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Mouse Anti-DUOX2 Recombinant Antibody (E-8) (CBMAB-D1867-YC)

Provided herein is a Mouse monoclonal antibody, which binds to Dual Oxidase 2 (DUOX2). The antibody can be used for immunoassay techniques, such as WB, IP, IF, ELISA.
See all DUOX2 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
E-8
Antibody Isotype
IgG
Application
WB, IP, IF, ELISA

Basic Information

Specificity
Human
Antibody Isotype
IgG
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Dual Oxidase 2
Introduction
DUOX2 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.
Entrez Gene ID
50506
UniProt ID
Q9NRD8
Alternative Names
Dual Oxidase 2; NADH/NADPH Thyroid Oxidase P138-Tox; NADPH Oxidase/Peroxidase DUOX2; NADPH Thyroid Oxidase 2; Nicotinamide Adenine Dinucleotide Phosphate Oxidase; Dual Oxidase-Like Domains 2; Flavoprotein NADPH Oxidase; P138 Thyroid Oxidase; Thyroid Oxidase 2; Large NOX 2;
Research Area
Generates hydrogen peroxide which is required for the activity of thyroid peroxidase/TPO and lactoperoxidase/LPO. Plays a role in thyroid hormones synthesis and lactoperoxidase-mediated antimicrobial defense at the surface of mucosa. May have its own peroxidase activity through its N-terminal peroxidase-like domain.
Biological Process
Cuticle development Source: UniProtKB
Cytokine-mediated signaling pathway Source: UniProtKB
Defense response Source: GO_Central
Hormone biosynthetic process Source: UniProtKB-KW
Hydrogen peroxide biosynthetic process Source: UniProtKB
Hydrogen peroxide catabolic process Source: UniProtKB-KW
Positive regulation of cell motility Source: UniProtKB
Positive regulation of wound healing Source: UniProtKB
Response to cAMP Source: UniProtKB
Response to oxidative stress Source: InterPro
Response to virus Source: UniProtKB
Superoxide anion generation Source: UniProtKB
Thyroid hormone generation Source: Reactome
Cellular Location
Apical cell membrane; Cell junction. Localizes to the apical membrane of epithelial cells. Localizes on internal membrane structures under resting conditions, translocates to the plasma membrane and cell-cell junctions upon challenge with enteric pathogens, such as Escherichia coli.
Involvement in disease
Thyroid dyshormonogenesis 6 (TDH6):
A disorder due to a defective conversion of accumulated iodide to organically bound iodine. The iodide organification defect can be partial or complete.
Defects in DUOX2 may play a role in the pathogenesis of very early onset inflammatory bowel disease (VEOIBD), a chronic, relapsing inflammation of the gastrointestinal tract with a complex etiology diagnosed before 6 years of age. VEOIBD is subdivided into Crohn disease and ulcerative colitis phenotypes. Crohn disease may affect any part of the gastrointestinal tract from the mouth to the anus, but the phenotype of children with onset of Crohn disease occurring younger than the age of 10 is predominantly colonic, with a lower risk of ileal disease. Bowel inflammation is transmural and discontinuous; it may contain granulomas or be associated with intestinal or perianal fistulas. In contrast, in ulcerative colitis, the inflammation is continuous and limited to rectal and colonic mucosal layers; fistulas and granulomas are not observed. Both diseases include extraintestinal inflammation of the skin, eyes, or joints.
Topology
Extracellular: 26-601
Helical: 602-622
Cytoplasmic: 623-1041
Helical: 1042-1062
Extracellular: 1063-1076
Helical: 1077-1097
Cytoplasmic: 1098-1128
Helical: 1129-1151
Extracellular: 1152-1185
Helical: 1186-1206
Cytoplasmic: 1207-1223
Helical: 1224-1244
Helical: 1245-1265
Cytoplasmic: 1266-1548
PTM
N-glycosylated.

Rudolf, A. M., Wu, Q., Li, L., Wang, J., Huang, Y., Togo, J., ... & Speakman, J. R. (2022). A single nucleotide mutation in the dual-oxidase 2 (DUOX2) gene causes some of the panda's unique metabolic phenotypes. National science review, 9(2), nwab125.

Lyu, P. W., Xu, X. D., Zong, K., & Qiu, X. G. (2022). Overexpression of DUOX2 mediates doxorubicin resistance and predicts prognosis of pancreatic cancer. Gland Surgery, 11(1), 115.

Gu, F., Krüger, A., Roggenkamp, H. G., Alpers, R., Lodygin, D., Jaquet, V., ... & Guse, A. H. (2021). Dual NADPH oxidases DUOX1 and DUOX2 synthesize NAADP and are necessary for Ca2+ signaling during T cell activation. Science Signaling, 14(709), eabe3800.

Bann, D. V., Jin, Q., Sheldon, K. E., Houser, K. R., Nguyen, L., Warrick, J. I., ... & Goldenberg, D. (2019). Genetic variants implicate dual oxidase-2 in familial and sporadic nonmedullary thyroid cancer. Cancer Research, 79(21), 5490-5499.

Cho, S. Y., Kim, S., Son, M. J., Kim, G., Singh, P., Kim, H. N., ... & Eun, H. S. (2019). Dual oxidase 1 and NADPH oxidase 2 exert favorable effects in cervical cancer patients by activating immune response. BMC cancer, 19(1), 1-12.

Sasivari, Z., Szinnai, G., Seebauer, B., Konrad, D., & Lang-Muritano, M. (2019). Double variants in TSHR and DUOX2 in a patient with hypothyroidism: case report. Journal of Pediatric Endocrinology and Metabolism, 32(11), 1299-1303.

Wu, Y., Konaté, M. M., Lu, J., Makhlouf, H., Chuaqui, R., Antony, S., ... & Doroshow, J. H. (2019). IL-4 and IL-17A cooperatively promote hydrogen peroxide production, oxidative DNA damage, and upregulation of dual oxidase 2 in human colon and pancreatic cancer cells. The Journal of Immunology, 203(9), 2532-2544.

Liu, S., Zhang, W., Zhang, L., Zou, H., Lu, K., Li, Q., ... & Ma, X. (2018). Genetic and functional analysis of two missense DUOX2 mutations in congenital hypothyroidism and goiter. Oncotarget, 9(4), 4366.

Kang, K. A., Ryu, Y. S., Piao, M. J., Shilnikova, K., Kang, H. K., Yi, J. M., ... & Hyun, J. W. (2018). DUOX2-mediated production of reactive oxygen species induces epithelial mesenchymal transition in 5-fluorouracil resistant human colon cancer cells. Redox biology, 17, 224-235.

Zheng, X., Ma, S. G., Guo, M. L., Qiu, Y. L., & Yang, L. X. (2017). Compound heterozygous mutations in the DUOX2/DUOXA2 genes cause congenital hypothyroidism. Yonsei Medical Journal, 58(4), 888-890.

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For research use only. Not intended for any clinical use.

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