Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Alle Spezies anzeigen
Weitere Synonyme anzeigen
Wählen Sie die Spezies und Applikation aus
anti-Mouse (Murine) Antikörper:
anti-Rat (Rattus) Antikörper:
Sie gelangen zu unserer vorgefilterten Suche.
Human Polyclonal CYBA Primary Antibody für IHC (fro), IF (p) - ABIN750538
Walton, Shin, Tajinda, Heusner, Kogan, Miyake, Chen, Tamura, Matsumoto: Adult neurogenesis transiently generates oxidative stress. in PLoS ONE 2012
Show all 4 Pubmed References
Human Monoclonal CYBA Primary Antibody für 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
Show all 3 Pubmed References
Human Monoclonal CYBA Primary Antibody für 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
Show all 2 Pubmed References
In a family study of a patient with chronic granulomatous disease, the mutation in the CYBB (zeige CYBB Antikörper) 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 (zeige NOX1 Antikörper) and Nox4 (zeige NOX4 Antikörper) but not Nox5 (zeige NOX5 Antikörper) exclusively depends on p22phox.
NOX5 (zeige NOX5 Antikörper)-p22phox complex drives monocytic differentiation into dendritic cells, and thus could be critical for immunity and inflammation.
PI3K (zeige PIK3CA Antikörper)/AKT (zeige AKT1 Antikörper) signaling only occurs when FLT3 (zeige FLT3 Antikörper)-ITD is expressed at the plasma membrane and is required for the production of NOX-generated ROS (zeige ROS1 Antikörper). ER retention of FLT3 (zeige FLT3 Antikörper)-ITD resulted in NOX4 (zeige NOX4 Antikörper) 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 (zeige CYBB Antikörper) activation and oxidative response to tumor necrosis factor-alpha (zeige TNF Antikörper) 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 (zeige PPARG Antikörper) --> NF-kappaB (zeige NFKB1 Antikörper) --> 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 (zeige NOX1 Antikörper)-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 (zeige ROS1 Antikörper) derived from NADPH (zeige FDXR Antikörper) oxidases and that the effects of NADPH oxidase (zeige NOX1 Antikörper) on vascular activation are mediated in part by protein kinase (zeige CDK7 Antikörper) CK1alpha (zeige CSNK1A1 Antikörper).
Enhanced p22(phox) expression causes vascular dysfunction through ERK1/2 (zeige MAPK1/3 Antikörper) and p38-mitogen-activated protein kinase (zeige MAPK14 Antikörper)-dependent mechanisms in male type 2 diabetic mice.
The first quantitative characterization of the interactions made between the cytosolic regulators NOXO1 (zeige NOXO1 Antikörper) and NOXA1 (zeige NOXA1 Antikörper) and membrane-bound p22(phox), is presented.
renal expression of Nox-2 (zeige CYBB Antikörper), p22(phox), and p47(phox), components of NADPH oxidase (zeige NOX1 Antikörper), are upregulated in GSD-Ia mice compared with controls
cytochrome b558 expression is downregulated via the reduction of heme availability after NADPH oxidase (zeige NOX1 Antikörper) is inhibited by HO-1 (zeige HMOX1 Antikörper)
LPS (zeige TLR4 Antikörper) treatment enhanced protein levels of p22(phox), a catalytic subunit of NADPH oxidase (zeige NOX1 Antikörper), and increased NADPH oxidase (zeige NOX1 Antikörper) activity and levels of superoxide radicals and hydrogen peroxide.
Upregulation of PPAR-gamma and NADPH oxidases are involved in restenosis.
CRP (zeige CRP Antikörper) inhibits endothelium-dependent NO-mediated dilation in coronary arterioles by producing superoxide from NAD(P)H (zeige NQO1 Antikörper) oxidase via p38 (zeige MAPK14 Antikörper) kinase activation
Reactive oxygen species generated by NADPH oxidase (zeige NOX1 Antikörper) 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 (zeige PRKCE Antikörper)-dependent activation of NADPH oxidase (zeige NOX1 Antikörper) 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