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anti-Human NOS2 Antikörper:
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Human Polyclonal NOS2 Primary Antibody für ICC, IF - ABIN4325968
Pulido, Shames, Fullerton, Sheridan, Selzman, Gamboni-Robertson, Bensard, McIntyre: Differential inducible nitric oxide synthase expression in systemic and pulmonary vessels after endotoxin. in American journal of physiology. Regulatory, integrative and comparative physiology 2000
Show all 35 Pubmed References
Human Polyclonal NOS2 Primary Antibody für IHC (p), WB - ABIN3044372
Tan, Chen, Guo, Ou, Xie, Quan: Relationship between macrophages in mouse uteri and angiogenesis in endometrium during the peri-implantation period. in Theriogenology 2014
Show all 25 Pubmed References
Human Polyclonal NOS2 Primary Antibody für WB - ABIN5518782
Sassenroth, Trinkmann: [Implantation of a Binkhorst lens in chronic simple glaucoma]. in Fortschritte der Ophthalmologie : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft 1985
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Human Polyclonal NOS2 Primary Antibody für IF, IHC - ABIN6711801
Fu, Chen, Wang, Guo, Xu, Wu: XJP-1, a novel ACEI, with anti-inflammatory properties in HUVECs. in Atherosclerosis 2012
Show all 9 Pubmed References
Dog (Canine) Polyclonal NOS2 Primary Antibody für IF (p), IHC (p) - ABIN677228
Pei, Wang et al.: Propofol attenuates LPS-induced tumor necrosis factor-?, interleukin-6 and nitric oxide expression in canine peripheral blood mononuclear cells possibly through down-regulation of nuclear factor ... in The Journal of veterinary medical science / the Japanese Society of Veterinary Science 2014
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Human Monoclonal NOS2 Primary Antibody für ELISA, FACS - ABIN4325979
Wang, Wang, Zhang, Zhao, Yang: Clinical significance of a myeloperoxidase gene polymorphism and inducible nitric oxide synthase expression in cirrhotic patients with hepatopulmonary syndrome. in Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban 2010
Show all 5 Pubmed References
Human Polyclonal NOS2 Primary Antibody für IHC (p), WB - ABIN966678
Chartrain, Geller, Koty, Sitrin, Nussler, Hoffman, Billiar, Hutchinson, Mudgett: Molecular cloning, structure, and chromosomal localization of the human inducible nitric oxide synthase gene. in The Journal of biological chemistry 1994
Show all 3 Pubmed References
Human Monoclonal NOS2 Primary Antibody für FACS, IHC - ABIN969551
Huang, Ratovitski: Phosphorylated TP63 induces transcription of RPN13, leading to NOS2 protein degradation. in The Journal of biological chemistry 2010
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Human Polyclonal NOS2 Primary Antibody für FACS, IF - ABIN6662456
Peng, Liu, Han, Luo, Cathopoulis, Lu, Li, Yang, Liu, Cai, Shi: Dynamic metabolic change is indicative of inflammation-induced transformation of hepatic cells. in The international journal of biochemistry & cell biology 2016
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Human Polyclonal NOS2 Primary Antibody für FACS, IF - ABIN3017570
Du, Tan, Zhao, Zhao, Xue, Wang, Xie, Wang: Molecular pathology of cerebral TNF-α, IL-1β, iNOS and Nrf2 in forensic autopsy cases with special regard to deaths due to environmental hazards and intoxication. in Forensic science, medicine, and pathology 2017
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Study showed that TRIP4 promoted melanoma growth through modulation of COX-2 and iNOS expression partially by activating NF-kappaB signaling indirectly and partially by the direct anchoring of itself at COX-2 and iNOS promoter via synergy with p300. Clinical data showed that high expression of TRIP4 was positively correlated with increased expression of COX-2 and iNOS and predicted poor prognosis in melanoma patients.
Toxoplasma utilizes human iNOS to antagonize IFN-gamma-induced IDO1-mediated cell-autonomous immunity via its GRA15 virulence factor.
The carriage of a mutant allele in the -954 NOS2 gene may have a protective effect on malaria among Southern Ghanaian children. We assessed the association of mutant allele frequencies of the NOS2 gene at two SNPs (-954 and -1173) with malaria disease severity in children from a malaria endemic area.
Both depression exacerbation and posttraumatic stress disorder led to elevated levels of iNOS (and HO-1,IL-33 and MIP-1beta).
