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Is there anything for NOS to SNO in the Antarctic? Paper-12252710.
Arg II coimmunoprecipited with NOS1 but not NOS3. Paper-11369523.
In the GCL, amacrine cells but not RGCs were nNOS(+). Paper-10752899.
Additionally, TLR4 expression was reduced by NOS inhibitor. Paper-12987626.
No mutation in the CACNA1A and NOS genes was found in CH patients. Paper-11454333.
NOS1 decreased by 35.6% in group DI and increased by 58.1% in group DIS. Paper-10658433.
NOS1 C5266T and NOS3 G894T were not associated with asthma, atopy or FeNO. Paper-11090168.
The effect of HSP90 is mediated by the enhancement of CaM binding to nNOS. Paper-9090071.
Endothelin regulates NOS1 and NOS3 isoforms in the renal medulla. Paper-12602849.
A common genetic variant in the NOS1 regulator NOS1AP modulates cardiac repolarization. Paper-12023390.
The NOS1 intron 2 GT repeat and STAT6 exon 1 GT repeat were associated with asthma. Paper-10224072.
PTCL/ NOS also show variable Ki-67 marking, with rates >80% heralding a worse prognosis. Paper-13057188.
PMCA is of particular interest since it may affect activity of calcineurin and nNOS. Paper-11374033.
One of these proteins, PSD-93, co-localizes with a subpopulation of nNOS in the macula densa. Paper-2141362.
NOS inhibition may have negative effects on CBF but further studies are required. Paper-10755582.
Expression of nNOS in these neurons was highly co-localized with p21ras and p16INK4a. Paper-2100638.
In CC, iNOS and nNOS decreased at 1 year, whereas there was no change in TGF-beta1 levels. Paper-13411466.
Moreover, the NOS inhibitor NMA partially reduced the angiogenic activity of icariin. Paper-13038985.
Endothelial NOS was evenly expressed in all groups while neuronal NOS was undetectable. Paper-8854537.
CaM-K Ialpha and CaM-K IV failed to phosphorylate nNOS at Ser(847) in transfected cells. Paper-9740553.
Effects of long term NOS inhibition on disease and the immune system in MOG induced EAE. Paper-11525933.
Conversely, N(G)-monomethyl-L-arginine, a NOS inhibitor, decreased PPARgamma binding. Paper-13134311.
These data demonstrate that the neuronal NOS is implicated in proliferative effect evoked by CCK. Paper-8297061.
No association was found between the estrogen or progesterone receptor status and nNOS expression. Paper-8623674.
The captured cells expressed neuronal NOS (marker of macula densa), NOX2, and NOX4 but not NOX1. Paper-13623399.
The PEP and PEPI decrease was larger in the MSA + NOS group than in the PD + NOH/PAF group (P < 0.05). Paper-13544012.
Finally, the inhibition of TRPV1 receptor by capsazepine caused a significant fall in NOS activity. Paper-12970136.
Other studies reported that smoking modified the risk of PD due to polymorphisms in the MAO-B and nNOS genes. Paper-11140464.
We therefore studied wild-type mice and mice with a congenital deficiency of NOS 1, NOS 2, or NOS 3. Paper-8626798.
The enhanced expression of NOS and ANP may play a compensatory role in GA-induced hypertension. Paper-13531393.
Effects of acute caffeine administration on NOS and Bax/ Bcl2 expression in the myocardium of rat. Paper-12746250.
The expression of CD34, CD105, NOS and HIF-1alpha was detected by immunohistochemistry (S-P). Paper-12088072.
However, in the caudal brain, increased iNOS expression did not profoundly suppress nNOS expression. Paper-12721161.
NOS1 polymorphism is associated with atopy but not exhaled nitric oxide levels in healthy children. Paper-9994185.
NOS inhibitors that bound tightly to CLL cell NOS1 and were hydrophobic potently induced CLL cell death. Paper-12788601.
Left ventricular expressions of eNOS, hsp90, iNOS, but not nNOS or caveolins, were increased. Paper-13587402.
The infiltrate in the dermis contained numerous cells expressing AQP1, AQP3, nNOS, iNOS, and eNOS. Paper-10120685.
Thus, we conclude that a decrease of dystrophin in human neurons is associated with a decrease of nNOS expression. Paper-10088009.
However, EPO augmented urinary NOx concentrations as well as the expression of NOS 1 and NOS 2 in the kidney. Paper-12789179.
