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Cytochrome b (-245) is composed of cytochrome b alpha (CYBA) and beta (CYBB) chain. Additionally we are shipping CYBB Antibodies (117) and CYBB Kits (11) and many more products for this protein.
Showing 4 out of 6 products:
The nox1 (show NOX1 Proteins), nox2/cybb expression in zebrafish during early nervous system development from 12 to 48 hours post fertilization
Data indicate that NADPH oxidase (show NOX1 Proteins) NOx2 inhibition attenuates endoplasmic reticulum (ER) stress and apoptosis.
We examined the pattern of NOX expression in spinal cords of patients and mouse models of ALS (show IGFALS Proteins) and analyzed the impact of genetic deletion of the NOX1 (show NOX1 Proteins) and 2 isoforms as well as pharmacological NOX inhibition in the SOD1 (show SOD1 Proteins)(G93A) ALS (show IGFALS Proteins) mouse model.In contrast to previous publications, survival of SOD1 (show SOD1 Proteins)(G93A) mice was not modified upon breeding with constitutive NOX1 (show NOX1 Proteins) and NOX2 deficient mice.
Recent studies reveal that AKT2 (show AKT2 Proteins)-NOX2 signaling has critical roles in Ca mobilization, ROS (show ROS1 Proteins) generation, degranulation, and control of the ligand-binding function of cell surface molecules, thereby promoting heterotypic cell-cell interactions in thromboinflammation.
Study demonstrate that Nox2 signaling via inactivation of phosphatase and tensin homolog and activation of the PI3K (show PIK3CA Proteins)/Akt (show AKT1 Proteins) pathway leads to membrane ruffling and macropinocytosis.
Our findings indicate that Nox2 deficiency results in exaggerated experimental asthma, which is caused by enhanced Th2 effector function in a T-cell-intrinsic manner.
In a family study of a patient with chronic granulomatous disease, the mutation in the CYBB gene was confirmed to be pathogenic, and the three variants in the CYBA (show CYBA Proteins) gene were benign.
Finally, overexpression of miR34a in EBNA1 (show EBNA-1 Proteins)-expressing SNU719 cells induced typical apoptosis, suggesting that reactivation of miR34a in EBNA1 (show EBNA-1 Proteins)-expressing gastric cancer cells could be a strategy for treatment of EBV-infected gastric cancer cells.
NOX2 expression was significantly higher in the cortex of asphyctic suicide subjects than in non-suicidal asphyxia and controls.
Acute myeloid leukemia (show BCL11A Proteins) cells -derived NOX2 drives transfer of mitochondria via the generation of superoxide.
NOX2, NOX4 (show NOX4 Proteins), and mitochondrial-derived reactive oxygen species contribute to angiopoietin-1 (show ANGPT1 Proteins) signaling and angiogenic responses in endothelial cells.
PFK-2 (show PFKFB3 Proteins) seems to be a strategic element that links NADPH oxidase (show NOX1 Proteins) activation and glycolysis modulation, and, as such, is proposed as a potential therapeutic target in inflammatory diseases.
Data indicate that the efficiency of NADPH oxidase (show NOX1 Proteins) enzymatic activity is higher at endoplasmic reticulum (ER).
A p47(phox) and Src kinase activation of peroxide production by Nox2 appears to be an important contributor to vascular contractile mechanisms mediated through activation of protein kinase C
Neurofibromin (show NF1 Proteins) regulates macrophage superoxide production via p21Ras.Neurofibromin-deficient smooth muscle cells are sensitive to oxidative stress.NADPH oxidase 2 is required for NF1 (show NF1 Proteins) arterial stenosis.Neurofibromatosis type 1 patients have evidence of chronic oxidative stress.
We examined the pattern of NOX expression in spinal cords of patients and mouse models of ALS and analyzed the impact of genetic deletion of the NOX1 (show NOX1 Proteins) and 2 isoforms as well as pharmacological NOX inhibition in the SOD1 (show SOD1 Proteins)(G93A) ALS mouse model.In contrast to previous publications, survival of SOD1 (show SOD1 Proteins)(G93A) mice was not modified upon breeding with constitutive NOX1 (show NOX1 Proteins) and NOX2 deficient mice.