NOS2 was confirmed to be expressed in both the glioma cell line and a human glioma primary culture, and overexpressed in relative derived neurospheres. Experiments that aimed to evaluate the influence of 1400W on U-87 MG, T98G (glioblastoma cell lines) and primary glioma cells sustained the crucial role played by NOS2 in proliferation, colony formation, migration, and neurosphere generation.
These findings link iNOS to Notch1 signaling in CD24(+)CD133(+) LCSCs through the activation of TACE/ADAM17.
the present findings were the first to show that KLF5 expression and nitration by iNOS-mediated peroxynitrite are necessary for the induction of TNF-alpha and IL-1beta expression in VSMCs of diabetic vascular tissues.
iNOS microsatellite polymorphism may contribute to the genetic background of atrial fibrillation in Chinese-Taiwanese patients.
High expression of iNOS and STAT3 in cells transfected with miR-34a mimic further validated it.
ur findings endorse polymorphic regulation of iNOS expression, altered oxidant-antioxidant components and evidences of risk association as the hallmark of malaria pathogenesis. iNOS/NO may serve as potential diagnostic marker in assessing clinical malaria.
NOS2A_ (CCTTT)n gene variations may influence inflammatory bowel disease susceptibility in the Moroccan population.
The results indicated that the expression levels of interleukin6 and inducible nitric oxide synthase (iNOS) were decreased, whereas collagen expression and deposition were increased in ketaminetreated SMCs. Conversely, treatment with CTX restored the expression of iNOS, which may prevent or limit oxidative damage
The present study demonstrated that iNOS C150T polymorphism did not show significant association with metabolic syndrome.
KLF4 activated the transcription activity of iNOS promoter in MH7A cells stimulated by TNF-alpha. This study indicates that KLF4 is important for regulating the expression of iNOS by TNF-alpha in human synoviocytes.
Coexpression of NOS2 and COX2 accelerates tumor growth and reduces survival in estrogen receptor-negative breast cancer.
NOS2 T allele of rs2297514 significantly increased the risk of a non-union during the fracture healing process by 38% compared to the C allele. Further stratification analyses conducted for this SNP using data from subgroups classified by different sites of fracture indicated that significance could only be observed in the tibial diaphysis subgroup.
NOS2 polymorphisms in prediction of benefit from first-line chemotherapy in metastatic colorectal cancer patients
PEDF protects human glomerular mesangial cells from diabetes-derived oxidative stress via NOXO1- iNOS suppression.
The studies established a potential link between leptin and adipocyte insulin responsiveness in an NOS2 dependent manner.
Collectively, our results demonstrated sanggenon C induced apoptosis of colon cancer cells by increased reactive oxygen species generation and decreased nitric oxide production, which is associated with inhibition of inducible nitric oxide synthase expression(iNOS) and activation of mitochondrial apoptosis pathway.
this paper shows that NOS2 enhances the survival of mice during Salmonella Typhimurium infection-induced sepsis by increasing reactive oxygen species, inflammatory cytokines and recruitment of neutrophils to the peritoneal cavity
High INOS expression is associated with sepsis.
iNOS-derived NO during the late phase of sepsis caused vasodilation-induced hypothermia and a lethal hypodynamic state.
study enables us to conclude that beta-cell stress is aggravated by the incapability of STAT5B to induce Nos2 resulting in HO accumulation and the ensuing oxidative stress enhances beta-cell damage.
Nitrated POPC showed anti-inflammatory potential, as assessed by the inhibition of inducible nitric oxide synthase (iNOS) expression in RAW 264.7 macrophages activated by the Toll-like receptor 4 (TLR4) agonist lipopolysaccharide (LPS) in a well-described in vitro model of inflammation
these data show a role for iNOS-produced reactive oxygen species in maintaining homeostasis of the gut microbiota
Results suggest that dopaminergic modulation of striatal function is altered in the iNOS KO mice. These alterations may be related to the decreased expression and activation of astrocytes and microglia in the iNOS KO mice. In conclusion, the phenotype profile of iNOS mutant mice corroborates iNOS constitutive function.
The role of miR-294 and miR-721 in the regulation of NOS2 expression during Leishmania replication in infected macrophages pointing these miRNAs as potential new targets for drug development.
Our results uncover the molecular mechanism behind the constricted regulation of Nos2 expression and open new therapeutic opportunities based on epigenetic activities of caspase-1 against infectious and inflammatory diseases.
Data suggest that, in biocatalytic cycle of iNos, deferred ET (electron tunneling) from substrate or undue ET from/to cofactor leads to side products. These studies involved quantum mechanics, DFT (Density Functional Theory), thermodynamics, nondynamical electron correlation, and molecular modeling.
iNOS-derived nitric oxide plays a role in telogen elongation under the inflammatory conditions associated with diabetes in mice.