EGF- induced formation of the nNOS- RSK1 complex was significantly decreased by PD98059 treatment. Paper-12378501.
Neither eNOS nor nNOS expression was associated with vascular density, tumor grade or the TNM status of the tumors. Paper-8623674.
In NPY(-/-) mice, there were significantly fewer nNOS-containing enteric neurons compared with wild-type (WT) mice. Paper-12263095.
NOS inhibitors and SOD mimetic also prevent O(2)- induced diminished brain mass and functional deficit. Paper-12298011.
NOS inhibition had no effect on the augmented dilation during exogenous VIP or hyperthermia (P > 0.05). Paper-11509554.
In OA chondrocytes NMDAR signalling requires extracellular calcium, association with PSD-95, and nNOS activity. Paper-13078653.
The results demonstrate that the nNOS variants are found at similar frequencies in MDD patients and healthy control subjects. Paper-9718307.
PRMT1 is the major type 1 PRMT in vivo, thus it is the primary producer of the competitive NOS inhibitor, ADMA. Paper-13008624.
The NOS inhibitor N(G)-nitro-l-arginine methyl ester (l-NAME) abolished the effect of eNOS transfection. Paper-12307235.
AT1 receptor blockade prevents the decrease in conduit artery flow- mediated dilatation during NOS inhibition in humans. Paper-13131557.
Sildenafil reduces cardiovascular remodeling associated with hypertensive cardiomyopathy in NOS inhibitor-treated rats. Paper-12151357.
In addition, the similar behavior of nNOS and SIN-1 provides further evidence for NO as initial product of the NOS reaction. Paper-12146329.
Conversely, overexpression of neuronal NOS within the PVN with adenoviral gene transfer significantly attenuated ANG II responses. Paper-11328121.
In addition, the inhibition of NOS and the antagonism of glutamatergic receptors decreased the NO fluorescence in the NTS. Paper-13667017.
Neuronal NOS ( nNOS) was expressed in normal (fetal and adult) human pituitary tissues and in GH-secreting adenomas. Paper-11051699.
In contrast, the expression of nNOS and eNOS gradually decreased in the hippocampal CA1 sector up to 14 days after ischemia. Paper-10531592.
In patients with COPD, neuronal NOS expression correlated negatively with the degree of the airway obstruction (%FEV1 predicted). Paper-10056023.
In rat islets, NOS inhibition decreased JNK and p38 activities induced by a 6-h exposure to IL-1beta. Paper-11103078.
Then we evaluated the contributions of neuronal NOS, endothelial NOS, and inducible NOS to NO production in brain cryosections. Paper-13668446.
Real-time PCR analysis of IFN-gamma-treated HMC1 showed a significant (P < 0.05) time-dependent increase in NOS1 and NOS3 mRNA. Paper-12688358.
The application of LPS to the pulp increased NOS activity, PGE(2), and MMP-3 production associated with iNOS overactivity. Paper-13703496.
RNS potentiate vascular and cellular injury by oxidation, by decreasing NO bioavailability, and by regulating NOS isoforms. Paper-13652256.
NOS exists in three distinct isoforms: neuronal NOS ( nNOS), inducible NOS ( iNOS), and endothelial NOS ( eNOS). Paper-10326365.
Positive associations were found between NOS1 and p53, bax and NOS2, bcl-2 and NOS2, bax and p53, and between bax and fasL. Paper-13568781.
The aim of this study was to determine whether allelic variation at the nNOS gene locus is associated with MS in an Australian cohort. Paper-10373114.
Here, we describe a novel interaction between the PDZ domain of nNOS and Vac14, the activator of the PtdIns(3)P 5-kinase PIKfyve. Paper-12360222.
CONCLUSIONS: Changes in muscle blood flow may affect the muscular size through actions of HSP-72, myostatin, and NOS-1. Paper-10739631.
Also, specific immunoreactivity for neurotransmitters SP, VIP, CGRP, ChAT and nNOS was mainly expressed by macrophagic cells. Paper-12043436.
Renin, NO synthase-1 ( NOS-1), and cyclooxygenase-2 ( COX-2) are key regulators of the RAS and TGF. Paper-12654979.
This NOS is regulated by its substrate L-arginine, by calcium, and by phosphorylation via PI3 kinase. Paper-11774975.
