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Validated All-in-One™ qPCR Primer for NOS1(NM_000620.4) Search again
Product ID:
HQP102929
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
IHPS1, N-NOS, NC-NOS, NOS, bNOS, nNOS
Gene Description:
nitric oxide synthase 1
Target Gene Accession:
NM_000620.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
Nitric oxide (NO) is a messenger molecule with diverse functions throughout the body. In the brain and peripheral nervous system, NO displays many properties of a neurotransmitter; it is implicated in neurotoxicity associated with stroke and neurodegenerative diseases, neural regulation of smooth muscle, including peristalsis, and penile erection. NO is also responsible for endothelium-derived relaxing factor activity regulating blood pressure. In macrophages, NO mediates tumoricidal and bactericidal actions, as indicated by the fact that inhibitors of NO synthase (NOS) block these effects. Neuronal NOS and macrophage NOS (MIM 163730) are distinct isoforms (Lowenstein et al., 1992 [PubMed 1379716]). Both the neuronal and the macrophage forms are unusual among oxidative enzymes in requiring several electron donors: FAD (see MIM 610595), flavin mononucleotide (FMN), NADPH, and tetrahydrobiopterin.[supplied by OMIM].
Gene References into function
- fine mapping and single nucleotide polymorphism association results of candidate genes for asthma and related phenotypes
- An alternative promoter of the human neuronal nitric oxide synthase gene is expressed specifically in Leydig cells.
- quantitative expression of nNOS first exon variants in different human tissues and the characterization of the basal nNOS exon 1c promoter
- ligand and protein vibrations at the substrate binding site. A study by FTIR.
- allelic association of the gene with schizophrenia
- assembly and activation of the heme-deficient neuronal enzyme with various porphyrins
- Data report a 89-nucleotide alternatively spliced exon in human neuronal nitric oxide synthase located in the 5'-untranslated region between exon 1 variants and a common exon 2 that contains the translational initiation codon.
- Association analysis of five polymorphic microsatellite markers in cluster headache (CH) patients reveals that genetic variations in the NOS1 gene do not contribute greatly to CH susceptibility.
- nitric oxide synthases(inducible, brain and endothelial) were expressed in human pregnant term uterus and did not change in the myometrium during labor
- expression in neurons of the Nuc. suprachiasmaticus (SCN) of depressed patients and matched controls
- calmodulin activates electron transfer in the flavin domain of human neuronal nitric oxide synthase
- Nitric oxide participates in the phosphorylation of eIF2alpha since nNOS processes are closely related to eIF2alpha(P) positive cells in temporal lobe epilepsy with hippocampal sclerosis
- rate of intramolecular electron transfer between the two flavins in the iNOS flavin domain was faster than that of the nNOS flavin domain.
- NOS1 is strongly expressed in most tubules of the human nephron. Epithelial cells may be major source of nitric oxide in human kidney under physiologic conditions.
- nNOS staining was found in nerve fibers branching within seminal vesicle tissue
- Results describe the expression of nitric oxide synthases 1, 2, and 3 in patients with chronic obstructive pulmonary disease, suggesting their involvement in muscle dysfunction in this disease.
- There is no obvious association between ecNOS polymorphism and preeclampsia.
- Variations in the NOS1 gene may contribute to atopy without this relationship being reflected by FENO.
- Nitric oxide liberated from enteric neurons participates in the chloride secretory response to stroking in human jejunum in vitro.
- nNOS can differentially regulate the ERK signal transduction pathway in a manner dependent on the presence of l-arginine and the production of NO*.
- The increased NO production with increased expression of iNOS and ncNOS may contribute to the pathological and physiological features of UVB-induced erythema and skin inflammation.
- Association analysis for the CA repeat polymorphism of the neuronal nitric oxide synthase (NOS1) gene and schizophrenia.
- Cu,Zn superoxide dismutase and nitric oxide synthase in neurodegenerative processes (review)
- MPP(+)-dependent aconitase inactivation, Tf-iron uptake, and oxidant generation result in the depletion of intracellular tetrahydrobiopterin, leading to the uncoupling of nNOS activity
- IFN-gamma regulates NOS-1 expression through posttranscriptional and posttranslational mechanisms.
- nitric noxide release by nitric oxide synthase 1 (neuronal) would significantly affect available smooth muscle nitric oxide
- human mast cell lines produce NO in both cytoplasmic and nuclear compartments, and endogenously produced NO can regulate leukotriene production.
- The nNOS gene polymorphism may not confer increased susceptibility to Tardive Dyskinesia, although more investigations on other populations are warranted.
- NOS1 gene may participate in pathogenesis of high total serum IgE levels in allergic diseases. NOS1 may be candidate gene for IgE-mediated allergy.
- Neuronal NOS expression in the prefrontal cortex was significantly higher in individuals with schizophrenia.
- Intron4 polymorphism of the nitric oxide synthase gene is associated with the development of lupus nephritis.
- Intracellular factors able to induce abnormalities in the nNOS monomer/dimer equilibrium could lead to pancreatic beta-cell dysfunction.
- In trained vastus lateralis, NOS 1 protein and immunostaining at myofibers II were significantly increased at the end of head-down-tilt bed rest.
- nNOS expression is regulated in the process of cutaneous wound repair.
- increased activity of nNOS may be involved in the neuroprotection conferred by 17beta-estradiol.
- Constitutive NOS activities are responsible for E2-induced NO production in neuroblastoma cells. Differential activation of NOS isoforms in these cells occurs in response to different treatments.
- neuronal nitric-oxide synthase activity through serine 741 phosphorylation is inhibited by Calcium/calmodulin-dependent protein kinase I
- NOS-1 mRNA and protein levels hint that not only NOS-3, but also NOS-1 may be involved in the regulation of systemic hyperdynamic circulation and portal hypertension.
