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Cytochrome b (-245) is composed of cytochrome b alpha (CYBA) and beta (CYBB) chain. 再加上，我们可以发CYBB 试剂盒 (9) 和 CYBB 蛋白 (6)和数多这个蛋白质的别的产品。
Showing 10 out of 115 products:
Human Polyclonal CYBB Primary Antibody for IF (cc), IF (p) - ABIN750688
Dalaklioglu, Tasatargil, Kale, Tanriover, Dilmac, Erin: Metastatic breast carcinoma induces vascular endothelial dysfunction in Balb-c mice: Role of the tumor necrosis factor-? and NADPH oxidase. in Vascular pharmacology 2013
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Human Polyclonal CYBB Primary Antibody for IHC (p), WB - ABIN3044252
Liao, Liu, Guo, Zhang, Zhang: Oxidative burst of circulating neutrophils following traumatic brain injury in human. in PLoS ONE 2013
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Mouse (Murine) Monoclonal CYBB Primary Antibody for IF, WB - ABIN968523
Jacobsen, Skalnik: YY1 binds five cis-elements and trans-activates the myeloid cell-restricted gp91(phox) promoter. in The Journal of biological chemistry 1999
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Human Polyclonal CYBB Primary Antibody for IHC, IHC (p) - ABIN4301440
Rajtik, Carnicka, Szobi, Giricz, O-Uchi, Hassova, Svec, Ferdinandy, Ravingerova, Adameova: Oxidative activation of CaMKIIδ in acute myocardial ischemia/reperfusion injury: A role of angiotensin AT1 receptor-NOX2 signaling axis. in European journal of pharmacology 2016
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Human Monoclonal CYBB Primary Antibody for ICC, IF - ABIN1042596
Burritt, Quinn, Jutila, Bond, Jesaitis: Topological mapping of neutrophil cytochrome b epitopes with phage-display libraries. in The Journal of biological chemistry 1995
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Human Polyclonal CYBB Primary Antibody for ELISA, IHC - ABIN4301436
Zhu, Lindsey, Konieczna, Eklund: Constitutive activation of SHP2 protein tyrosine phosphatase inhibits ICSBP-induced transcription of the gene encoding gp91PHOX during myeloid differentiation. in Journal of leukocyte biology 2008
Human Monoclonal CYBB Primary Antibody for WB - ABIN1042597
Baniulis, Burritt, Taylor, Dinauer, Heyworth, Parkos, Magnusson, Jesaitis: Monoclonal antibody CL5 recognizes the amino terminal domain of human phagocyte flavocytochrome b558 large subunit, gp91phox. in European journal of haematology 2005
Human Polyclonal CYBB Primary Antibody for WB - ABIN2781794
Fink, Duval, Martel, Soucy-Faulkner, Grandvaux: Dual role of NOX2 in respiratory syncytial virus- and sendai virus-induced activation of NF-kappaB in airway epithelial cells. in Journal of immunology (Baltimore, Md. : 1950) 2008
The nox1 (显示 NOX1 抗体), nox2/cybb expression in zebrafish during early nervous system development from 12 to 48 hours post fertilization
Data indicate that NADPH oxidase (显示 NOX1 抗体) NOx2 inhibition attenuates endoplasmic reticulum (ER) stress and apoptosis.
NOX2, NOX4 (显示 NOX4 抗体), and mitochondrial-derived reactive oxygen species contribute to angiopoietin-1 (显示 ANGPT1 抗体) signaling and angiogenic responses in endothelial cells.
PFK-2 (显示 PFKFB3 抗体) seems to be a strategic element that links NADPH oxidase (显示 NOX1 抗体) 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 (显示 CD8A 抗体) 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 (显示 CD8A 抗体)+ T cells in close contact with target T cells release NADPH oxidase 2-containing microvesicles that inhibit TCR activation by elevating ROS (显示 ROS1 抗体) and thereby reducing phosphorylation of the TCR-associated kinase ZAP70 (显示 ZAP70 抗体).
Thioredoxin (显示 TXN 抗体) attenuates oxidized low-density lipoprotein induced oxidative stress in human umbilical vein endothelial cells by reducing NOX2-NOX4 (显示 NOX4 抗体) activity.
