseOpen Targets
0.05Suggestive
ChΓ©diak-Higashi syndromeOpen Targets
0.05Suggestive
Autosomal recessive malignant osteopetrosisOpen Targets
0.04Suggestive
hemolytic uremic syndrome, atypical, 8, with rhizomelic short statureOpen Targets
0.04Suggestive
Camurati-Engelmann diseaseOpen Targets
0.04Suggestive
Hypocalcemic vitamin D-dependent ricketsOpen Targets
0.03Suggestive
Shwachman-Diamond syndromeOpen Targets
0.03Suggestive
Albers-SchΓΆnberg osteopetrosisOpen Targets
0.03Suggestive
cartilage-hair hypoplasiaOpen Targets
0.03Suggestive
Aplasia cutis congenita - intestinal lymphangiectasiaOpen Targets
0.03Suggestive
aplasia cutis congenita-intestinal lymphangiectasia syndromeOpen Targets
0.03Suggestive
immunoskeletal dysplasia with neurodevelopmental abnormalitiesOpen Targets
0.03Suggestive
Skeletal dysplasia - intellectual disabilityOpen Targets
0.03Suggestive
Thyroid dyshormonogenesis 5UniProt
Pathogenic Variants27
NM_207581.4(DUOXA2):c.340+1G>ALikely pathogenic
Thyroglobulin synthesis defect|not provided
β˜…β˜…β˜†β˜†2025
NM_207581.4(DUOXA2):c.738C>G (p.Tyr246Ter)Pathogenic
Thyroglobulin synthesis defect|Familial thyroid dyshormonogenesis|Inborn genetic diseases
β˜…β˜…β˜†β˜†2025β†’ Residue 246
NM_207581.4(DUOXA2):c.396G>A (p.Trp132Ter)Likely pathogenic
Thyroglobulin synthesis defect
β˜…β˜…β˜†β˜†2025β†’ Residue 132
NM_207581.4(DUOXA2):c.413dup (p.Tyr138Ter)Pathogenic
Thyroglobulin synthesis defect|Familial thyroid dyshormonogenesis
β˜…β˜…β˜†β˜†2024β†’ Residue 138
NM_207581.4(DUOXA2):c.95dup (p.Leu32fs)Pathogenic
Thyroglobulin synthesis defect|not provided
β˜…β˜…β˜†β˜†2024β†’ Residue 32
NM_207581.4(DUOXA2):c.770-19_780delLikely pathogenic
Thyroglobulin synthesis defect
β˜…β˜†β˜†β˜†2024
NM_207581.4(DUOXA2):c.769+2T>ALikely pathogenic
Thyroglobulin synthesis defect
β˜…β˜†β˜†β˜†2024
NM_207581.4(DUOXA2):c.753G>A (p.Trp251Ter)Likely pathogenic
Thyroglobulin synthesis defect
β˜…β˜†β˜†β˜†2024β†’ Residue 251
NM_207581.4(DUOXA2):c.465_466dup (p.Tyr156fs)Likely pathogenic
Thyroglobulin synthesis defect
β˜…β˜†β˜†β˜†2024β†’ Residue 156
NM_207581.4(DUOXA2):c.1A>G (p.Met1Val)Likely pathogenic
Thyroglobulin synthesis defect
β˜…β˜†β˜†β˜†2024β†’ Residue 1
NM_207581.4(DUOXA2):c.382G>T (p.Glu128Ter)Likely pathogenic
Thyroglobulin synthesis defect
β˜…β˜†β˜†β˜†2024β†’ Residue 128
NM_207581.4(DUOXA2):c.205+1G>ALikely pathogenic
Thyroglobulin synthesis defect
β˜…β˜†β˜†β˜†2024
NM_207581.4(DUOXA2):c.147+1G>TLikely pathogenic
Thyroglobulin synthesis defect
β˜…β˜†β˜†β˜†2024
NM_207581.4(DUOXA2):c.136del (p.Arg46fs)Pathogenic
Thyroglobulin synthesis defect
β˜…β˜†β˜†β˜†2024β†’ Residue 46
NM_207581.4(DUOXA2):c.768del (p.Gly257fs)Likely pathogenic
Thyroglobulin synthesis defect
β˜…β˜†β˜†β˜†2024β†’ Residue 257
NM_207581.4(DUOXA2):c.860del (p.Lys287fs)Likely pathogenic
Thyroglobulin synthesis defect
β˜…β˜†β˜†β˜†2024β†’ Residue 287
NM_207581.4(DUOXA2):c.205+1G>TLikely pathogenic
Thyroglobulin synthesis defect
β˜…β˜†β˜†β˜†2024
NM_207581.4(DUOXA2):c.37C>T (p.Gln13Ter)Pathogenic
Thyroglobulin synthesis defect
β˜…β˜†β˜†β˜†2023β†’ Residue 13
NM_207581.4(DUOXA2):c.611T>C (p.Leu204Pro)Likely pathogenic
Thyroglobulin synthesis defect
β˜…β˜†β˜†β˜†2023β†’ Residue 204
NM_207581.4(DUOXA2):c.573G>A (p.Trp191Ter)Pathogenic
Thyroglobulin synthesis defect
β˜…β˜†β˜†β˜†2023β†’ Residue 191
View on ClinVar β†—
Related Genes
NOX5Protein interaction100%IYDProtein interaction85%SLC26A4Protein interaction74%TGProtein interaction74%TPOProtein interaction74%DUOX2Protein interaction64%
Tissue Expression6 tissues
Lung
100%
Ovary
25%
Liver
16%
Bone Marrow
6%
Brain
5%
Heart
0%
Gene Interaction Network
Click a node to explore
DUOXA2NOX5IYDSLC26A4TGTPODUOX2
PROTEIN STRUCTURE
Preparing viewer…
AlphaFoldAI-predicted Β· UniProt Q1HG44
View on AlphaFold β†—
Constraintβ“˜
LOEUFβ“˜
1.16LoF Tolerant
pLIβ“˜
0.00Tolerant
Observed/Expected LoF0.81 [0.58–1.16]
RankingsWhere DUOXA2 stands among ~20K protein-coding genes
  • #13,177of 20,598
    Most Researched24
  • #1,921of 5,498
    Most Pathogenic Variants27
  • #12,124of 17,882
    Most Constrained (LOEUF)1.16
Genes detectedDUOXA2
Sources retrieved10 papers
Response timeβ€”
πŸ“„ Sources
10β–Ό
1
PMID: 32425884
Front Endocrinol (Lausanne) Β· 2020
1.00
2
The genetic characteristics of congenital hypothyroidism in China by comprehensive screening of 21 candidate genes.
PMID: 29650690
Eur J Endocrinol Β· 2018
0.90
3
Dual Oxidase System Genes Defects in Children With Congenital Hypothyroidism.
PMID: 33631011
Endocrinology Β· 2021
0.80
4
Genetic and Phenotypic Characteristics of Congenital Hypothyroidism in a Chinese Cohort.
PMID: 34539567
Front Endocrinol (Lausanne) Β· 2021
0.70
5
The role of DUOXA2 in the clinical diagnosis of paediatric congenital hypothyroidism.
PMID: 39673194
Ann Med Β· 2025
0.60