- CHIP is an E3 ligase for nNOS whose action is facilitated by (and possibly requires) its interaction with nNOS-bound hsp70
- The T/T genotype of the neuronal nitric oxide synthase C276T SNP seems to be associated wtith Alzheimer's disease in Italy population, particularly with early onset.
- The 5' repeat variant of the nNOS gene is the more functional variant expressing gene information that could affect NO synthesis and result in diseased states. However, no association with migraine was seen in the case-control cohort.
- Nocodazole treatment inhibited TRAIL-increased NOS activity, indicating that, on cultured HUVEC, TRAIL ability to affect NO production by regulating eNOS sub-cellular distribution is mediated by cytoskeleton and Golgi complex modifications.
- Regulatory polymorphisms of NOS1 contribute to the genetic risk for shizophrenia, and modulate prefrontal brain functioning.
- The expression of the different exon 1-related splice variants of NOS1 mRNA is controlled directly (at least in part) by the associated 5'flanking sequences.
- intracellular generation of NO* by nNOS leads to S-nitrosylation of H-Ras, which interferes with Raf-1 activation and propagation of signalling through ERK1/2
- nNOS is a new p60(src) kinase substrate essential for SST5-mediated anti-proliferative action
- NOS gene polymorphisms are not involved in the susceptibility to and nature of the clinical course of sporadic achalasia.
- current findings provide evidence for expression of all 3 of the NOS isoforms at all of the airway levels studied in the developing lung and in all of the levels studied of the developing vascular tree from 22 weeks to term
- describe a novel interaction between the PDZ domain of nNOS and Vac14
- CD95 alters NOS1 expression to contribute to diabetic gastroparesis.
- We conclude, therefore, that estrogen opens BK(Ca) channels in HCASMC by stimulating nNOS via a transduction sequence involving PI3-kinase and Akt.
- reduced activity of respiratory chain complexes with mitochondrial encoded subunits and a lower nNOS amount in amyotrophic lateral sclerosis muscles
- For C276T polymorphism distribution of CC, TC, TT and genotypes was 31%, 29%, and 40% in primary nocturnal enuresis compared with 10%, 43%, and 47% in the controls
- Therefore, short alleles of the NOS1 exon 1f-VNTR are likely to be susceptibility factors for AD, and interact with the epsilon 4 allele to markedly increase the AD risk.
- nNOS mu protein expression is greater in endurance-trained individuals when compared with sedentary individuals
- inflammation is associated with a differential expression of VIP and nNOS neuronal subpopulations within the two major enteric plexi, likely due to phenotypic switch in Crohn disease
- eNOS and nNOS were not detectable by Western blotting in both peripheral and cord-blood eEPCs upon 3 weeks, and their mRNA levels were lower than 2% relative to those present in HUVECs
- NOS1 exon 29 CA-repeat may be a risk factor for asthma susceptibility and mite specific IgE response in a Colombian population.
- a possible involvement of NOS-I(nitric oxide synthase 1) gene variants in suicidal behavior and related intermediate phenotypes.
- Suggest that NO generation via nNOS, but not NO generation via eNOS, is reduced in low-flow postural tachycardia syndrome.
- Total NOS1 protein content was reduced by 41% in patients with critical illness myopathy compared to controls
- Proteolytic degradation of NOS1 by calpain is modulated by the expression levels of HSP90.
- NOS1 was elevated during tourniquet-induced ischemia/reperfusion.
- The C276T SNP acts as risk factor for sporadic FTLD, possibly influencing NOS1 transcription. Studies in larger populations are needed to confirm its role in PSP and CBD.
- nNOS isoform has distinct physiological roles in cardiovascular control mechanisms in humans, in vivo. nNOS isoform affects NO increases and vasodilatation during centrally mediated, reflex responses to whole-body heat stress.
- this study provides evidence for an association of variants in the NOS1 gene and RLS, and suggests the involvement of the NO/arginine pathway in the pathogenesis of RLS.
- functional polymorphism in NOS1 was associated with lower loudness dependence of auditory evoked potentials
- Basal forearm blood flow in humans is regulated by nNOS-derived nitric oxide. Vascular nNOS has a distinct local role in the physiological regulation of human microvascular tone in vivo.
- Expression of this isoform is reduced in skeletal muscle in type 1 diabetes.
- Cardiomyocyte NOS1 may be a useful target against cardiac deterioration during chronic pressure-overload-induced heart failure through modulation of calcium cycling.
- Our results strongly support a previous hypothesis that NOS1 contributes to the genetic risk of schizophrenia
- These results establish an SNTA1-based nNOS complex attached to SCN5A as a key regulator of sodium current and suggest that SNTA1 be considered a rare long QT syndrome-susceptibility gene.
- AMPK alpha2 activity, AMPK alpha2 Thr172 phosphorylation, and ACC-beta Ser222 phosphorylation were increased immediately after exercise. These increases had all returned to basal levels at 3 and 24 h after exercise.
- Data show that nNOS expression in glial tumors is significantly positive correlated with malignancy and tumor proliferation.
- nNOS was more frequently expressed in normal than in osteoarthritic chondrocytes, whereas the opposite was found for iNOS; IL-1 induced the degradation of both enzymes, but iNOS disappeared more rapidly
- Sarcolemmal nNOS staining was decreased in patient biopsies from a large number of distinct myopathies
- A diminished NO generation by injured endothelium and loss of macula densa neuronal NOS could impair the vasodilatory ability of the renal vasculature and contribute to the reduction in the glomerular filtration rate in postischemic acute kidney injury.
- A novel functional promoter polymorphism in NOS1 was associated with traits related to impulsivity, including hyperactive and aggressive behaviors.