Cytochrome B-245, beta Polypeptide Proteins (CYBB)

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

1. 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. 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.

2. 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.

3. 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.

4. 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.

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

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

7. 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)

8. 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.

9. 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.

10. 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.

11. 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.

12. 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

13. 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.

14. We demonstrated that small interfering RNA (siRNA)-mediated knockdown of PRR, Nox2 and Nox4 significantly reduced the HG-induced stimulation of VEGF. On the other hand, Nox4 overexpression significantly potentiated PRR-induced stimulation of VEGF under hyperglycemia in ARPE-19 cells.

15. NOX2 isoform in blood samples has been considered as biomarker of disease severity and treatment efficacy in neurodegenerative disease. (Review)

16. 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.

17. Hyperinsulinemia modulates arteriolar flow-induced dilation via Nox2-mediated superoxide production.

18. this study shows that aging-associated metabolic disorder induces Nox2 activation and oxidative damage of endothelial function

19. Results show that Nox2 knockdown attenuated HIV-1 Tat-induced HDAC6 expression and subsequent expression of chemokines. Also, the data provide evidence that HDAC6 mediates HIV-1 Tat-induced reactive oxygen species generation by regulating the activity and expression of Nox2-based NADPH oxidase in astrocytes, and demonstrate the existence of a crosstalk between HDAC6 and NADPH oxidase in HIV-1 Tat-stimulated astrocytes.

20. Porphyromonas gingivalis modulates the danger signal eATP-induced NOX2 signaling and also induces host glutathione synthesis to likely avoid HOCl mediated clearance.

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

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

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

4. 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

5. 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

6. Proximal point of bifurcation in cardiac insulin signaling through the simultaneous activation of both NOX2 and NOX4 was identified. Each NOX isoform generates H2O2 in cardiac myocytes with distinct time courses, with H2O2 derived from NOX2 augmenting Akt-dependent metabolic effects of insulin, while H2O2 from NOX4 blocks beta adrenergic increases in inotropy.

7. AIF activated AMPK-dependent Nox2 signaling pathway.

8. Nox2 may be a therapeutic target for AII-induced skeletal muscle atrophy.

9. These results indicated that integrin CD11b mediates alpha-synuclein-induced NOX2 activation through a RhoA-dependent pathway.

10. These results showed that CR3 regulated Nox2 activation and dopaminergic neurodegeneration through a Src-Erk-dependent pathway in a two pesticide-induced Parkinson's disease (PD) model, providing novel insights into the immune pathogenesis of PD.

11. 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.

12. Echocardiography revealed that ALDH-2(-/-)/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

13. Nox2 activation favors thioredoxin-1 (TRX-1)/p40phox interaction, which leads to exclusion of TRX-1 from the nucleus.

14. these observations indicate that Nox2-mediated ROS production promotes arterial EC specification in differentiating miPSCs by activating the Notch signaling pathway and contributes to the angiogenic potency of transplanted miPSC-derived ECs.

15. in addition to a secretory role, VAMP8-mediates trafficking of NOX2 to endosomes and phagosomes and this promotes induction of cytolytic T cell immune responses

16. This study for the first time establishes the significant role of Nox2 in mediating the NE-induced pathological adrenergic signaling in cardiac myoblasts.

17. We propose that NOX2-derived ROS 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

18. NOX2 knockout mice was used to study the role of NOX2 in mediating NLRP3 inflammasome expression and activation following a controlled cortical impact.

19. Myricitrin attenuated the generation of intracellular ROS by inhibiting the assembly of components of the gp91(phox) and p47(phox). Suppression of ROS generation using NAC or apocynin or by silencing gp91(phox) and p47(phox) all demonstrated that decreasing the level of ROS inhibited the LPS-induced inflammatory response.

20. Ablation of NOX2 prevented inflammation-induced axon initial segment plasticity.

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.