On the other hand, dexamethasone increases basal nNOS expression but decreases LPS + IFNgamma- induced iNOS expression. Paper-13609796.
CONCLUSIONS: These data suggest a possible link between the NOS1 gene locus and the rate of decline in lung function in patients with CF. Paper-10361487.
The PSD95- nNOS interface: a target for inhibition of excitotoxic p38 stress-activated protein kinase activation and cell death. Paper-10742331.
Endothelin-1 inhibited NKCC2 activity, an effect that was blocked by dominant-negative Akt and NOS inhibition. Paper-13570825.
Residual relaxation in eNOS knockdown mouse aorta was further inhibited by the selective inhibition of nNOS with L-ArgNO2-L-Dbu. Paper-13483717.
Cellular compartmentalization of phosphorylated eIF2alpha and neuronal NOS in human temporal lobe epilepsy with hippocampal sclerosis. Paper-9693607.
Similarly, both myogenin (P = 0.001) and MyoD1 (P < 0.001) had significantly higher expression for ARMS than RMS, not otherwise specified ( NOS). Paper-12070991.
Moreover, a NOS inhibitor abolished MAPK phosphorylation as well as neurite outgrowth in genipin-treated cells. Paper-12734487.
Moreover, NOS inhibitor ( L-NAME) and anti-TLR 4mAb reduced the LPS-induced NO, IL-8 and VEGF production and ICAM-1 expression. Paper-12987626.
All NOS isoforms were expressed and active in unlesioned animals. nNOS and iNOS were detected in some small cells in the parenchyma. Paper-12243579.
Both EFS and LS led to fluorescence emission from a fiber network associated with neuronal NO synthase ( nNOS) immunoreactive nerves. Paper-12655790.
Thus these studies provide direct evidence demonstrating that HSP90 enhances nNOS catalytic function in vitro and in intact cells. Paper-9090071.
This study investigated the expression of NO synthases ( NOS) and their relationship with expression of ET-1 and angiogenic markers in PTC. Paper-12014329.
The presence of L-NAME, an inhibitor of NOS, abrogated the inhibitory effect of ammonia on PRL secretion from APs from control and PH rats. Paper-12418269.
Topical application of dynorphin A (1-17) antiserum significantly attenuated neuronal NOS up-regulation in the adjacent T9 and T12 segments. Paper-11838826.
The expression of nitric oxide synthase-1 ( NOS-1) mRNA increased (P < 0.01), whereas that of IGF-1 mRNA showed no significant change (P = 0.36). Paper-10739631.
Thus, NO binding to the NOS heme may be a fundamental feature of catalysis and functions to down-regulate NO synthesis by neuronal NOS. Paper-369203.
Immunoreactivities for VAChT and nNOS, VAChT and VIP, and nNOS and VIP, were generally found in the same varicose nerve terminals. Paper-8420466.
This occurred in the absence of modifications in NFH, NFM or neuronal nitric oxide synthase (Type I NOS; nNOS) steady state mRNA levels. Paper-2029557.
Neuronal NOS, renin, and AT2 receptor expression in PRVs were upregulated in the newborn and decreased with age to lowest levels in the adult. Paper-13552101.
To test whether variants of NOS1, NOS2, and NOS3 relate to asthma, a genetic association study was conducted in a British population (n = 300). Paper-2121910.
In building our recombinant system, we used human kidney embryonic cells, HEK 293, as host for transfection of nNOS and NMDA receptor proteins. Paper-9491874.
PCA therefore not only increases the expression of nNOS but also induces the expression of iNOS and NT in both neurones and astrocytes. Paper-12302754.
We conclude that mitochondrial Arg II negatively regulates NOS1 activity, most likely by limiting substrate availability in its microdomain. Paper-11369523.
The receptor tyrosine phosphatase-like protein ICA512 binds the PDZ domains of beta2-syntrophin and nNOS in pancreatic beta-cells. Paper-8563994.
Associations between ACS and the AAT repeat in intron 13 (formerly intron 20) of the NOS1, and with NOS3 T-786C polymorphism were explored. Paper-13163808.
However, some interactions between NOS gene polymorphisms and HLA-DRB1 alleles confer and increased risk of developing CV events in patients with RA. Paper-13688942.
Northern blot analysis revealed that DAN mRNA was detected in OS-KH and RMS-NK cells, but was not detectable in SAOS-2, NOS-1, and ASPS-KY cells. Paper-8612720.
