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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 抗体 (117) 和 CYBB 蛋白 (6)和数多这个蛋白质的别的产品。
Showing 5 out of 11 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 (显示 NOX1 ELISA试剂盒), 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 ELISA试剂盒) NOx2 inhibition attenuates endoplasmic reticulum (ER) stress and apoptosis.
Finally, overexpression of miR34a in EBNA1-expressing SNU719 cells induced typical apoptosis, suggesting that reactivation of miR34a in EBNA1-expressing gastric cancer cells could be a strategy for treatment of EBV-infected gastric cancer cells.
NOX2 expression was significantly higher in the cortex of asphyctic suicide subjects than in non-suicidal asphyxia and controls.
Acute myeloid leukemia (显示 BCL11A ELISA试剂盒) cells -derived NOX2 drives transfer of mitochondria via the generation of superoxide.
NOX2, NOX4 (显示 NOX4 ELISA试剂盒), and mitochondrial-derived reactive oxygen species contribute to angiopoietin-1 (显示 ANGPT1 ELISA试剂盒) signaling and angiogenic responses in endothelial cells.
PFK-2 (显示 PFKFB3 ELISA试剂盒) seems to be a strategic element that links NADPH oxidase (显示 NOX1 ELISA试剂盒) 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 ELISA试剂盒) 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 ELISA试剂盒)+ 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 ELISA试剂盒) and thereby reducing phosphorylation of the TCR-associated kinase ZAP70 (显示 ZAP70 ELISA试剂盒).
Thioredoxin (显示 TXN ELISA试剂盒) attenuates oxidized low-density lipoprotein induced oxidative stress in human umbilical vein endothelial cells by reducing NOX2-NOX4 (显示 NOX4 ELISA试剂盒) activity.
Nox4 (显示 NOX4 ELISA试剂盒)-derived H2O2 in part activates Nox2 to increase mitochondrial ROS (显示 ROS1 ELISA试剂盒) via pSer36-p66Shc (显示 SHC1 ELISA试剂盒), thereby enhancing VEGFR2 (显示 KDR ELISA试剂盒) signaling and angiogenesis in endothelial cells.
Cytochrome b558 (显示 CYBA ELISA试剂盒) also traffics from a lysosomal pool to phagosomes and this is required to replenish oxidatively damaged NOX2.
Data indicate that the efficiency of NADPH oxidase (显示 NOX1 ELISA试剂盒) enzymatic activity is higher at endoplasmic reticulum (ER).
A p47(phox) and Src kinase (显示 CSK ELISA试剂盒) 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 ELISA试剂盒)
Virus infection activates endosomal NOX2 oxidase and restricts TLR7 (显示 TLR7 ELISA试剂盒) signaling, and that an endosomal NOX2 inhibitor decreases viral pathogenicity.
These data suggest that endothelial SHIP2 (显示 INPPL1 ELISA试剂盒) is required to maintain normal systemic glucose homeostasis and prevent oxidative stress-induced (显示 SQSTM1 ELISA试剂盒) endothelial dysfunction.
NOX2 is a negative regulator of maximal glucose stimulation of insulin (显示 INS ELISA试剂盒) secretion in C57BL/6J mouse islets.
Nox2- and Nox4 (显示 NOX4 ELISA试剂盒)-derived reactive oxygen species contribute to stem cell pluripotency maintenance and self-renewal.
Redox-dependent regulation of EGFR (显示 EGFR ELISA试剂盒) activation in airway epithelial cells was found to strongly depend on activation of either DUOX1 (显示 DUOX1 ELISA试剂盒) 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 ELISA试剂盒) activity of peroxiredoxin 6 (显示 PRDX6 ELISA试剂盒) 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 (显示 SHROOM1 ELISA试剂盒)-115 treatment decreased NADPH oxidase (显示 NOX1 ELISA试剂盒) (Nox) Nox1 (显示 NOX1 ELISA试剂盒), Nox2, and Nox4 (显示 NOX4 ELISA试剂盒) protein expression in the kidney.
sub-vasomotor concentration of ET-1 (显示 EDN1 ELISA试剂盒) leads to vascular dysfunction by impairing endothelium-dependent NO-mediated dilation via p38 (显示 MAPK14 ELISA试剂盒) kinase-mediated production of superoxide from NADPH oxidase (显示 NOX1 ELISA试剂盒) following ETA receptor activation
Reactive oxygen species generated by NADPH oxidase (显示 NOX1 ELISA试剂盒) 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