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Validated All-in-One™ qPCR Primer for DUOX2(NM_014080.4) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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. [provided by RefSeq].
Gene References into function
- the dual oxidase 2 N-terminal region is targeted to the plasma membrane
- Expression of dual oxidase 2 in human colon and Caco-2 cells.
- These data suggest that Duox1 and 2 are the major NADPH oxidases expressed in airway epithelia and therefore contributors of hydrogen peroxide production in the airway lumen.
- post-translational modifications during the maturation process of Duox2 could be implicated in the mechanism of H2O2 formation by favoring intramolecular superoxide dismutation
- Results demonstrate the regulation of Duox1 and 2 expression by Th1 and Th2 cytokines, and suggest a mechanism by which ROS production can be regulated in the respiratory tract as part of the host defense response.
- Heterozygous mutations in the DUOX2 gene are responsible for iodide organification defect and congenital hypothyroidism.
- In conclusion, incubation of normal or GD thyrocytes with Th1 cytokines induces a significant reduction in TSH-increased expression of both TPO and ThOXs, an effect partially mediated by NO.
- co-expression with DUOXA2, an ER-resident transmembrane protein, allows ER-to-Golgi transition, maturation, and translocation to the plasma membrane of functional DUOX2 in a heterologous system
- DUOXA2 allows rapid ER exit of folded DUOX2 or enhanced degradation of mutant DUOX2 proteins not competent for ER exit.
- Analysis of point mutations opens possibility to ascertain whether transiency or permanency of DUOX2 phenotypes relate to monoallelic or biallelic inactivation of gene, or if degree of pathogenic severity of mutations may also influence outcome. (Review)
- Results imply that the airway expression of Duox2 is diversely associated with smoking and chronic obstructive pulmonary disease.
- Results suggest that an area on chromosome 15 that includes DUOX1, DUOX2, and their maturation factors is a frequent target for epigenetic silencing in lung cancer.
- Loss of DUOX2 activity results in transient congenital hypothyroidism and transient congenital hypothyroidism caused by DUOX2 mutations is inherited as an autosomal recessive trait.