Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Alle Spezies anzeigen
Weitere Synonyme anzeigen
Wählen Sie die Spezies und Applikation aus
anti-Human NCF1 Antikörper:
anti-Mouse (Murine) NCF1 Antikörper:
anti-Rat (Rattus) NCF1 Antikörper:
Sie gelangen zu unserer vorgefilterten Suche.
Human Polyclonal NCF1 Primary Antibody für IHC, WB - ABIN6713141
Irita, Okura, Jotoku, Nagao, Enomoto, Kurata, Desilva, Miyoshi, Matsui, Uede, Denhardt, Rittiling, Higaki: Osteopontin deficiency protects against aldosterone-induced inflammation, oxidative stress, and interstitial fibrosis in the kidney. in American journal of physiology. Renal physiology 2011
Show all 5 Pubmed References
Human Polyclonal NCF1 Primary Antibody für WB - ABIN2801889
Volpp, Nauseef, Donelson, Moser, Clark: Cloning of the cDNA and functional expression of the 47-kilodalton cytosolic component of human neutrophil respiratory burst oxidase. in Proceedings of the National Academy of Sciences of the United States of America 1989
Show all 4 Pubmed References
Mouse (Murine) Polyclonal NCF1 Primary Antibody für IHC, ELISA - ABIN1531722
Lee, Ko, Jeong, Park, Kim: β-Lapachone suppresses neuroinflammation by modulating the expression of cytokines and matrix metalloproteinases in activated microglia. in Journal of neuroinflammation 2015
Show all 2 Pubmed References
Cow (Bovine) Polyclonal NCF1 Primary Antibody für ELISA, WB - ABIN546711
Underhill, Rossnagle, Lowell, Simmons: Dectin-1 activates Syk tyrosine kinase in a dynamic subset of macrophages for reactive oxygen production. in Blood 2005
Human Polyclonal NCF1 Primary Antibody für ELISA, IHC (p) - ABIN256632
Davidson-Moncada, Lopez-Lluch, Segal, Dekker: Involvement of protein kinase D in Fc gamma-receptor activation of the NADPH oxidase in neutrophils. in The Biochemical journal 2002
Human Polyclonal NCF1 Primary Antibody für IHC, ELISA - ABIN1531718
Kröller-Schön, Steven, Kossmann, Scholz, Daub, Oelze, Xia, Hausding, Mikhed, Zinßius, Mader, Stamm, Treiber, Scharffetter-Kochanek, Li, Schulz, Wenzel, Münzel, Daiber: Molecular mechanisms of the crosstalk between mitochondria and NADPH oxidase through reactive oxygen species - studies in white blood cells and in animal models. in Antioxidants & redox signaling 2013
Show all 2 Pubmed References
Mouse (Murine) Polyclonal NCF1 Primary Antibody für IHC, WB - ABIN3021551
Sun, Ji, Guo, Liu, Wang, Ma, Hu, Wang, Jiang: Early adventitial activation characterized by NADPH oxidase expression and neovascularization in an aortic transplantation model. in Experimental and molecular pathology 2016
Human Polyclonal NCF1 Primary Antibody für IF (p), IHC (p) - ABIN1385194
Chen, Ye, Zhang, Tang, Li, Lu, Wu, Yu, Kou: Limb Remote Ischemic Postconditioning Reduces Ischemia-Reperfusion Injury by Inhibiting NADPH Oxidase Activation and MyD88-TRAF6-P38MAP-Kinase Pathway of Neutrophils. in International journal of molecular sciences 2016
Mouse (Murine) Polyclonal NCF1 Primary Antibody für ELISA, WB - ABIN4338257
Roos, Kuhns, Maddalena, Bustamante, Kannengiesser, de Boer, van Leeuwen, Köker, Wolach, Roesler, Malech, Holland, Gallin, Stasia: Hematologically important mutations: the autosomal recessive forms of chronic granulomatous disease (second update). in Blood cells, molecules & diseases 2010
Our findings in experiments on activated human retinal endothelial cells provide translational corroboration of studies in experimental models of retinal vasculopathy and support the therapeutic application of Nox4 inhibition by GKT136901 and GKT137831 in patients with retinal vascular diseases.
