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Mouse (Murine) NOS2 ELISA Kit for Sandwich ELISA - ABIN415396
Campo, Avenoso, Nastasi, Micali, Prestipino, Vaccaro, DAscola, Calatroni, Campo: Hyaluronan reduces inflammation in experimental arthritis by modulating TLR-2 and TLR-4 cartilage expression. in Biochimica et biophysica acta 2011
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Rat (Rattus) NOS2 ELISA Kit for Sandwich ELISA - ABIN416102
Tang, Fang, Zhou, Zhuang, Zhang, Gu, Hu: A novel mechanism of formaldehyde neurotoxicity: inhibition of hydrogen sulfide generation by promoting overproduction of nitric oxide. in PLoS ONE 2013
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Rat (Rattus) NOS2 ELISA Kit for Sandwich ELISA - ABIN579874
Hattiwale, Saha, Yendigeri, Jargar, Dhundasi, Das: Protective effect of L-ascorbic acid on nickel induced pulmonary nitrosative stress in male albino rats. in Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine 2013
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Human NOS2 ELISA Kit for Sandwich ELISA - ABIN415084
Kim, Koppula, Hong, Jeon, Kwon, Hwang, Park, Choi: Regulation of microglia activity by glaucocalyxin-A: attenuation of lipopolysaccharide-stimulated neuroinflammation through NF-?B and p38 MAPK signaling pathways. in PLoS ONE 2013
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Human NOS2 ELISA Kit for Sandwich ELISA - ABIN365871
Hazam, Deka, Kar: Role of nitric oxide synthase genes in hepatitis E virus infection. in Journal of viral hepatitis 2014
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Mouse (Murine) NOS2 ELISA Kit for Sandwich ELISA - ABIN366306
Hayakawa, Okazaki, Morioka, Nakamura, Tanaka, Ogata: Lipopolysaccharide preconditioning facilitates M2 activation of resident microglia after spinal cord injury. in Journal of neuroscience research 2014
ATM (show ATM ELISA Kits)-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 rs2779248, NOS2 rs1137933, and NOS3 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 with Marfan syndrome showed elev (show ADAMTS1 ELISA Kits)ated NOS2 and decreased ADAMTS1 protein levels in the aorta.
the model demonstrated that although TNF-alpha (show TNF ELISA Kits) contributed towards a more rapid response time, measured as time to reach maximum iNOS production, IFN-gamma (show IFNG ELISA Kits) 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 ELISA Kits) 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
During cell transdifferentiation, innate immune activation increases iNOS generation of nitric oxide to S-nitrosylate RING1A.
These results were associated with a long-term improvement in function, which suggests, in light of the current work, that an acute and temporally restricted inhibition of iNOS is needed for the provision of therapeutic benefit.
iNOS showed significantly higher expression with increasing tumour grade in malignant mucinous tumours
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 ELISA Kits)) prevents impairment of liver mitochondria during sepsis; melatonin/antioxidant treatment prevents liver damage.
PHLPP1 (show PHLPP1 ELISA Kits) reduced IFN-gamma (show IFNG ELISA Kits)-stimulated but not LPS (show TLR4 ELISA Kits)-induced ERK1/2 (show MAPK1/3 ELISA Kits) phosphorylation, and inhibition of ERK1/2 (show MAPK1/3 ELISA Kits) abolished IFN-gamma-induced (show SAMHD1 ELISA Kits) ser (show SIGLEC1 ELISA Kits)(727) STAT1 (show STAT1 ELISA Kits) 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 ELISA Kits)-deficient mice and in a mouse model of Marfan syndrome.
iNOS plays a critical role in burn-induced Sirt1 (show SIRT1 ELISA Kits) S-nitrosylation and acetylation and activation of p65 NF-kappaB (show NFkBP65 ELISA Kits) and p53 (show TP53 ELISA Kits) 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 ...
Stat3 (show STAT3 ELISA Kits) plays a compensatory anti-apoptotic role in IL-17A (show IL17A ELISA Kits)/iNOS-mediated cardiomyocyte apoptosis via inhibiting iNOS transcription, providing a novel molecular mechanism of apoptosis regulation and complicated interactions between IL-17A (show IL17A ELISA Kits)/iNOS and IL-17A (show IL17A ELISA Kits)/Stat3 (show STAT3 ELISA Kits) signalings.
this study shows that iNOS-derived oxidative stress plays a key role in psoriasis induced kidney dysfunction
stability of LPS (show TLR4 ELISA Kits)-induced iNOS mRNA was increased by GlcN under normal glucose conditions. These results suggest that GlcN regulates inflammation by sensing energy states of normal and fuel excess.
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 ELISA Kits) 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 ELISA Kits) activity.
Data suggest distinct localizations of iNOS along the radial arteries and eNOS (show NOS3 ELISA Kits) at the spiral arteries/arterial sinuses in the developing placenta.
Ulinastatin (show AMBP ELISA Kits) effectively inhibited the increased expression of MMP-2 (show MMP2 ELISA Kits), MMP-3 (show MMP3 ELISA Kits), and iNOS in degenerated NP cells induced by IL-1beta (show IL1B ELISA Kits) in vitro.
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 ELISA Kits) 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 ELISA Kits) and eNOS (show NOS3 ELISA Kits), 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 ELISA Kits) 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 (show NOS ELISA Kits) 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 ELISA Kits) and iNOS pathways in the regulation of this pathological condition.
Differential cell-specific and spatiotemporal expression of the EDN1 (show EDN1 ELISA Kits) system and NOS (show NOS ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) 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 (show NOS ELISA Kits) isomers, which probably lowers the concentrations of nitric oxide, a common precursor of inflammation.
In swine, IL-8 (show IL8 ELISA Kits), TNF-ALPHA (show TNF ELISA Kits), INOS AND MIP-1BETA (show CCL4 ELISA Kits) were increased during mechanical ventilation in a time-related fashion.
Data suggest that pig sperm contain bNOS (show NOS1 ELISA Kits), iNOS, and eNOS (show NOS3 ELISA Kits); up-regulation of NOS (show NOS ELISA Kits) by leptin (show LEP ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) was similar to NADPH-d (show NQO1 ELISA Kits) staining. Clear iNOS immunoreactivity was detected in the luminal epithelium, endometrial stroma and individual endometrial glands.
We demonstrated that NOS (show NOS ELISA Kits) 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
This gene encodes an inositol-3-phosphate synthase enzyme. The encoded protein plays a critical role in the myo-inositol biosynthesis pathway by catalyzing the rate-limiting conversion of glucose 6-phosphate to myoinositol 1-phosphate. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene, and a pseudogene of this gene is located on the short arm of chromosome 4.
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
, MI-1-P synthase
, MIP synthase
, myo-inositol 1-phosphate synthase A1
, inducible nitric oxide synthase
, macrophage NOS
, nitric oxide synthase 2, inducible, macrophage
, Nitric oxide synthase, inducible
, nitric oxide synthase 2, inducible
, nitric oxide synthase 2A
, nitric oxide synthase-like protein
, nitric-oxide synthase like protein