DUOX2 Antibody

1. Our study demonstrates the existence of a TET1/DUOX2/ROS/EMT axis that could play a role in colon cancer chemo-resistance and the aggressiveness of this cancer. PMID: 29715584
2. Letter/Case Report: biallelic, inactivating DUOX2 mutations described here might license overgrowth of mucosa-associated bacteria, which triggers colitis. PMID: 28683258
3. DUOX2 knockdown with short interfering RNA significantly decreased IFN-gamma-induced VEGF-A or HIF-1alpha up-regulation. PMID: 27637085
4. High expression of DUOX2 is associated with dilated cardiomyopathy and impaired left ventricular function accompanied by increased risk of death. PMID: 29320567
5. Human neutrophil elastase is involved in transactivation of TLR4 through activation of DUOX-2/EGFR and synergistically enhances IL-12p40 production by macrophages stimulated with LPS. PMID: 27282560
6. Monoallelic TSHR mutations are significantly associated with positive newborn screen for congenital hypothyroidism, and the association is further strengthened by the coexistence of monoallelic DUOX2 mutations. PMID: 29092890
7. In addition to thyroid hormonogenesis, the DUOX2 N-terminal domain may play a role in thyroid development. PMID: 28666341
8. This study reports the pedigree with goitrous congenital hypothyroidism (GCH) due to the coexistence of heterozygous mutations in the DUOX2 and DUOXA2 genes. PMID: 28541007
9. DUOX2 nonsense mutation plays a role in the pathogenesis of congenital hypothyroidism. PMID: 28633507
10. 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 IgG or VacA in the serum had lower DUOX2 expression levels than those infected with H. pylori without either virulence factor. PMID: 27048452
11. xome sequencing identified candidate variants, including a missense mutation in DUOX2 that impaired its function and a frameshift mutation in CSF2RB that was associated with Crohn's Disease in an independent cohort of Ashkenazi Jewish individuals. PMID: 27373512
12. 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. PMID: 27166716
13. DUOX2 Mutation is associated with Congenital Hypothyroidism. PMID: 27557340
14. Nox4 and Duox1/Duox2 mediate redox activation of mesenchymal cell migration by PDGF. PMID: 27110716
15. The high prevalence of DUOX2 mutations in this cohort of children with Congenial hypothyroidism appears striking and surprising. The clinical implications were discussed. PMID: 27498126
16. study expanded the mutational spectrum of the DUOX2 and thyroglobulin 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 PMID: 27108200
17. 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) were identified as the mutations underlying congenital hypothyroidism. PMID: 26709262
18. Transient congenital hypothyroidism is caused by compound heterozygous mutations affecting the NADPH-oxidase domain of DUOX2. PMID: 26565538
19. the house dust mite-dependent TLR2-Duox2 signalling axis promotes NF-kappaB activation, which induces IL-8 and CCL20 production and mediates epidermal keratinocyte inflammation PMID: 26174504
20. Results identified 2 mutations in DUOX2 gene from patient with congenital hypothyroidism and report new cryptic splicing sites in the intron 17 and exon 18. PMID: 26506010
21. inactivating mutations in the DUOXA2 (p.Y246X) and DUOX2 (p.R885Q) genes were identified in a set of dizygotic twins with congenital hypothyroidism PMID: 27349010
22. Prevalence of DUOX2 pathogenic variants is 29% among patients with congenital hypothyroidism in Guangxi, China. Monoallelic and biallelic DUOX2 variants are associated with transient, while triallelic variants are associated with permanent disease. PMID: 26349762
23. The prognosis of Japanese patients with DUOX2 defects was usually transient Congenital hypothyroidism. Delayed improvement of thyroglobulin indicates that these patients have subclinical hypothyroidism. PMID: 26742565
24. Data indicate dual oxidase 2 protein (DUOX2) mutation-carrying pedigree presenting pseudodominant inheritance of nonautoimmune hypothyroidism. PMID: 25263060
25. The folding of DUOX2 appears to be a key event in the trafficking of the DUOX2/DUOXA2 complex as it promotes an appropriate conformation of the N-terminal region, which is propitious to subsequent covalent interactions with the maturation factor, DUOXA2. PMID: 25761904
26. Mucosal dysbiosis leads to increased expression of DUOX2, which might be a marker of perturbed mucosal homeostasis in patients with early-stage inflammatory bowel disease. PMID: 26261005