Such genes include those for monoamine oxidase ( MAO-A isoform), nitric oxide synthase ( nNOS isoform) and the peripheral-type benzodiazepine receptor. Paper-10126564.
Although pre-incubation with AM251 (CB1 antagonist) or AM630 ( CB2 antagonist) had no effect, co-incubation with both antagonists induced NOS activity. Paper-12970136.
Immunohistochemical double labeling for nNOS and SP or enkephalin further confirmed that nNOS is found in boutonal and cap-like endings in the CG. Paper-2044486.
In conclusion, both decreased ROS production and increased NOS activity appear to participate in the BP changes after NAC treatment in young SHRs. Paper-11341396.
Thus, we attempted to study whether or not a decrease of dystrophin expression would induce a modification in nNOS expression in cultured human neurons. Paper-10088009.
Serum TNF-alpha, sTNFR-I, and asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NOS, in CD were significantly higher than in UD or NS. Paper-11626063.
ICA512 also interacted in vitro with the PDZ domain of nNOS and ICA512- nNOS complexes were co-immunoprecipitated from INS-1 cells. Paper-8563994.
Confocal and biochemical analysis confirmed subcellular co-localisation and protein-protein interaction of RyR1 with nitric oxide (NO)-synthase type-1 ( NOS1). Paper-12765175.
Resveratrol exerts its antiproliferative effect on HepG2 hepatocellular carcinoma cells, by inducing cell cycle arrest, and NOS activation. Paper-12304474.
Water-soluble heteroatomic basic classes detected at >1% relative abundance include N, NO, NO2, NS, NS2, NOS, NO2S, N2, N2O, N2O2, OS, O2S, and O2S2. Paper-13265698.
CONCLUSIONS: DDAH2 upregulated the expression of VEGF through Sp1-dependent and NO/ NOS system-independent promoter activation. Paper-12046531.
CBT, which has proven to be the most useful behavioral treatment for bulimia, has now been shown to be effective for patients in the NOS category. Paper-13772759.
Two cases classified as nonkeratinizing SQCC and 2 cases of large cell neuroendocrine carcinoma on histology were misclassified as ADC- NOS by FNA. Paper-13394845.
Immunohistochemistry studies were performed for the detection of cGMP and nNOS, while Western blot analysis was employed for the detection of SHP-1. Paper-11363473.
On the other hand, CRF significantly increased the number of spinally projecting neurons triple- labeled with Fos and nNOS only in the ventral part of the PVN. Paper-13758249.
As classic neurotransmitters, VIP is stored in vesicles in the nerve endings, while NO is synthetized on demand by the neuronal isoform of NO synthase ( nNOS). Paper-10536889.
The expression of NHE3, NBC1, nNOS and iNOS proteins was determined in the cortex of the kidney by immunoblotting and immunohistochemistry. Paper-12752771.
To date, 3 distinct NOS isoforms have been identified: neuronal NOS ( NOS1), inducible NOS ( NOS2), and endothelial NOS ( NOS3). Paper-11281116.
These results demonstrate that E2-stimulated NO production occurs via estrogen receptor-mediated activation of the constitutive NOSs, neuronal NOS and eNOS. Paper-10611477.
In mice, Meis2-expressing ( Meis2+) AM cells are not cholinergic or dopaminergic, but some are immunoreactive for neuronal nitric oxide synthase ( bNOS). Paper-13419718.
It is established that neuronal NO synthase ( nNOS) is associated with the chaperone hsp90, although the functional role for this interaction has not been defined. Paper-9163703.
The administration of AST-120 to CRF rats significantly increased urine levels of NOx and the expression of glomerular eNOS and tubulointerstitial nNOS. Paper-12665123.
These data provide evidence that the NOS1 gene is not only associated with the variability of FENO, but also with P. aeruginosa colonization of airways in CF patients. Paper-8551324.
The syntrophins are PDZ-domain-containing proteins that facilitate the recruitment of signalling proteins such as nNOS (neuronal nitric oxide synthase) to the DPC [4]. Paper-8634394.
Activation of ERbeta increases levels of phosphorylated nNOS and NO production through a Src/ PI3K/Akt-dependent pathway in hypothalamic neurons. Paper-12994725.
In addition, six genes ( DPYSL2, DTNBP1, G30/ G72, GRID1, GRM4, and NOS1) showed overlapping suggestive evidence of association in both disorders. Paper-11451435.