Nox4 (显示 NOX4 抗体)-derived H2O2 in part activates Nox2 to increase mitochondrial ROS (显示 ROS1 抗体) via pSer36-p66Shc (显示 SHC1 抗体), thereby enhancing VEGFR2 (显示 KDR 抗体) signaling and angiogenesis in endothelial cells.
Cytochrome b558 (显示 CYBA 抗体) also traffics from a lysosomal pool to phagosomes and this is required to replenish oxidatively damaged NOX2.
Nox4 (显示 NOX4 抗体) should contribute to the pathological processes insubarachnoid hemorrhage(SAH (显示 ACSM3 抗体))-induced early brain injury (EBI (显示 TBL1X 抗体)), and there was not an overlay effect of Nox2 inhibition and Nox4 (显示 NOX4 抗体) inhibition on preventing SAH (显示 ACSM3 抗体)-induced EBI (显示 TBL1X 抗体).
NADPH oxidase (显示 NOX1 抗体) promotes Parkinsonian phenotypes by impairing autophagic flux in an mTORC1-independent fashion in a cellular model of Parkinson's disease
TLR4 (显示 TLR4 抗体)- and TLR2 (显示 TLR2 抗体)-induced IRAK (显示 IRAK1 抗体)-ERK (显示 EPHB2 抗体) pathway cross-talks with p67phox (显示 NCF2 抗体)-Nox-2 for reactive oxygen species generation, thus regulating IL-1beta (显示 IL1B 抗体) transcription and processing in monocytic cells.
Data indicate that the efficiency of NADPH oxidase (显示 NOX1 抗体) enzymatic activity is higher at endoplasmic reticulum (ER).
A p47(phox) and Src kinase (显示 CSK 抗体) activation of peroxide production by Nox2 appears to be an important contributor to vascular contractile mechanisms mediated through activation of protein kinase C (显示 PKC 抗体)
Redox-dependent regulation of EGFR (显示 EGFR 抗体) activation in airway epithelial cells was found to strongly depend on activation of either DUOX1 (显示 DUOX1 抗体) 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 (显示 YWHAZ 抗体) activity of peroxiredoxin 6 (显示 PRDX6 抗体) 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 (显示 SUPT6H 抗体)-NOX-inhibitor APX (显示 SHROOM1 抗体)-115 treatment decreased NADPH oxidase (显示 NOX1 抗体) (Nox) Nox1 (显示 NOX1 抗体), Nox2, and Nox4 (显示 NOX4 抗体) protein expression in the kidney.
NOX2 regulates proinflammatory TLR signaling and alveolar remodeling induced by a single dose of lipopolysaccharides.
a deficiency in MyD88 (显示 MYD88 抗体) 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 (显示 NCF1 抗体), p67phox (显示 NCF2 抗体), p40phox (显示 NCF4 抗体), and Rac1 or Rac2 (显示 RAC2 抗体)) and a membrane-associated cytochrome b558 (显示 CYBA 抗体) reductase made up of gp91phox and p22phox (显示 CYBA 抗体) subunits.
Macrophage-produced HMGB1 (显示 HMGB1 抗体) leads to aortic inflammation and acts as a trigger for CD4 (显示 CD4 抗体)(+) T-cell-produced IL-17 (显示 IL17A 抗体) during abdominal aortic aneurysm formation. HMGB1 (显示 HMGB1 抗体) release is dependent on Nox2 activation, which can be inhibited by MSCs leading to attenuation of proinflammatory cytokines and protection against AAA (显示 AAAS 抗体) formation.
NOX2 is important for ROS (显示 ROS1 抗体) generation induced by both the GPCR (显示 GPBAR1 抗体) and the GPVI (显示 GP6 抗体)/ITAM signaling pathways in blood platelets.
sub-vasomotor concentration of ET-1 (显示 EDN1 抗体) leads to vascular dysfunction by impairing endothelium-dependent NO-mediated dilation via p38 (显示 MAPK14 抗体) kinase-mediated production of superoxide from NADPH oxidase (显示 NOX1 抗体) following ETA receptor activation
Reactive oxygen species generated by NADPH oxidase (显示 NOX1 抗体) contribute to the aberrant pulmonary arterial responses in piglets exposed to 3 days of hypoxia.
Upregulation of PPAR-gamma (显示 PPARG 抗体) and NADPH (显示 NQO1 抗体) 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