IFN-gamma-iNOS axis are an essential pathway in the pathogenesis of arenavirus hemorrhagic fever.
tibias of botulin A toxin-treated and tail-suspended mice, which featured unloading and decreased bone mass, showed higher expression of IL-1beta, Lcn2 and Nos2, suggesting their pathophysiologic involvement in endothelial cell-osteoblast crosstalk.
Results demonstrate that TLR2 signal plays an important role in the regulation of iNOS expression after C. sinensis infection. TLR2 signal is also beneficial to limiting worm growth and development and contributing to the susceptibility to C. sinensis in which the iNOS/NO reactions possibly participate.
Influence of 1mM MbetaCD on the fenoterol-driven changes in both contractility and NO level was strongly attenuated by inhibition of Gi-protein (pertussis toxin), Akt (Akt 1/2 kinase inhibitor) or NO-synthase (L-NAME)..Obtained results suggest that slight cholesterol depletion upregulates Gi-protein/Akt/NO-synthase signaling that attenuates the positive inotropic response to b2-adrenergic stimulation
Diphenyleneiodonium selectively interacts with heme protein of iNOS, inhibiting nitric oxide production.
Bone marrow mesenchymal stromal cells induce the rapid differentiation of CD11b+ myeloid cells from bone marrow progenitors, and such an activity requires the expression of nitric oxide synthase-2.
omega-alkynyl arachidonic acid may promote the anti-inflammatory M2 polarization of macrophages in acute myocardial infarction via regulating the cross-talk between PKM2, HIF-1alpha and iNOS.
Inducible nitric oxide synthase (NOS2)-deficiency enhanced survival and reduced tumor severity in genetically engineered mouse model of pancreatic cancer (KPC mouse).
The expression of iNOS participates in the pathogenesis of cochlear damage caused by acoustic trauma.
Our data demonstrate that both iNOS and nNOS represent sources for nitric oxide overproduction in ileal myenteric plexus during ischemia and reperfusion
Salvia miltiorrhiza injection had no effect on the expression of nNOS and eNOS, but could inhibit iNOS in choclea.
iNOS and AChE expression increases in spiral ganglia treated with streptomycin. Salvia miltiorrhiza injection reduces ototoxicity by reducing the levels of iNOS and AChE.
The auditory brainstem response threshold increases and the expression of iNOS strengthens in streptomycin ototoxicity.
polymorphism of the NOS2 gene may contribute to the susceptibility of Holstein cattle to bovine tuberculosis
Vitamin D receptor activation, and inducible nitric oxide synthase (NOS2), were strongly induced during Cooperia oncophora reinfection. Several canonical pathways associated with NOS2 were impacted.
The expression, localization, and distribution of 3 nitric oxide synthase enzymes through the estrous cycle in bovien fallopian tubes are reported.
These results provide evidence for a high prevalence of subclinical endometritis in repeat breeding cows as well as the involvement of TNFalpha and iNOS pathways in the regulation of this pathological condition.
Differential cell-specific and spatiotemporal expression of the EDN1 system and NOS in the bovine utero-placental unit may be associated with regulation of vascular and cellular functions during pregnancy.
All infected calves had an increased number of cells expressing iNOS, nitrotyrosine and manganese superoxide dismutase in the inflamed lung tissue
iNOS is expressed in ruminant granulosa cells and is regulated by gonadotrophins and oestradiol
Expression level of NOS2 mRNA in endometrial biopsies from cows with puerperal endometritis is high. Highest expression of is found in cows with clinical endometritis.
data suggest that the transcriptional inducible NOS response to octacalcium phosphate crystals involved both the p38 and the JNK MAPK pathways, probably under the control of activator protein-1
The expression of iNOS and NRAMP1 in the lymph nodes, lungs, and tuberculous granulomas in 8 bovine tuberculosis cases is reported.
identified a 3471bp transcript for iNOS, isolated from RNA from alveolar macrophages stimulated with the intracellular pathogen Mycobacterium bovis
The results showed that the expression of TNF-alpha, iNOS, and IL-6 in alveolar macrophages was up-regulated by stimulation with the recombinant Mce4A protein of M. bovis; in contrast, expression of IL-12 was unaffected.
fibronectin fragment induced iNOS and COX-2 expression is downregulated in chondrocyte/agarose constructs
study investigated hypothesis that CD40 signalling is impaired in Mycobacterium avium subspecies paratuberculosis(MAP)-infected macrophages; propose that MAP interferes with gene expression of iNOS and IL-12p40 genes downstream of p38
Isoforms of NOS (eNOS and iNOS) are present in oocytes of cattle from early folliculogenesis up to maturation; in vitro maturation influences amount of mRNA and NOS activity.
iNOS was shown to be constitutively expressed within porcine LV. Its level decreases during the progression of systolic nonischemic HF in the pig model.
