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Cytochrome b (-245) is composed of cytochrome b alpha (CYBA) and beta (CYBB) chain.
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.
Translated to human pathophysiology, (show ALDH2 Proteins)we found increased gp91(phox) expression in endomyocardial biopsies of Alcoholic cardiomyopathy (ACM) patients. In conclusion, ACM is promoted by ACA-driven mitochondrial dysfunction and can be improved by ablation of NOX2/gp91(phox). NOX2/gp91(phox) therefore might be a potential pharmacological target to treat ACM.
We demonstrated that small interfering RNA (siRNA)-mediated knockdown of PRR (show PVRL1 Proteins), Nox2 and Nox4 (show NOX4 Proteins) significantly reduced the HG-induced stimulation of VEGF (show VEGFA Proteins). On the other hand, Nox4 (show NOX4 Proteins) overexpression significantly potentiated PRR (show PVRL1 Proteins)-induced stimulation of VEGF (show VEGFA Proteins) under hyperglycemia in ARPE-19 cells.
NOX2 isoform in blood samples has been considered as biomarker of disease severity and treatment efficacy in neurodegenerative disease. (Review)
Study demonstrates that there is no increase of NOX2 expression in schizophrenic patients. Unexpectedly, however, the study found that NOX2 expression was decreased in patients with bipolar disorder.
Hyperinsulinemia modulates arteriolar flow-induced dilation via Nox2-mediated superoxide production.
this study shows that aging-associated metabolic disorder induces Nox2 activation and oxidative damage of endothelial function
Results show that Nox2 knockdown attenuated HIV-1 Tat (show TAT Proteins)-induced HDAC6 (show HDAC6 Proteins) expression and subsequent expression of chemokines. Also, the data provide evidence that HDAC6 (show HDAC6 Proteins) mediates HIV-1 Tat (show TAT Proteins)-induced reactive oxygen species generation by regulating the activity and expression of Nox2-based NADPH oxidase (show NOX1 Proteins) in astrocytes, and demonstrate the existence of a crosstalk between HDAC6 (show HDAC6 Proteins) and NADPH oxidase (show NOX1 Proteins) in HIV-1 Tat (show TAT Proteins)-stimulated astrocytes.
Porphyromonas gingivalis modulates the danger signal eATP-induced NOX2 signaling and also induces host glutathione synthesis to likely avoid HOCl mediated clearance.
the increased oxidative stress was mediated by nox2 dependent reactive oxygen species overproduction that could downregulate whole-cell K(+) currents
Nox2 activity efficiently contributes to the mechanism of oxidative stress-induced (show SQSTM1 Proteins) increase in premature aging conferred by doxorubicin. The importance of modulation of Nox2 in human EPCs could reveal a useful tool to restore endothelial progenitor cells physiological function and properties.
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
These results showed that CR3 (show ITGAM Proteins) regulated Nox2 activation and dopaminergic neurodegeneration through a Src (show SRC Proteins)-Erk (show EPHB2 Proteins)-dependent pathway in a two pesticide-induced Parkinson's disease (PD) model, providing novel insights into the immune pathogenesis of PD.
High levels of NOX2 were found in mouse adult neurogenic brain regions. NOX2-deficient brain showed decrease in neuroprecursor cell pool and lowered expression of genes involved in neural differentiation.
Echocardiography revealed that ALDH-2 (show ALDH2 Proteins)(-/-)/gp91(phox-/-) mice were protected from ACA-overload-induced HF after 5 weeks of 2% EtOH-diet, demonstrating that NOX2-derived O2(*-) contributes to the development of ACM
Nox2 activation favors thioredoxin-1 (TRX-1 (show TXN Proteins))/p40phox (show NCF4 Proteins) interaction, which leads to exclusion of TRX-1 (show TXN Proteins) from the nucleus.
these observations indicate that Nox2-mediated ROS (show ROS1 Proteins) production promotes arterial EC specification in differentiating miPSCs by activating the Notch (show NOTCH1 Proteins) signaling pathway and contributes to the angiogenic potency of transplanted miPSC-derived ECs.
in addition to a secretory role, VAMP8 (show VAMP8 Proteins)-mediates trafficking of NOX2 to endosomes and phagosomes and this promotes induction of cytolytic T cell immune responses
This study for the first time establishes the significant role of Nox2 in mediating the NE-induced pathological adrenergic signaling in cardiac myoblasts.
We propose that NOX2-derived ROS (show ROS1 Proteins) facilitate metastasis of melanoma cells by downmodulating NK-cell function and that inhibition of NOX2 may restore IFNgamma-dependent, NK cell-mediated clearance of melanoma cells
NOX2 knockout mice was used to study the role of NOX2 in mediating NLRP3 (show NLRP3 Proteins) inflammasome expression and activation following a controlled cortical impact.
Myricitrin attenuated the generation of intracellular ROS (show ROS1 Proteins) by inhibiting the assembly of components of the gp91(phox) and p47(phox). Suppression of ROS (show ROS1 Proteins) generation using NAC or apocynin or by silencing gp91(phox) and p47(phox) all demonstrated that decreasing the level of ROS (show ROS1 Proteins) inhibited the LPS (show TLR4 Proteins)-induced inflammatory response.
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