The neutrophil cytosolic factor 1 (NCF1), also known as p47phox gene, spanning 15kb with 11 exons, is mapped to human chromosome 7q11.23. The gene codes for a 390 amino acid protein, which is a novel component of the NADPH oxidase complex.
면역원
The antiserum was produced against synthesized peptide derived from human p47 phox around the phosphorylation site of Ser345.
Immunogen Range: 311-360
생화학적/생리학적 작용
Neutrophil cytosolic factor 1 (NCF1) stimulates the production of reactive oxygen species (ROS) under hyperoxic condition. The above process can be inhibited by the NCF1 inhibitor diphenylene iodonium (DPI) and apocynin. Mutation in the gene leads to a rare congenital immune deficiency called, chronic granulomatous disease (CGD). Deletion of NCF1 gene, which is a vital component of NADPH oxidase complex implicated in generation of oxidative stress, leads to Williams syndrome. It also act as a modifier of vascular stiffness.
특징 및 장점
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물리적 형태
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
면책조항
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American journal of human genetics, 47(3), 483-492 (1990-09-01)
Chronic granulomatous disease (CGD) is a heterogeneous group of inherited disorders of impaired superoxide production in phagocytes. The most common X-linked recessive form involves the CYBB locus in band Xp21.1 that encodes the membrane-bound beta subunit of the cytochrome b558
Biochimica et biophysica acta, 1832(10), 1662-1672 (2013-05-22)
Chronic granulomatous disease (CGD) is a rare congenital disorder in which phagocytes cannot generate superoxide (O2(-)) and other microbicidal oxidants due to mutations in one of the five components of the O2(-)-generating NADPH oxidase complex. The most common autosomal subtype
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology, 32(1), 59-62 (2016-01-06)
To observe the effects of NADPH oxidase inhibitor diphenylene iodonium (DPI) and apocynin on the generation of reactive oxygen species (ROS) induced by p47phox and the mechanism of p47phox-induced ROS production under hyperoxic conditions. Peripheral blood mononuclear cells (PBMCs) were
Williams syndrome is caused by the deletion of 26 to 28 genes, including elastin, on human chromosome 7. Elastin insufficiency leads to the cardiovascular hallmarks of this condition, namely focal stenosis and hypertension. Extrapolation from the Eln(+/-) mouse suggests that
Angiotensin-converting enzyme inhibitors (ACEIs) are used by millions of patients to treat hypertension, diabetic kidney disease, and heart failure. However, these patients are often at increased risk of infection. To evaluate the impact of ACEIs on immune responses to infection