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Human Polyclonal CYBA Primary Antibody for IHC (fro), IF (p) - ABIN750538
Walton, Shin, Tajinda, Heusner, Kogan, Miyake, Chen, Tamura, Matsumoto: Adult neurogenesis transiently generates oxidative stress. in PLoS ONE 2012
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Human Monoclonal CYBA Primary Antibody for WB - ABIN1042639
Taylor, Jesaitis: Immunoaffinity purification of human phagocyte flavocytochrome b and analysis of conformational dynamics. in Methods in molecular biology (Clifton, N.J.) 2008
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Human Monoclonal CYBA Primary Antibody for IHC (fro), FACS - ABIN1042638
Taylor, Burritt, Baniulis, Foubert, Lord, Dinauer, Parkos, Jesaitis: Site-specific inhibitors of NADPH oxidase activity and structural probes of flavocytochrome b: characterization of six monoclonal antibodies to the p22phox subunit. in Journal of immunology (Baltimore, Md. : 1950) 2004
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In a family study of a patient with chronic granulomatous disease, the mutation in the CYBB (show CYBB Antibodies) gene was confirmed to be pathogenic, and the three variants in the CYBA gene were benign.
We demonstrated that rapid deletion of p22phox is possible and that the activity of Nox1 (show NOX1 Antibodies) and Nox4 (show NOX4 Antibodies) but not Nox5 (show NOX5 Antibodies) exclusively depends on p22phox.
NOX5 (show NOX5 Antibodies)-p22phox complex drives monocytic differentiation into dendritic cells, and thus could be critical for immunity and inflammation.
PI3K (show PIK3CA Antibodies)/AKT (show AKT1 Antibodies) signaling only occurs when FLT3 (show FLT3 Antibodies)-ITD is expressed at the plasma membrane and is required for the production of NOX-generated ROS (show ROS1 Antibodies). ER retention of FLT3 (show FLT3 Antibodies)-ITD resulted in NOX4 (show NOX4 Antibodies) deglycosylation and p22(phox) protein degradation.
CYBA gene ()49A>G polymorphism modifies the risk of coronary artery disease
The study demonstrated that the genetic variants of rs9932581 and rs1049255 in CYBA might not be associated with preeclampsia.
p22phox C242T polymorphism has a possible role in changing the genetic susceptibility to late-onset AD in ApoE 4 carriers of northern Han Chinese origin.
CYBA mutations lead to one of the autosomal recessive forms of chronic granulomatous disease (AR220CGD) clinically characterized by recurrent and severe infections in early chilA large number of genetic variations of CYBA have been reported, among them the C242T polymorphism, which has been extensively studied in association with coronary artery and heart diseases, but conflicting results continue to be reported. [Review]
C242T single-nucleotide polymorphism causes p22(phox) structural changes that inhibit endothelial Nox2 (show CYBB Antibodies) activation and oxidative response to tumor necrosis factor-alpha (show TNF Antibodies) or high-glucose stimulation. C242T single-nucleotide polymorphism may represent a natural protective mechanism against inflammatory cardiovascular diseases.
CYBA C242T correlates with microalbuminuria onset in the French DT1 cohort.
Identification of a PPAR-gamma (show PPARG Antibodies) --> NF-kappaB (show NFKB1 Antibodies) --> p22phox neuroprotective signaling cascade opens a new avenue for protecting the brain against ischemic insult.
Knockout of the cytochrome P450 reductase by CRISPR/Cas9 technology (POR(-/-)) in HEK293 cells overexpressing Nox4 or Nox5 did not interfere with ROS production in intact cells. However, POR(-/-) abolished the signal in NADPH-stimulated assays using membrane fractions from the very same cells. Moreover, membranes of rat smooth muscle cells treated with angiotensin II showed an increased NADPH-dependent signal with lucigen
p22phox mRNA expression was increased in diet-induced obese (DIO) mice.
The present study provides evidence that augmented EGFRtk impairs vascular function by NADPH oxidase (show NOX1 Antibodies)-dependent mechanism. Therefore, EGFRtk and oxidative stress should be potential targets to treat vascular dysfunction in TD2.
Vascular hnRNP-C expression is regulated by ROS (show ROS1 Antibodies) derived from NADPH (show FDXR Antibodies) oxidases and that the effects of NADPH oxidase (show NOX1 Antibodies) on vascular activation are mediated in part by protein kinase (show CDK7 Antibodies) CK1alpha (show CSNK1A1 Antibodies).
Enhanced p22(phox) expression causes vascular dysfunction through ERK1/2 and p38-mitogen-activated protein kinase (show MAPK14 Antibodies)-dependent mechanisms in male type 2 diabetic mice.
The first quantitative characterization of the interactions made between the cytosolic regulators NOXO1 (show NOXO1 Antibodies) and NOXA1 (show NOXA1 Antibodies) and membrane-bound p22(phox), is presented.
renal expression of Nox-2 (show CYBB Antibodies), p22(phox), and p47(phox), components of NADPH oxidase (show NOX1 Antibodies), are upregulated in GSD-Ia mice compared with controls
cytochrome b558 expression is downregulated via the reduction of heme availability after NADPH oxidase (show NOX1 Antibodies) is inhibited by HO-1 (show HMOX1 Antibodies)
LPS (show TLR4 Antibodies) treatment enhanced protein levels of p22(phox), a catalytic subunit of NADPH oxidase (show NOX1 Antibodies), and increased NADPH oxidase (show NOX1 Antibodies) activity and levels of superoxide radicals and hydrogen peroxide.
Upregulation of PPAR-gamma and NADPH oxidases are involved in restenosis.
CRP (show CRP Antibodies) inhibits endothelium-dependent NO-mediated dilation in coronary arterioles by producing superoxide from NAD(P)H (show NQO1 Antibodies) oxidase via p38 (show MAPK14 Antibodies) kinase activation
Reactive oxygen species generated by NADPH oxidase (show NOX1 Antibodies) contribute to the aberrant pulmonary arterial responses in piglets exposed to 3 days of hypoxia.
Angiotensin II inhibits the Na+/K+ pump via protein kinase c epsilon (show PRKCE Antibodies)-dependent activation of NADPH oxidase (show NOX1 Antibodies) subunits.
Cytochrome b is comprised of a light chain (alpha) and a heavy chain (beta). This gene encodes the light, alpha subunit which has been proposed as a primary component of the microbicidal oxidase system of phagocytes. Mutations in this gene are associated with autosomal recessive chronic granulomatous disease (CGD), that is characterized by the failure of activated phagocytes to generate superoxide, which is important for the microbicidal activity of these cells.
, cytochrome b-245, alpha polypeptide
, predicted cytochrome b-245, alpha polypeptide
, Cytochrome b(558) alpha chain
, Cytochrome b558 subunit alpha
, Neutrophil cytochrome b 22 kDa polypeptide
, Superoxide-generating NADPH oxidase light chain subunit
, cytochrome b-245 light chain
, flavocytochrome b558 (p22phox)
, p22 phagocyte B-cytochrome
, cytochrome b light chain
, cytochrome b(558) alpha chain
, cytochrome b(558) alpha-subunit
, cytochrome b, alpha polypeptide
, cytochrome b558 subunit alpha
, flavocytochrome b-558 alpha polypeptide
, neutrophil cytochrome b 22 kDa polypeptide
, superoxide-generating NADPH oxidase light chain subunit
, cytochrome beta-558
, p22 phox
, cytochrome b558 alpha-subunit
, NADPH oxidase light chain subunit