Furthermore, isorhynchophylline increased the NO content and NOS activity, and suppressed Ang II-induced over-expression of c-fos, OPN and PCNA. Paper-13088661.
Experimental evidence suggested that CGRP stimulated both constitutive NOS activity and generation of NO via nitrosothiol degradation within the first hour. Paper-12084472.
Androgen deficiency diminishes protein expression and enzymatic activity of nitric oxide synthases ( eNOS and nNOS) and phosphodiesterase type 5 ( PDE5). Paper-11228485.
Incubation of B-CLL cells with TLR-7 agonists effectively resulted in an increased resistance to apoptosis that was reverted with the NOS inhibitor L-NMMA. Paper-12883959.
ROS expression and catalase, glucose-6-phosphate-dehydrogenase ( G6PHD), and NOS/NADPH-diaphorase activity were investigated by using histochemical reactions. Paper-12109361.
NO production in the brain is catalyzed by three isoforms of NO synthase ( NOS) including neuronal NOS ( nNOS), inducible NOS and endothelial NOS. Paper-13761243.
Within minutes of adding EGF to transfected cells, RSK1 associated with nNOS and subsequently dissociated following more prolonged agonist stimulation. Paper-12378501.
This short variant came along with decreased transcriptional activity of the NOS1 exon 1f promoter and alterations in the neuronal transcriptome including RGS4 and GRIN1. Paper-13565732.
Effect of Buthus martensi Karsch on aromatase activity and cytokine-inducted NOS and NO production in osteoblasts and leukaemic cell line FLG 29.1. Paper-12156850.
Notably, SUMOylation of CtBP1 was inhibited by the PDZ domain of nNOS, correlating with the known inhibitory effect of nNOS on the nuclear accumulation of CtBP1. Paper-9728240.
RESULTS: Urine levels of NOx and the expression of glomerular eNOS and tubulointerstitial nNOS were significantly decreased in CRF rats compared with normal rats. Paper-12665123.
Using the selective ERbeta agonist, DPN (10nM), we show that activation of ERbeta rapidly increases phosphorylation levels of nNOS at Ser(1412) and NO production. Paper-12994725.
Furthermore, an acute bout of exercise did not alter AMPK alpha1, AMPK alpha2, ACC-beta, or nNOS mu protein expression during the 24-h period after exercise. Paper-13082265.
CONCLUSION: NOS activity decreases AQP2 expression/traffick in the inner collecting duct principal cells in response to hemorrhage and this effect is lower with aging. Paper-12880834.
Inducible-NOS but not neuronal-NOS participate in the acute effect of TNF-alpha on hypothalamic insulin-dependent inhibition of food intake. Paper-12176694.
Furthermore, NO produced from newly induced neuronal NOS was reported to induce expression of thioredoxin and several other genes for preconditioning-induced neuroprotection. Paper-9491883.
With heat, arteriolar blood flow increased (187.2 +/- 28.5%, P = 0.00003), which was significantly attenuated with NOS plus sensorineural blockade (88.6 +/- 37.2%, P = 0.04). Paper-13263020.
The VEGF promoter activity was increased by DDAH2 transfection, which was not blocked by an NO synthase ( NOS) inhibitor but required the Sp1 sites. Paper-12046531.
Data on the effects of NOS inhibition on lesion volume (mm3, %) and cerebral blood flow ( CBF; %, ml * min(-1) * g(-1)) were analyzed using the Cochrane Review Manager software. Paper-10755582.
Citrulline formed as a by-product of the NOS reaction can be recycled to arginine by argininosuccinate synthetase (AS) and argininosuccinate lyase ( AL). Paper-13247789.
NOS activity - measured by conversion of [(3)H]-L-arginine to [(3)H]-L-citrulline - was enhanced under treatment with both drugs due to inhibition of HMG-CoA reductase. Paper-12521178.
We found that 60% and 65% of AT1 receptors immunoreactive neurons coexpressed nNOS in the hypothalamic paraventricular nucleus and supraoptic nucleus, respectively. Paper-13761787.
The NO synthase ( NOS) inhibitor N(G)-monomethyl-L-arginine (1 mM) reduced basal levels of c-GMP by 50% but had no effect on telomerase activity or replicative capacity. Paper-13405655.
