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Cytochrome b (-245) is composed of cytochrome b alpha (CYBA) and beta (CYBB) chain. Additionally we are shipping CYBB Antibodies (116) and CYBB Proteins (6) and many more products for this protein.
Showing 3 out of 9 products:
Human CYBB ELISA Kit for Sandwich ELISA - ABIN418998
Tassone, Perticone, Sciacqua, Mafrici, Settino, Malara, Mollace, Sesti, Perticone: Low dose of acetylsalicylic acid and oxidative stress-mediated endothelial dysfunction in diabetes: a short-term evaluation. in Acta diabetologica 2015
Rat (Rattus) CYBB ELISA Kit for Sandwich ELISA - ABIN433568
Du, Wang, Wang: Role of RhoA/MERK1/ERK1/2/iNOS signaling in ocular ischemic syndrome. in Graefe's archive for clinical and experimental ophthalmology 2016
The nox1 (show NOX1 ELISA Kits), nox2/cybb expression in zebrafish during early nervous system development from 12 to 48 hours post fertilization
Data indicate that NADPH oxidase (show NOX1 ELISA Kits) NOx2 inhibition attenuates endoplasmic reticulum (ER) stress and apoptosis.
Acute myeloid leukemia (show BCL11A ELISA Kits) cells -derived NOX2 drives transfer of mitochondria via the generation of superoxide.
NOX2, NOX4 (show NOX4 ELISA Kits), and mitochondrial-derived reactive oxygen species contribute to angiopoietin-1 (show ANGPT1 ELISA Kits) signaling and angiogenic responses in endothelial cells.
PFK-2 (show PFKFB3 ELISA Kits) seems to be a strategic element that links NADPH oxidase (show NOX1 ELISA Kits) activation and glycolysis modulation, and, as such, is proposed as a potential therapeutic target in inflammatory diseases.
data support NOX2 as a critical component of the suppressive machinery of CD8 (show CD8A ELISA Kits) Tregs and suggest that repairing NOX2 deficiency in these cells may protect older individuals from tissue-destructive inflammatory disease, such as large-vessel vasculitis.
CD8 (show CD8A ELISA Kits)+ T cells in close contact with target T cells release NADPH oxidase 2-containing microvesicles that inhibit TCR activation by elevating ROS (show ROS1 ELISA Kits) and thereby reducing phosphorylation of the TCR-associated kinase ZAP70 (show ZAP70 ELISA Kits).
Thioredoxin (show TXN ELISA Kits) attenuates oxidized low-density lipoprotein induced oxidative stress in human umbilical vein endothelial cells by reducing NOX2-NOX4 (show NOX4 ELISA Kits) activity.
Nox4 (show NOX4 ELISA Kits)-derived H2O2 in part activates Nox2 to increase mitochondrial ROS (show ROS1 ELISA Kits) via pSer36-p66Shc (show SHC1 ELISA Kits), thereby enhancing VEGFR2 (show KDR ELISA Kits) signaling and angiogenesis in endothelial cells.
Cytochrome b558 (show CYBA ELISA Kits) also traffics from a lysosomal pool to phagosomes and this is required to replenish oxidatively damaged NOX2.
Nox4 (show NOX4 ELISA Kits) should contribute to the pathological processes insubarachnoid hemorrhage(SAH (show ACSM3 ELISA Kits))-induced early brain injury (EBI (show TBL1X ELISA Kits)), and there was not an overlay effect of Nox2 inhibition and Nox4 (show NOX4 ELISA Kits) inhibition on preventing SAH (show ACSM3 ELISA Kits)-induced EBI (show TBL1X ELISA Kits).
NADPH oxidase (show NOX1 ELISA Kits) promotes Parkinsonian phenotypes by impairing autophagic flux in an mTORC1-independent fashion in a cellular model of Parkinson's disease
Data indicate that the efficiency of NADPH oxidase (show NOX1 ELISA Kits) enzymatic activity is higher at endoplasmic reticulum (ER).
A p47(phox) and Src kinase (show CSK ELISA Kits) activation of peroxide production by Nox2 appears to be an important contributor to vascular contractile mechanisms mediated through activation of protein kinase C (show PKC ELISA Kits)
Nox2- and Nox4 (show NOX4 ELISA Kits)-derived reactive oxygen species contribute to stem cell pluripotency maintenance and self-renewal.
Redox-dependent regulation of EGFR (show EGFR ELISA Kits) activation in airway epithelial cells was found to strongly depend on activation of either DUOX1 (show DUOX1 ELISA Kits) or NOX2.
NOX2 signaling in macrophages participates in the pathogenesis of obesity, and reinforce a key role for macrophage inflammation in diet-induced metabolic and neurologic decline
Studies in knockout and knock-in mice showed that the phospholipase A2 (show YWHAZ ELISA Kits) activity of peroxiredoxin 6 (show PRDX6 ELISA Kits) activates NOX2 in cultured pulmonary endothelial cells and alveolar macrophages, clarifying the metabolism of lysophosphatidyl chold to lysophosphatidic acid.
NOX2 knockout mice had significantly lower blood pressure than littermate controls, with both endothelial cells and myeloid cells having a deficiency in NOX2.
Data show that pan-NOX-inhibitor APX (show SHROOM1 ELISA Kits)-115 treatment decreased NADPH oxidase (show NOX1 ELISA Kits) (Nox) Nox1 (show NOX1 ELISA Kits), Nox2, and Nox4 (show NOX4 ELISA Kits) protein expression in the kidney.
NOX2 regulates proinflammatory TLR signaling and alveolar remodeling induced by a single dose of lipopolysaccharides.
a deficiency in MyD88 (show MYD88 ELISA Kits) or CybB is associated with impaired bacterial clearance and increased granuloma formation in the lung.
NOX2 isoform was first discovered as a component of the oxidative burst in neutrophils and is a complex consisting of several cytosolic subunits (p47phox (show NCF1 ELISA Kits), p67phox (show NCF2 ELISA Kits), p40phox (show NCF4 ELISA Kits), and Rac1 or Rac2 (show RAC2 ELISA Kits)) and a membrane-associated cytochrome b558 (show CYBA ELISA Kits) reductase made up of gp91phox and p22phox (show CYBA ELISA Kits) subunits.
sub-vasomotor concentration of ET-1 (show EDN1 ELISA Kits) leads to vascular dysfunction by impairing endothelium-dependent NO-mediated dilation via p38 (show MAPK14 ELISA Kits) kinase-mediated production of superoxide from NADPH oxidase (show NOX1 ELISA Kits) following ETA receptor activation
Reactive oxygen species generated by NADPH oxidase (show NOX1 ELISA Kits) 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