Spinal cord injury leads to a significant increase in NOX2 expression. The reduction in M2 polarization is associated with a peak in NOX2 expression.
NOX2 has a role in leukocyte activation and in thrombus formation
mice deficient in reactive oxygen species production by NOX2 due to the absence of the gp91 (show LILRB3 Proteins) subunit had significantly more severe pathology in the later stages of infection with Leishmania amazonensis
indicate that following traumatic brain injury NOX2 inhibition promotes a robust anti-inflammatory response in macrophages/microglia that is mediated by the IL-10 (show IL10 Proteins)/STAT3 (show STAT3 Proteins) signaling pathway
The results suggest that Nrf2 (show NFE2L2 Proteins) is an important regulator of the retinal milieu during tissue ischemia, and that the Nrf2 (show NFE2L2 Proteins)/NOX2 balance may play a critical role in determining the fate of ischemic revascularization.
North American ginseng inhibits myocardial NOX2-ERK1/2-TNF-alpha (show TNF Proteins) signaling pathway and improves cardiac function in endotoxemia, suggesting that NA ginseng may have the potential in the prevention of clinical sepsis.
Study demonstrate that Nox2 signaling via inactivation of phosphatase and tensin homolog and activation of the PI3K/Akt (show AKT1 Proteins) pathway leads to membrane ruffling and macropinocytosis.
our results demonstrate that 5-HT (show DDC Proteins) induces the invasion of commensal E. coli into gut (show GUSB Proteins) submucosa by amplifying commensal bacteria-induced epithelial signaling (superoxide production and the inductions of NOX2 and TLR2/TLR4 (show TLR4 Proteins)). The authors suggest that these changes may constitute the molecular basis for the pathogenesis of inflammatory bowel disease (IBD).
These results suggested that resveratrol strongly enhances the RA-induced O2(-)-generating activity via up-regulation of gp91-phox gene expression in U937 cells.
sub-vasomotor concentration of ET-1 (show EDN1 Proteins) leads to vascular dysfunction by impairing endothelium-dependent NO-mediated dilation via p38 (show MAPK14 Proteins) kinase-mediated production of superoxide from NADPH oxidase (show NOX1 Proteins) following ETA receptor activation
Reactive oxygen species generated by NADPH oxidase (show NOX1 Proteins) contribute to the aberrant pulmonary arterial responses in piglets exposed to 3 days of hypoxia.
Upregulation of PPAR-gamma and NADPH oxidases are involved in restenosis.
Cytochrome b (-245) is composed of cytochrome b alpha (CYBA) and beta (CYBB) chain. It has been proposed as a primary component of the microbicidal oxidase system of phagocytes. CYBB deficiency is one of five described biochemical defects associated with chronic granulomatous disease (CGD). In this disorder, there is decreased activity of phagocyte NADPH oxidase\; neutrophils are able to phagocytize bacteria but cannot kill them in the phagocytic vacuoles. The cause of the killing defect is an inability to increase the cell's respiration and consequent failure to deliver activated oxygen into the phagocytic vacuole.
cytochrome b-245, beta polypeptide
, NADPH oxidase 2
, cytochrome b-245, beta polypeptide (chronic granulomatous disease)
, Cytochrome b-245 heavy chain
, NADPH oxidase heavy chain subunit
, NADPH oxidase 1
, NADPH oxidase flavocytochrome b subunit
, cytochrome b-245 heavy chain
, cytochrome b(558) subunit beta
, cytochrome b558 subunit beta
, heme-binding membrane glycoprotein gp91phox
, neutrophil cytochrome b 91 kDa polypeptide
, p22 phagocyte B-cytochrome
, superoxide-generating NADPH oxidase heavy chain subunit
, endothelial type gp91-phox
, predicted NADPH oxidase-2