In addition, subcellular localization of both NOS1 and NOS3 has been shown to regulate enzymatic activity and influence the ability of NOS to produce nitric oxide (NO). Paper-12692695.
Nitric oxide synthase ( NOS) type 1 or neuronal NOS ( nNOS) is expressed in the macula densa and NOS type II or endothelial NOS ( eNOS) in the afferent arteriole. Paper-10067446.
We have discovered that inhibition of hsp90 by radicicol or geldanamycin nearly prevents the heme- mediated activation and assembly of heme-deficient apo- nNOS in insect cells. Paper-9163703.
A role similar to that of NOS/NO signaling has been postulated for carbon monoxide (CO) produced in mammals from heme catabolism by heme oxygenase ( HO) enzyme. Paper-13590325.
In endothelial cells, eNOS and CAV-1 were present throughout the vasculature, whereas nNOS and CAV-3 were absent except in capillaries, which reacted for nNOS. Paper-2012232.
It appears that both NOS uncoupling and the activation of NADPH oxidase participate in the changes of reactive oxygen concentrations seen in cerebral hypoxic-ischemic injury. Paper-13024745.
The impaired reendothelialization with CRP was mimicked by NOS antagonism in CF1 mice; conversely, in cultured ECs CRP attenuation of migration was prevented by exogenous NO. Paper-13255698.
We concluded that, estrone rapid action on vascular tissue involves a cross talk between NOS and COX system, and the activation of PLC/ DAG/PKC transduction pathways. Paper-12198970.
Fluvastatin increased eNOS [ endothelial NOS (NO synthase)] expression, but NOS inhibitors failed to reverse the effect of fluvastatin on vWF secretion. Paper-13305019.
These results, taken together, indicate that the NOS activation is essential for water maze learning, which may be triggered via the CaM-kinase II activation in hippocampus. Paper-13618225.
These data suggest that NO generated by neuronal NOS exacerbates oxidative damage to cones in RP and that combined therapy to reduce NO and oxidative stress should be considered. Paper-13039847.
Incubation of ferric P420 nNOS with BH4 alone or BH4 and L-arginine resulted in time-dependent reactivation of catalysis and associated recovery of P450 character. Paper-1741961.
While GABAergic genes might underlie reduced anxiety, dysregulation of the glucocorticoid receptor can well contribute to a blunted stress response as found in NOS1 knockdown mice. Paper-12539670.
Insulin treatment decreased platelet adhesion to endothelial cells through insulin stimulation of endothelial NO production and NOS inhibition interfered with this process. Paper-12766174.
PTCL/ NOS are characterised by erratic expression of T cell associated antigens, including CD4 and CD52, which have recently been proposed as targets for ad hoc immunotherapies. Paper-13057188.
EDHF-dependent dilatations to acetylcholine ( ACh) were measured in the presence of L-NNA (100 microM, NOS inhibitor) and indomethacin ( INDO; 10 microM, COX inhibitor). Paper-12104178.
Overexpression of NOS- interacting protein ( NOSIP) induces translocation of eNOS from the plasma membrane to intracellular compartments, thereby impairing NO production. Paper-10759169.
Statistical analysis indicated that there is no association of this nNOS variant and MS and hence the gene does not appear to play a genetically significant role in disease susceptibility. Paper-10373114.
The relative contribution of constitutive forms of NOS and COX, as well as interactions between IP, PPARbeta and guanylyl cyclase pathways in vessels and platelets, is discussed. Paper-12673661.
High salt resulted in decreased expression of preproET as well as all three NOS isoforms in the Obese, while cytokine induced NOS ( iNOS) and neuronal NOS ( nNOS) increased in Leans. Paper-13034679.
BACKGROUND: The role of endothelial nitric oxide synthase 3 ( NOS-3) in the hyperdynamic circulation associated with cirrhosis is established but not that of the neuronal ( NOS-1) isoform. Paper-10525949.
Both methods revealed that SNPs in genes within the 6q22.3-23.2 and 8q11-q12 linkage peaks, and also the ARG2, FLT1, HAO2 and NOS1 genes were associated with the HbF response to HU. Paper-12622903.
AM404 completely prevented the overproduction of NO and the overexpression of nNOS, inhibited the increase in tumour necrosis factor alpha (TNFalpha) and enhanced the production of interleukin-10. Paper-12159260.
Two different consensus sequences were identified: GIQVD present in nNOS, in DNA cytosine methyl transferase and also in GKAP, where it is present twice in the protein sequence. Paper-9049788.
