Cytochrome B-245, beta Polypeptide (CYBB) Kits ELISA

Zebrafish Cytochrome B-245, beta Polypeptide (CYBB) interaction partners

1. our results show that Nox2/Cybb is important for retinotectal development in zebrafish

2. The nox1, nox2/cybb expression in zebrafish during early nervous system development from 12 to 48 hours post fertilization

Rabbit Cytochrome B-245, beta Polypeptide (CYBB) interaction partners

1. Data indicate that NADPH oxidase NOx2 inhibition attenuates endoplasmic reticulum (ER) stress and apoptosis.

Human Cytochrome B-245, beta Polypeptide (CYBB) interaction partners

1. The observation leads to the hypothesis that, in adults, regular exercise preserves artery dilation through Nox2 decreased activity.

2. Inhibition of NOX2 and NOX1 with siRNA or chemical inhibitors significantly suppresses reactive oxygen species production and DNA damage induced by acidic bile salts.

3. Levels of NADPH oxidase subunits NOX2 and NOX4 proteins in peripheral blood mononuclear cells of the sevoflurane group were lower than the propofol group (p=0.033, p<0.001, p<0.001and p<0.001, respectively).

4. Characterization of 4 New Mutations in the CYBB Gene in 10 Iranian Families With X-linked Chronic Granulomatous Disease.

5. In children exposed to passive smoking, Nox2-derived oxidative stress is upregulated and inversely associated with impaired artery dilation.

6. Exon skipping in CYBB mRNA and skewed inactivation of X chromosome cause late-onset chronic granulomatous disease.

7. Expression of functional gp91(phox) in hematopoietic cells did not affect their homing properties, which engrafted at high levels in mice. Extensive in vitro and in vivo genotoxicity studies found no evidence for adverse mutagenesis related to vector treatment. These studies paved the way for the approval of clinical trials in Europe and in the United States for the treatment of XCGD patients with G1XCGD gene-modified aut

8. We describe a 17-year old girl with X-linked chronic granulomatous disease caused by the expression of a heterozygous frameshift mutation in the CYBB gene at Xp21.1 causing a premature stop codon in exon 9 of the complementary DNA, leading to a truncated gp91phox protein due to skewed inactivation of the normal X chromosome. To our knowledge, this is the first report of a patient carrying this mutation in the CYBB gene.

9. platelet aggregation resulted to be higher in patients with atrial fibrillation carrying the C2238 ANP gene variant with respect to non-carriers. In conclusions, C2238/alphaANP promotes platelet aggregation through the activation of Nox2 and the reduction of cAMP.

10. These results suggest the specific involvement of Nox4 and Nox2 subunits as physiologically relevant endothelial sources of H2O2 generation that contribute to the endothelium-dependent vasodilatation of renal arteries and therefore have a protective role in kidney vasculature.

11. The activity of Nox2 is lowered in neutrophils of untreated hypercholesterolemic patients. Finally oxysterols (25-hydroxy-cholesterol or 5alpha, 6alpha - epoxy-cholesterol) do not induce effects different from that of non-oxidized cholesterol.

12. indicated that miR-27b exerted its protective role in retinal pigment epithelium cells under PDGF-BB stimulation was partially through regulation of Nox2

13. Findings show that under elevated glucose concentration, NOX2 is activated by SMIT1 triggering ROS production in the heart.

14. Human post-mortem and animal studies have identified elevated NOX2 and NOX4 levels in the injured brain, suggesting that these two NOXs are involved in the pathogenesis of Traumatic brain injury (TBI)

15. To further elucidate the mAb 7D5 epitope on human gp91(phox) , chimeric DNA expressed human and mouse gp91(phox) recombinant protein were constructed. The fusion proteins were immunostained for mAb 7D5 and analyzed by FACS and western blot analysis.

16. Phorbol 12-myristate-13-acetate-stimulated NOX2-NIS (NOX-specific Insertion Sequence) phosphorylation by ATM kinase causes a dynamic switch that deactivates NOX2 activity. This downregulation may be defective in NOX2-NIS3 mutant because of the absence of Ser486.

17. This study identifies one novel mutation in the IL2RG gene and another, previously described mutation in the CYBB genes. It is the first report establishing a diagnosis of X-SCID and X-CGD using WES in Chinese patients.

18. 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.

