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We found that lowering the glucose concentration increased expression of genes coding for inducible nitric oxide syntheas, NOS2 (show NANOS2 Proteins) and NOS2A resulting in enhanced production of nitric oxide
Downregulation of inducible NO synthetase (iNOS) resulted in downregulation of heme oxygenase 1 (HO-1 (show HMOX1 Proteins)), and, conversely, upregulation of iNOS enhanced HO-1 (show HMOX1 Proteins) activity.
Data suggest that NOS1 and NOS2 play roles in stress-induced surge in nitric oxide (NO) production; NO serves as mediator for development of secondary neurological disorders associated with stress such as anxiety and anxiety disorders. [REVIEW]
ATM (show ATM Proteins)-reactive oxygen species-iNOS axis regulates nitric oxide mediated cellular senescence.
The risk of developing chronic pancreatitis is not increased by the presence of the iNOS-2087A>G polymorphism.
NOS2 (show NANOS2 Proteins) rs2779248, NOS2 (show NANOS2 Proteins) rs1137933, and NOS3 (show NANOS3 Proteins) rs3918188 genetic polymorphisms are potentially related to the susceptibility to type 2 diabetes mellitus (T2DM), and the rs1800783 polymorphism might be considered as genetic risk factors for diabetic nephropathy.
Patients wi (show NANOS2 Proteins)th Marfan syndrome showed elev (show ADAMTS1 Proteins)ated NOS2 and decreased ADAMTS1 protein levels in the aorta.
the model demonstrated that although TNF-alpha (show TNF Proteins) contributed towards a more rapid response time, measured as time to reach maximum iNOS production, IFN-gamma (show IFNG Proteins) stimulation was significantly more significant in terms of the maximum expression of iNOS and the concentration of NO produced.
iNOS-derived NO plays a crucial role during atherosclerosis by regulating the endocytic-lysosomal degradation of ILK (show ILK Proteins) in endothelial cells.
analysis of inhibition interaction between AR and iNOS, suggesting a new pathophysiological mechanism and providing a new insight into the therapeutic mechanism of diabetic cataract
results indicate that in addition to its function in caveolae biogenesis, Cavin-2 (show SDPR Proteins) plays a critical role in endothelial cell maintenance and function by regulating eNOS (show NOS3 Proteins) activity.
iNOS is not involved in the cardioprotective effects of late-phase remote preconditioning of trauma.
Data (including data from studies using knockout mice) suggest that expression of iNOS mRNA/protein is elevated in liver cytosol/mitochondria in sepsis; these changes are related to enhanced oxidative/nitrosative stress in liver in sepsis; absence of iNOS (but not nNOS (show NOS1 Proteins)) prevents impairment of liver mitochondria during sepsis; melatonin/antioxidant treatment prevents liver damage.
PHLPP1 reduced IFN-gamma (show IFNG Proteins)-stimulated but not LPS (show TLR4 Proteins)-induced ERK1/2 phosphorylation, and inhibition of ERK1/2 abolished IFN-gamma-induced (show SAMHD1 Proteins) ser (show SIGLEC1 Proteins)(727) STAT1 (show STAT1 Proteins) phosphorylation and iNOS expression.
this study shows that knockout of Nos2 in mice lacking Arginase1 ameliorates allergic contact hypersensitivity
Aortic Nos2 levels were higher in Adamts1 (show ADAMTS1 Proteins)-deficient mice and in a mouse model of Marfan syndrome.
iNOS plays a critical role in burn-induced Sirt1 (show SIRT1 Proteins) S-nitrosylation and acetylation and activation of p65 NF-kappaB (show NFkBP65 Proteins) and p53 (show TP53 Proteins) in mouse skeletal muscle.
gammadelta T cells express NOS2 not only in vitro after t-cell receptor triggering, but also directly ex vivo. Nos2 deficient mice have fewer gammadelta T cells in peripheral lymph nodes than their wild-type counterparts, and these cells exhibit a reduced ability to produce IL-2. the inactivation of endogenous NOS2 significantly reduced gammadelta T cell proliferation and glycolysis metabolism that can be restored in ...
The expression of iNOS participates in the pathogenesis of cochlear damage caused by acoustic trauma.
Our data demonstrate that both iNOS and nNOS (show NOS1 Proteins) 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 (show NOS1 Proteins) and eNOS (show NOS3 Proteins), 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 (show VDR Proteins) 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 (show TNF Proteins) 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 (show SOD2 Proteins) 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 (show SLC11A1 Proteins) in the lymph nodes, lungs, and tuberculous granulomas in 8 bovine tuberculosis cases is reported.
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 (show IL8 Proteins), TNF-ALPHA (show TNF Proteins), INOS AND MIP-1BETA (show CCL4 Proteins) were increased during mechanical ventilation in a time-related fashion.
Data suggest that pig sperm contain bNOS (show NOS1 Proteins), iNOS, and eNOS (show NOS3 Proteins); up-regulation of NOS by leptin (show LEP Proteins) 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 (show NOS1 Proteins) 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.
expression of inducible nitric-oxide synthase by infected mucosa was without detriment to overall barrier function and may serve to promote clearance of infected enterocytes
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 (show NOS3 Proteins) was similar to NADPH-d (show NQO1 Proteins) staining. Clear iNOS immunoreactivity was detected in the luminal epithelium, endometrial stroma and individual endometrial glands.
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 (show ARG2 Proteins) 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 (show NOS3 Proteins) activity.
Data suggest distinct localizations of iNOS along the radial arteries and eNOS (show NOS3 Proteins) at the spiral arteries/arterial sinuses in the developing placenta.
Ulinastatin (show AMBP Proteins) effectively inhibited the increased expression of MMP-2 (show MMP2 Proteins), MMP-3 (show MMP3 Proteins), and iNOS in degenerated NP cells induced by IL-1beta (show IL1B Proteins) 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
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
, nanos homolog 2