27. DUOX2 played an important role in innate immunity against Klebsiella pneumoniae cytoinvasion through the reactive oxygen species pathway in T24 cells. PMID: 26046128
28. Taken together these data suggest that chemopotentiation by LDFRT in gastric cancer cells may be due, at least in part, to increased ROS production (DUOX2) without upregulation of the DNA repair machinery PMID: 26207686
29. findings demonstrate that PKCalpha plays a critical role in HCC development by inducing DUOX2 expression and ROS generation, and propose a strategy to target PKCalpha/DUOX2 as a potential adjuvant therapy for HCC treatment PMID: 26056003
30. DUOX2 variants are a relatively common cause of congenital hypothyroidism with normal-sized or enlarged eutopic thyroid PMID: 25248169
31. Duox2 proteins possessing the A-loops of Nox1 or Nox5 co-expressed with DuoxA2 showed enhanced O2 () release, and Duox1 proteins possessing the A-loops of Nox1 or Nox5 co-expressed with DuoxA1 acquired O2 () leakage PMID: 25586178
32. Heterozygous mutations in DUOX2 may affect protein function and cause congenital hypothyroidism. PMID: 25616291
33. Genotypes and phenotypes of congenital goitre and hypothyroidism caused by mutations in dual oxidase 2 genes. PMID: 24735383
34. An increase of DUOX2 expression was seen in association with an expansion of Proteobacteria in both ulcerative colitis and Crohn disease, while expression of APOA1 gene was downregulated and associated with Crohn disease-specific alterations in Firmicutes PMID: 25003194
35. Further, ROS generated by Duox enzymes localized adjacent to nuclear speckles altered the splicing of viral genes PMID: 24128054
36. Despite the high sequence similarity shared between DUOX1 and DUOX2, the two isoforms present distinct regulations, tissue expression and catalytic functions PMID: 24161126
37. family showed potential linkage to DUOX2 locus and we detected a nonsense mutation (R434X) in both cases and the mutation segregated with disease status in the family PMID: 24127536
38. The present data open new perspectives for a better understanding of the pathophysiology of thyroid autoimmune diseases considering DUOX2-mediated oxidative damages. PMID: 23010498
39. DUOX2 is Significantly Upregulated in Active Ulcerative Colitis and during Progression to Dysplasia. PMID: 24492313
40. The most robust clinical parameters for selecting patients for DUOX2 analysis have been identified, and several DUOX2 variants have been functionally characterized. PMID: 24423310
41. Underscore the importance of DUOX1 and DUOX2 in vesicant-induced IL-6 secretion in human airway epithelial cells. PMID: 24164541
42. upregulated in chronic rhinosinusitis as a part of inflammatory response PMID: 23281318
43. A key function of DUOX2 in the establishment of a late antiviral state triggered by the synergistic autocrine/paracrine action of IFNbeta and TNFalpha secreted during respiratory virus infection. PMID: 23545780
44. Duox2 was expressed at elevated levels in many human cancers, most notably tumors of the prostate, lung, colon and breast. PMID: 23404210
45. p.G488R missense mutation in the DUOX2 gene of the congenital hypothyroidism patients is associated with thyroid dysfunction that presents during the neonatal period. PMID: 23457309
46. Report shows that ROS levels in PC3 cells are constitutively maintained by DUOX 1 and 2 enzymes, and these ROS positively regulate AKT signalling through inactivating phosphatases, leading to increased resistance to apoptosis. PMID: 23225414
47. Study indicates a complex profile of protein interactions required for activity and localization of the DUOX1 and DOOX2 enzymes. PMID: 23362256
48. p.Arg376Trp mutation in DUOX2 was found in newborns of congenital hypothyroidism. PMID: 22336364
49. The dramatic increase in reactive oxygen species induced in pancreatic cancer cells by the combination of lipopolysaccharide and interferon-gamma depends critically on the upregulation of, and signaling through, the Toll-like receptor (TLR)4 pathway. PMID: 23296709
50. Two functionally important single-nucleotide polymorphisms within the promoter differentially regulate DUOX2/DUOXA2 transcription in response to exogenous double-stranded DNA. PMID: 22592922

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HGNC: 13273

OMIM: 606759

KEGG: hsa:50506

STRING: 9606.ENSP00000373691

UniGene: Hs.71377