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Cytochrome b (-245) is composed of cytochrome b alpha (CYBA) and beta (CYBB) chain. Zusätzlich bieten wir Ihnen CYBB Kits (12) und CYBB Proteine (6) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 137 products:
Human Polyclonal CYBB Primary Antibody für 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 für 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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Human Polyclonal CYBB Primary Antibody für 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 für 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 Monoclonal CYBB Primary Antibody für 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 für 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
The nox1 (zeige NOX1 Antikörper), nox2/cybb expression in zebrafish during early nervous system development from 12 to 48 hours post fertilization
Data indicate that NADPH oxidase (zeige NOX1 Antikörper) NOx2 inhibition attenuates endoplasmic reticulum (ER) stress and apoptosis.
This study identifies one novel mutation in the IL2RG (zeige IL2RG Antikörper) gene and another, previously described mutation in the CYBB genes. It is the first report establishing a diagnosis of X-SCID (zeige PRKDC Antikörper) and X-CGD using WES in Chinese patients.
In a male patient suffering from X-linked chronic granulomatous disease (CGD) we found a c.389G>T mutation in exon 5 of the CYBB gene.
The potency of RTK inhibition by BJ-1301 was lower than that of sunitinib (a multi-RTK inhibitor), but the inhibition of downstream signaling pathways (e.g., ROS (zeige ROS1 Antikörper) generation) and subsequent biological changes (e.g., NOX2 induction) by BJ-1301 was superior
Translated to human pathophysiology, (zeige ALDH2 Antikörper)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 (zeige PVRL1 Antikörper), Nox2 and Nox4 (zeige NOX4 Antikörper) significantly reduced the HG-induced stimulation of VEGF (zeige VEGFA Antikörper). On the other hand, Nox4 (zeige NOX4 Antikörper) overexpression significantly potentiated PRR (zeige PVRL1 Antikörper)-induced stimulation of VEGF (zeige VEGFA Antikörper) 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 (zeige TAT Antikörper)-induced HDAC6 (zeige HDAC6 Antikörper) expression and subsequent expression of chemokines. Also, the data provide evidence that HDAC6 (zeige HDAC6 Antikörper) mediates HIV-1 Tat (zeige TAT Antikörper)-induced reactive oxygen species generation by regulating the activity and expression of Nox2-based NADPH oxidase (zeige NOX1 Antikörper) in astrocytes, and demonstrate the existence of a crosstalk between HDAC6 (zeige HDAC6 Antikörper) and NADPH oxidase (zeige NOX1 Antikörper) in HIV-1 Tat (zeige TAT Antikörper)-stimulated astrocytes.
Data indicate that the efficiency of NADPH oxidase (zeige NOX1 Antikörper) enzymatic activity is higher at endoplasmic reticulum (ER).
A p47(phox) and Src kinase (zeige CSK Antikörper) activation of peroxide production by Nox2 appears to be an important contributor to vascular contractile mechanisms mediated through activation of protein kinase C (zeige PKC Antikörper)
Nox2 may be a therapeutic target for AII (zeige ARG2 Antikörper)-induced skeletal muscle atrophy.
These results indicated that integrin CD11b (zeige ITGAM Antikörper) mediates alpha-synuclein-induced NOX2 activation through a RhoA (zeige RHOA Antikörper)-dependent pathway.
These results showed that CR3 (zeige ITGAM Antikörper) regulated Nox2 activation and dopaminergic neurodegeneration through a Src (zeige SRC Antikörper)-Erk (zeige EPHB2 Antikörper)-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 (zeige ALDH2 Antikörper)(-/-)/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 (zeige TXN Antikörper))/p40phox (zeige NCF4 Antikörper) interaction, which leads to exclusion of TRX-1 (zeige TXN Antikörper) from the nucleus.
these observations indicate that Nox2-mediated ROS (zeige ROS1 Antikörper) production promotes arterial EC specification in differentiating miPSCs by activating the Notch (zeige NOTCH1 Antikörper) signaling pathway and contributes to the angiogenic potency of transplanted miPSC-derived ECs.
in addition to a secretory role, VAMP8 (zeige VAMP8 Antikörper)-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 (zeige ROS1 Antikörper) 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
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 (zeige EDN1 Antikörper) leads to vascular dysfunction by impairing endothelium-dependent NO-mediated dilation via p38 (zeige MAPK14 Antikörper) kinase-mediated production of superoxide from NADPH oxidase (zeige NOX1 Antikörper) following ETA receptor 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.
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