![Purified Mouse Anti-gp91[phox]](/content/dam/bdb/products/global/reagents/microscopy-imaging-reagents/immunofluorescence-reagents/611xxx/6114xx/611415_base/G95320_611415_image1.png)
![Purified Mouse Anti-gp91[phox]](/content/dam/bdb/products/global/reagents/microscopy-imaging-reagents/immunofluorescence-reagents/611xxx/6114xx/611415_base/G95320_611415_image2.png)
Preparation And Storage
Product Notices
- Since applications vary, each investigator should titrate the reagent to obtain optimal results.
- Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
- Source of all serum proteins is from USDA inspected abattoirs located in the United States.
- Please refer to www.bdbiosciences.com/us/s/resources for technical protocols.
Although dormant in resting granulocytes, macrophages, and B lymphocytes, the neutrophil respiratory burst oxidase (NADPH-oxidase) generates superoxide and secondary oxygen-derived toxic products in response to bacteria or a variety of soluble stimuli. It is an integral membrane cytochrome, b558, which consists of two subunits, gp91[phox] and p21[phox]. Upon stimulation, cytochrome b558 forms a complex with cytosolic proteins, p67[phox], p47[phox], p40[phox], and rac2 and produces superoxide anions in a NADPH-dependent manner. In chronic granulomatous disease (CGD), severe recurrent bacterial and fungal infections result from defective NADPH-oxidase activity. The majority of CGD cases are caused by a defective gp91[phox] gene. gp91[phox], implicated as a docking site for p47[phox], is membrane glycoprotein with multiple N-terminal hydrophobic domains and a hydrophilic C-terminus. The expression of gp91[phox] is restricted to terminally differentiated phagocytes and B lymphocytes. This cell type- and developmental stage-specific expression may be controlled by transcriptional activators, such as PU.1 and YY1, and transcriptional repressors, such as CCAAT displacement protein (CDP). Endogenous mouse gp91phox shows 58 kDa band, instead of 91 kDa observed in human. Both mouse and human deglycosylated gp91 are 54 kDa. This difference may be due to less glycosylation sites in the mouse sequence.
Development References (5)
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Agarwal D, Dange R, Vila J, Otamendi A, Francis J. Detraining differentially preserved beneficial effects of exercise on hypertension: effects on blood pressure, cardiac function, brain inflammatory cytokines and oxidative stress. PLoS ONE. 2012; 7(12):e52569. (Clone-specific: Western blot). View Reference
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Jacobsen BM, Skalnik DG. YY1 binds five cis-elements and trans-activates the myeloid cell-restricted gp91(phox) promoter. J Biol Chem. 1999; 274(42):29984-29993. (Biology). View Reference
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Suzuki S, Kumatori A, Haagen IA. PU.1 as an essential activator for the expression of gp91(phox) gene in human peripheral neutrophils, monocytes, and B lymphocytes. Proc Natl Acad Sci U S A. 1998; 95(11):6085-6090. (Biology). View Reference
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Yu L, Quinn MT, Cross AR, Dinauer MC. Gp91(phox) is the heme binding subunit of the superoxide-generating NADPH oxidase. Proc Natl Acad Sci U S A. 1998; 95(14):7993-7998. (Biology). View Reference
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Zhen L, Yu L, Dinauer MC. Probing the role of the carboxyl terminus of the gp91phox subunit of neutrophil flavocytochrome b558 using site-directed mutagenesis. J Biol Chem. 1998; 273(11):6575-6581. (Biology). View Reference
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For Research Use Only. Not for use in diagnostic or therapeutic procedures.