Tyrosine kinase substrate (Tks) proteins, analogous to the related proteins p47(phox), p40(phox) and NoxO1, also facilitate local generation of reactive oxygen species (ROS), which aid in signaling at invadopodia and/or podosomes to promote their activity. As their name suggests, Tks adaptor proteins are substrates for tyrosine kinases, especially Src. [review]
IL-27 enhances the potential of reactive oxygen species generation from monocyte-derived macrophages and dendritic cells by induction of p47(phox).
p47phox, but not p67phox or p40phox, binds to and activates Nrf2, enhancing the function of Nrf2 in suppressing inflammation.
p47phox S-glutathionylation plays an essential key role in the sustained ROS generation by human neutrophils.
patients with hereditary p47phox deficiency show reduced platelet activation suggesting a role for this Nox cytosolic subunit in platelet activation.
Decreased and increased copy numbers of NCF1 predispose to and protect against SLE.
Lysophosphatidylcholines prime polymorphonuclear neutrophil through Hck-dependent activation of PKCdelta, which stimulates PKCgamma, resulting in translocation of phosphorylated p47(phox).
There was an increased frequency of the NCF1-339 T allele in patients with systemic lupus erythematosus. The NCF1-339 T allele reduced extracellular ROS production in neutrophils and led to an increase expression of type 1 interferon-regulated genes.
Skeletal muscle protein expression of the NADPH oxidase subunits p22(phox), p47(phox), and p67(phox) was increased in obese relative to lean subjects, where p22(phox) and p67(phox) expression was attenuated by exercise training in obese subjects.
A novel role for Spns2 and S1P1&2 in the activation of p47(phox) and production of reactive oxygen species involved in hyperoxia-mediated lung injury.
Study provides evidence for a novel PKC-zeta to p47phox interaction that is required for cell transformation from blebbishields and ROS production in cancer cells.
Overexpression of p47phox is associated with increased migration/metastasis rate in melanoma.
A rare mutation in NCF1 encoding p47phox of the leukocyte NADPH oxidase causes lack of superoxide generation, leads to chronic granulomatous disease and was recently (1200-2300 years ago) introduced into the Kavkazi Jewish population
Data show that diphenylene iodonium (DPI) and apocynin can reduce hyperoxia-induced reactive oxygen species (ROS) production by decreasing the translocation and level of NADPH Oxidase p47phox.
increased levels of gp91phox, p47phox and p22phox likely account for the interferon-gamma mediated enhancement of dimethyl sulfoxide-induced Nox2 activity.
Results identifies p47phox-dependent NADPH oxidase activity as a critical component of Angpt-1-mediated endothelial barrier defense against classic inflammatory permeability factors.
DCLRE1C and NCF1 mutations have been found by whole-genome sequencing to cause primary immunodeficiency in unrelated patients.
TLR8, but not TLR7, is involved in priming of human neutrophil reactive oxygen species production by inducing the phosphorylation of p47phox and p38 MAPK.
Reduced carotid but not coronary artery atherosclerosis in patients with chronic granulomatous disease despite the high prevalence of traditional risk factors raises questions about the role of NADPH oxidase in the pathogenesis of atherosclerosis.
oxLDL-mediated cellular senescence is associated with increased p47phox recruitment to caveolae and its binding to Cav1.
ROS production stimulated by NoxO1 and p47phox limit endothelium-dependent relaxation and maintain blood pressure in mice. However, NoxO1 and p47phox cannot substitute each other despite their similar effect on vascular function. Deletion of NoxO1 induced an anti-inflammatory phenotype, whereas p47phox deletion rather elicited a hyper-inflammatory response.
we found that ROS formation and expression of p47(phox) and p67(phox), subunits of NADPH oxidase, were increased in AppTg mice but attenuated in AppTg/Cebpd(-/-) mice. Cebpd can up-regulate p47(phox) and p67(phox) transcription via a direct binding on their promoters, which results in an increase in intracellular oxidative stress
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.