19. 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 generation) and subsequent biological changes (e.g., NOX2 induction) by BJ-1301 was superior

20. Translated to human pathophysiology, 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.

Cow (Bovine) Cytochrome B-245, beta Polypeptide (CYBB) interaction partners

1. Data indicate that the efficiency of NADPH oxidase enzymatic activity is higher at endoplasmic reticulum (ER).

2. 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

Mouse (Murine) Cytochrome B-245, beta Polypeptide (CYBB) interaction partners

1. Increased reactive oxygen species production from NOX2 is a possible molecular mechanism responsible for developmental origins of cardiovascular disease in offspring of diabetic mothers.

2. NOX2 deficiency results in both granulomas and the accumulation of antitumoural immune cells in the lungs that probably mediate the decreased pulmonary metastatic colonization.

3. Exosomes from ACE2-expressing endothelial progenitor cells protect ageing endothelial cells against hypoxia/reoxygenation-induced injury through the miR-18a/Nox2/ROS pathway.

4. report illustrates that BI1 functions as a novel microvascular guardian in cardiac IR injury that operates via inhibition of the Syk-Nox2-Drp1-mitochondrial fission signaling axis.

5. Attenuation of oxidative stress-induced lesions in skeletal muscle in a mouse model of obesity-independent hyperlipidemia and atherosclerosis through the inhibition of Nox2 activity has been demonstrated.

6. Adoptive transfer of Tregs confirmed that Nox2-deficient cells had greater inhibitory effects on Ang II-induced heart remodeling than WT cells. These results identify a previously unrecognized role of Nox2 in modulating suppression of Tregs, which acts to enhance hypertension and cardiac remodeling.

7. Eliminating Nox2 reactive oxygen species production prevents microtubule disorganization and reduces fibrosis and muscle stiffness in Duchenne muscular dystrophy diaphragm.

8. this study shows that oxidant signaling mediated by Nox2 in neutrophils promotes regenerative myelopoiesis and tissue recovery following ischemic damage

9. mice lacking the Cybb subunit of Phox suffered from a specific defect in tolerance, which was caused by unregulated Caspase-1 activation, IL-1beta production, and neutrophil influx into the lung.

10. AGEs-related and NOX-triggered oxidative stress of vascular endothelial cells leads to angiogenesis impairment at the bone-implant interface in diabetes

11. evidence of a cell-specific anti-inflammatory role for Nox2 in alveolar macrophages.

12. Reactive oxygen species regulate axonal regeneration through the release of exosomal NADPH oxidase 2 complexes which are taken up into injured axons.

13. Nox1(-/-) and Nox2(-/-) mice showed higher susceptibility to avirulent type III Toxoplasma gondii infection than wild-type mice

14. We propose that NOX2-derived ROS may contribute to the progression of KRAS-induced leukemia and that strategies to target NOX2 merit further evaluation in RAS-mutated hematopoietic cancer.

15. The results strongly suggest that Nox2 destabilization through disrupting TRPC3-Nox2 complex underlies attenuation of hyperglycemia-induced heart failure by TRPC6.

16. Our data collectively suggest that Nox2 is implicated in high-fat diet-induced deleterious bone remodeling by enhancing bone marrow adipogenesis and osteoclastogenesis

17. Combination of exogenous and endogenous environmental factors with minimally toxic dose synergistically propagates dopaminergic neurodegeneration through activating microglial NOX2.

18. Reducing NADPH oxidase-2 by impeding p67(phox) activation in infected mouse macrophages reduced viral entry and inflammation.

19. the study reports a novel mechanistic pathway of leptin-mediated renal inflammation that is dependent on NOX-2-miR21 axis in ectopic manifestations underlying non-alcoholic fatty liver disease-induced co-morbidities

20. Whereas the oxidative burst in myeloid cells is mainly catalyzed by the NOX2 isotype, in epithelial cells other isotypes of the NADPH oxidases family are involved, especially NOX4

Pig (Porcine) Cytochrome B-245, beta Polypeptide (CYBB) interaction partners

1. These results suggested that resveratrol strongly enhances the RA-induced O2(-)-generating activity via up-regulation of gp91-phox gene expression in U937 cells.

2. sub-vasomotor concentration of ET-1 leads to vascular dysfunction by impairing endothelium-dependent NO-mediated dilation via p38 kinase-mediated production of superoxide from NADPH oxidase following ETA receptor activation

3. activated during ischemia/reperfusion in a complement-dependent manner, and may contribute to the renal damage

4. Reactive oxygen species generated by NADPH oxidase contribute to the aberrant pulmonary arterial responses in piglets exposed to 3 days of hypoxia.

5. Upregulation of PPAR-gamma and NADPH oxidases are involved in restenosis.