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This study reports the pedigree with goitrous congenital hypothyroidism (GCH (show GCH1 ELISA Kits)) due to the coexistence of heterozygous mutations in the DUOX2 and DUOXA2 (show DUOXA2 ELISA Kits) genes.
DUOX2 nonsense mutation plays a role in the pathogenesis of congenital hypothyroidism.
Expression of DUOX2 mRNA and protein was lower in gastric mucosa of patients with H. pylori infection compared to the uninfected. Among the H. pylori-infected patients, those having CagA (show S100A8 ELISA Kits) IgG or VacA in the serum had lower DUOX2 expression levels than those infected with H. pylori without either virulence factor.
xome sequencing identified candidate variants, including a missense mutation in DUOX2 that impaired its function and a frameshift mutation in CSF2RB (show CSF2RB ELISA Kits) that was associated with Crohn's Disease in an independent cohort of Ashkenazi Jewish individuals.
Data suggest that mutations in DUOX2 may be the most common cause of both permanent congenital hypothyroidism and transient hypothyroidism; severity of disease due to DUOX2 mutations may be milder than that due to other causes. This study involved neonatal screening of 48 Japanese boys and girls.
DUOX2 Mutation is associated with Congenital Hypothyroidism.
Nox4 (show NOX4 ELISA Kits) and Duox1/Duox2 (show DUOX1 ELISA Kits) mediate redox activation of mesenchymal cell migration by PDGF (show PDGFA ELISA Kits).
The high prevalence of DUOX2 mutations in this cohort of children with Congenial hypothyroidism appears striking and surprising. The clinical implications were discussed.
study expanded the mutational spectrum of the DUOX2 and thyroglobulin (show TG ELISA Kits) genes and provided the best estimation of the DUOX2 mutation rate (29%) for congenital hypothyroidism/subclinical congenital hypothyroidism patients in Guangxi Zhuang Autonomous Region of China
Seven different recurrent mutations [p.G488R (n=13), p.A649E (n=3), p.R885Q (n=3), p.I1080T (n=2), and p.A1206T (n=2) in DUOX2; p.Y138X (n=9) in DUOXA2 (show DUOXA2 ELISA Kits)) were identified as the mutations underlying congenital hypothyroidism.
the dual oxidase 2 N-terminal region is targeted to the plasma membrane
DUOX2 (show DUOX1 ELISA Kits) regulates interactions between the intestinal microbiota and the mucosa to maintain immune homeostasis in mice.
these data indicate that the gut (show GUSB ELISA Kits) microbiota uses two distinct signaling pathways to induce Duox2 (show DUOX1 ELISA Kits) expression in the ileum and colon epithelium.
Data suggest that proteinase-activated receptor 2 (show F2RL1 ELISA Kits) activation leads to up-regulation of the dual oxidase-2 (show DUOX1 ELISA Kits)/reactive oxygen species pathway in airway epithelial cells (AECs).
DUOX2 (show DUOX1 ELISA Kits)-generated ROS (show ROS1 ELISA Kits) induce AEC death.
a spontaneously generated valine 674-to-glycine mutation of murine Duox2 (show DUOX1 ELISA Kits) results in a translocation defect and complete loss of function that explains the severe congenital hypothyroid phenotype of the thyd/thyd mouse strain
DUOX2 (show DUOX1 ELISA Kits) plays pivotal roles in TLR5 (show TLR5 ELISA Kits)-dependent inflammatory response of nasal airway epithelium.
DUOX2 (show DUOX1 ELISA Kits) and NOD2 (show NOD2 ELISA Kits) cooperatively facilitate antibacterial action.
The protein encoded by this gene is a glycoprotein and a member of the NADPH oxidase family. The synthesis of thyroid hormone is catalyzed by a protein complex located at the apical membrane of thyroid follicular cells. This complex contains an iodide transporter, thyroperoxidase, and a peroxide generating system that includes this encoded protein and DUOX1. This protein is known as dual oxidase because it has both a peroxidase homology domain and a gp91phox domain.
dual oxidase 2
, dual oxidase 2-like
, NADH/NADPH thyroid oxidase p138-tox
, NADPH oxidase/peroxidase DUOX2
, NADPH thyroid oxidase 2
, dual oxidase-like domains 2
, flavoprotein NADPH oxidase
, large NOX 2
, long NOX 2
, nicotinamide adenine dinucleotide phosphate oxidase
, p138 thyroid oxidase
, thyroid oxidase 2
, NADH/NADPH thyroid oxidase THOX2