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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 - 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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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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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
The Oncogenic Properties Of The Redox Inflammatory Protein Inducible Nitric Oxide Synthase In ER(-) Breast Cancer.
Exploration into the mechanisms of the cGMP-mediated protection identified a role for the iNOS/NO/cGMP pathway in the activation of ADAM17 (TACE (show ADAM17 ELISA Kits)), which is a sheddase that cleaves a number of cell surface receptors including TNF (show TNF ELISA Kits) receptor type 1 (TNFR1 (show TNFRSF1A ELISA Kits)).
results suggest that NOS2 polymorphisms may influence the risk of aggressive prostate cancer and that these polymorphisms could have an impact on disease pathogenesis, possibly by affecting intracellular nitric oxide levels.
no significant difference in frequency of NOS2-1659C/T polymorphism was observed between patients and controls. None of the studied SNPs were associated with erosive disease, seropositivity or extra-articular manifestations. The -277A/G and -1026 G/T promoter polymorphisms in iNOS may confer susceptibility to rheumatoid arthritis (RA). in South Indian Tamils.
This is the first reported evidence for NO-enhanced bystander aggressiveness in the context of PDT (show TWIST1 ELISA Kits). In the clinical setting, such effects could be averted through pharmacologic use of iNOS inhibitors as non-ionizing photodynamic therapy adjuvants
This increase was inhibited in the presence of the nonspecific iNOS inhibitor aminoguanidine (AG).
our study shows that the expression of iNOS is increased in both central airways and the alveolar parenchyma, but not in BAL cells, in uncontrolled asthmatics as compared to controlled asthmatics and healthy controls.
We found that lowering the glucose concentration increased expression of genes coding for inducible nitric oxide syntheas, NOS2 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 ELISA Kits)), and, conversely, upregulation of iNOS enhanced HO-1 (show HMOX1 ELISA Kits) 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]
These results suggested that Fyn (show FYN ELISA Kits) has a regulatory role in iNOS expression in astrocytes during neuroinflammatory responses.
Inducible NO synthase (iNOS) mRNA levels were significantly increased immediately after exposure to hypergravity.
results indicate that in addition to its function in caveolae biogenesis, Cavin-2 (show SDPR ELISA Kits) plays a critical role in endothelial cell maintenance and function by regulating eNOS (show NOS3 ELISA Kits) 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 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.
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.
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.
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
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