Our results suggest that the presence of low mycotoxin doses in feed slows down the mRNA expression of both nitric oxide synthase isomers, which probably lowers the concentrations of nitric oxide, a common precursor of inflammation.
In swine, IL-8, TNF-ALPHA, INOS AND MIP-1BETA were increased during mechanical ventilation in a time-related fashion.
Data suggest that pig sperm contain bNOS, iNOS, and eNOS; up-regulation of NOS by leptin during acrosome reaction and inhibition of acrosome reaction by inhibitors of nitric oxide synthases suggests these enzymes are involved in acrosome reaction.
Periodic acceleration (pGz) acutely increases endothelial and neuronal nitric oxide synthase expression in endomyocardium of normal swine.
Regional difference in blood flow has no effect on iNOS protein content in different size conduit arteries.
Along with several single loci, the epistatic QTLs, SLC9A3R1 and NOS2 control for total number of piglets born and number of piglets born alive in a F(2) Iberian by Meishan intercross.
In this study, neuronal iNOS expression and increase of NO production were found in the acute phase of hypoxia-ischemia. Brain biopterin did not increase in hypoxia-ischemia although plasma biopterin was five-fold elevated.
Immunoreactivity of eNOS was similar to NADPH-d staining. Clear iNOS immunoreactivity was detected in the luminal epithelium, endometrial stroma and individual endometrial glands.
The increase in NOS protein seen in both the endothelium and vascular smooth muscle in response to cerebral vasospasm is enhanced by dopamine in a D(2)R-dependent mechanism
sustained regional ischemia induces myocardial iNOS expression in pigs, which contributes to contractile dysfunction at the cardiomyocyte level.
results suggest that endothelial (eNOS) and inducible (iNOS) nitric oxide synthase are responsible for regulation of blood circulation in umbilical cord
Kidneys from circulation-restricted fetuses showed increased inducible nitric oxide synthase messenger RNA.
The hypotestosteronemia observed in diabetic rabbits could be a consequence of the increased expression of iNOS and could contribute to the hyperreactivity of the rabbit carotid artery to testosterone.
The result demonstrate that mechanical stress on synovial cells induces gene expressions of iNOS.
In heart failure, increased iNOS and arginase II expression results in unchanged NO species and protein S-nitrosylation; with substrate limitation, uncoupled iNOS produces superoxide anions and contributes to contractile dysfunction.
amyloid and oxidative stress-related disease proteins like NOS 2 is increased in expression and form localized accumulations in diabetic muscle in this rabbit model of diabetes.
Pulmonary ischaemia-reperfusion up-regulates inducible nitric oxide synthesis and/activity, which coincides with reduced endothelial nitric oxide synthase activity.
Data suggest distinct localizations of iNOS along the radial arteries and eNOS at the spiral arteries/arterial sinuses in the developing placenta.
Ulinastatin effectively inhibited the increased expression of MMP-2, MMP-3, and iNOS in degenerated NP cells induced by IL-1beta in vitro.
We demonstrated that NOS family genes are expressed in caprine peripheral blood mononuclear cells and higher expression of these genes with HSPs during thermal stress suggest possible involvement of them to ameliorate deleterious effect of thermal stress so as to maintain cellular integrity and homeostasis in goats
synthesized and stored in a part of the male reproductive tract, then transferred to the femaleduring ejaculation
Nitric oxide is a reactive free radical which acts as a biologic mediator in several processes, including neurotransmission and antimicrobial and antitumoral activities. This gene encodes a nitric oxide synthase which is expressed in liver and is inducible by a combination of lipopolysaccharide and certain cytokines. Three related pseudogenes are located within the Smith-Magenis syndrome region on chromosome 17.
NOS type II
, NOS, type II
, hepatocyte NOS
, inducible NO synthase
, inducible NOS
, nitric oxide synthase 2A (inducible, hepatocytes)
, nitric oxide synthase, inducible
, nitric oxide synthase, macrophage
, peptidyl-cysteine S-nitrosylase NOS2
, inducible nitric oxide synthase
, macrophage NOS
, nitric oxide synthase 2, inducible, macrophage
, nitric oxide synthase 2, inducible
, nitric oxide synthase 2A
, nitric oxide synthase-like protein
, nitric-oxide synthase like protein