Results show that Ncf1 is not needed during juvenility to protect from autoimmune arthritis later on, but conditional Ncf1 suppresses arthritis even if activated after the disease priming. The study presents in vivo evidence that Ncf1/reactive oxygen species-regulated mechanisms are different in priming than in the effector phase.
we used the Ang II infused hph-1 mice to examine the roles of NOX isoforms in the development of AAA. We generated double mutants of hph-1-NOX1, hph-1-NOX2, hph-1-p47phox, and hph-1-NOX4
Mice bearing point mutation in the Ncf1-gene develop fewer osteoclasts after ovariectomy (ovx) than wild-type mice. However, irrespective of genotype, bone mineral density decreases after ovx, indicating that a compensatory mechanism retains bone degradation after ovx.
The authors demonstrated a significant role of the host NADPH oxidase in promoting chronic inflammatory pathology in the oviduct following chlamydial infection.
Colitis susceptibility in p47(phox-/-) mice is mediated by the microbiome.
data partly explains the discrepancy of the phenotypes reported earlier utilizing the Ncf1m1J mice or Ncf1 knockout mice.
Data (including data from studies in transgenic mice) suggest that ability to generate Ncf1-derived superoxide, specifically in CD4-positive T-lymphocytes, is key for development of autoimmune responses in type 1 diabetes.
The Park7 binds to p47(phox), a subunit of the NADPH oxidase, to promote NADPH oxidase-dependent production of ROS.
p47(phox)-dependent NADPH oxidases are a major glomerular source of reactive oxygen species, contributing to kidney injury
p47phox mRNA expression was increased in diet-induced obese (DIO) mice. p47phox suppresses collateral vessel growth after femoral artery ligation in DIO mice.
These findings suggest that a p47(phox)-dependent NAD(P)H oxidase mediates the increase in diaphragm oxidants and contractile dysfunction in chronic heart failure.
The present study provides evidence that augmented EGFRtk impairs vascular function by NADPH oxidase-dependent mechanism. Therefore, EGFRtk and oxidative stress should be potential targets to treat vascular dysfunction in TD2.
NOX2/ROS activity in macrophages signals the development of antigen-specific CD8(+)T cell response.
p47phox plays a critical role in the regulation of adventitial fibroblast proliferation and migration and may be a new therapeutic target for neointimal hyperplasia
p47phox-Nox2-dependent physiological reactive oxygen species signaling suppresses inflammation in aging.
Differential Roles of Protein Complexes NOX1-NOXO1 and NOX2-p47phox in Mediating Endothelial Redox Responses to Oscillatory and Unidirectional Laminar Shear Stress.
two novel splice variants designed as NCF1-TV1 (retained intron 6) and NCF1-TV2 (retained part of intron 8)encoding two putative truncated proteins (239AA and 283AA). Two splice variants were up-regulated in the mastitis-infected cows' mammary tissues, blood and neutrophils compared with these of healthy cows.
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.
Angiotensin II inhibits the Na+/K+ pump via PKC-dependent activation of NADPH oxidase subunits.
The protein encoded by this gene is a 47 kDa cytosolic subunit of neutrophil NADPH oxidase. This oxidase is a multicomponent enzyme that is activated to produce superoxide anion. Mutations in this gene have been associated with chronic granulomatous disease.
47 kDa autosomal chronic granulomatous disease protein
, 47 kDa neutrophil oxidase factor
, NADPH oxidase organizer 2
, SH3 and PX domain-containing protein 1A
, neutrophil NADPH oxidase factor 1
, neutrophil cytosol factor 1
, neutrophil cytosolic factor 1, (chronic granulomatous disease, autosomal 1)
, nox organizer 2
, nox-organizing protein 2
, NADPH oxidase subunit (47 kD)
, NADPH oxidase subunit (47kDa)
, phagocyte oxidase 47 kDa
, neutrophil cytosolic factor 1 (47kDa, chronic granulomatous disease, autosomal 1)
, NADPH oxidase p47-phox
, predicted neutrophil cytosolic factor 1