DPI (a dual inhibitor of NADPH-oxidase and NOS), ABAH ( MPO inhibitor) and BAPTA-AM (calcium chelator) significantly reduced 80 mM KCl or NO mediated free radical generation. Paper-13732414.
Sheep at high altitude relative to sea level had significantly greater total lung NOS activity and eNOS protein, but reduced sGC and HO expression and carbon monoxide production. Paper-12676463.
PMCA4b transgenic mice (PMCA4b-TG) showed a significant reduction in nNOS and total NOS activities as well as in cGMP levels in the heart compared with their wild type (WT) littermates. Paper-13736058.
Following MTB treatment, the cellular NOS activities were significantly enhanced with a concomitant increase in the levels of constitutive NOS ( cNOS) protein mass (110-178%). Paper-8663274.
Also, the increase in NOS activity and/or content in AP induced NO production that directly inhibited PRL secretion from the AP, without the participation of the dopaminergic system. Paper-12418269.
Inhibition of leptin secretion that had been induced by the IFN-gamma-LPS mixture was completely nullified by NOS inhibitors such as Nomega-monomethyl-L-arginine and aminoguanidine. Paper-12173875.
These results indicate that the NMDAR/ nNOS cascade, activated via MORs, provide the free zinc ions required for inactive PKCgamma to bind to HINT1/ RGSZ complex at the C terminus of the receptor. Paper-12975238.
These results demonstrate that AT(1) receptor blockade prevents the decrease in conduit artery FMD during NOS inhibition in humans, suggesting the development of a compensatory endothelial mechanism. Paper-13131557.
L-NAME (a nonselective NOS inhibitor) or aminoguanidine (a selective iNOS inhibitor) was given p.o. twice daily for 6 days starting from the termination of DSS treatment. Paper-12879609.
The inhibition of NOS activity by Nomega-nitro-L-arginine methyl ester abrogated the effect of Dicer overexpression to rescue the cells from serum withdrawal-induced apoptosis. Paper-13483722.
Mean SUV(max) was 8.3 g/ml in the 12 sites with NLP, 11.2 g/ml in the 147 sites affected with NS, 14.6 g/ml in the 36 sites with MC, and 13.1 g/ml in the 13 sites with CHL- NOS ( ANOVA, p = 0.002). Paper-12217590.
Exogenous ADMA significantly enhanced the increase in both TF mRNA level and activity induced by LPS, whereas L-arginine, the NOS substrate, markedly attenuated the LPS-induced TF increment. Paper-13221717.
Together, our results show that Src kinase mediates ERbeta- induced increases in phosphorylation levels of nNOS at Ser(1412) and NO production by activating the PI3K/Akt pathway. Paper-12994725.
We conducted a pilot study to investigate whether genes encoding neurotransmitters ( TAC1, TAC3, VIP, NOS1) and receptors ( TACR1, TACR2, TACR3, KIT) could be responsible for STC. Paper-13197129.
We also observed that a regulatory protein, Protein Inhibitor of NOS-1 (PIN) was down-regulated by IFN-gamma treatment, and more ubiquitinated PIN accumulated in IFN-gamma treated neurons. Paper-12342971.
Here we show that nNOS-derived NO produced during PC was crucial for the down-regulation of astrocytic GLT-1, and this down-regulation coincided with an increased survival rate of neurons. Paper-11334349.
Binding of both fluorinated analogues to the NOS active site was also investigated using a spectral binding assay employing a heme domain construct of the inducible NOS isoform (iNOS(heme)). Paper-13652536.
In CA from normal rabbits, Ad.nNOS generated high levels of functional nNOS protein predominantly in endothelial cells and increased vascular NOS activity by 3.4-fold relative to sham-infected control CA. Paper-1644883.
In the present study, the expression of endothelial NO synthase ( eNOS), neuronal NO synthase ( nNOS) and of inducible NO synthase ( iNOS) in the human brain after subarachnoid haemorrhage were studied. Paper-12460294.
NADPH oxidase-derived superoxide avidly interacts with eNOS-derived NO to form peroxynitrite (ONOO(-)), which oxidizes the essential NOS cofactor (6R-)5,6,7,8-tetrahydrobiopterin (BH(4)). Paper-12335917.
CONCLUSIONS: In vivo adenovirus-mediated endovascular delivery of nNOS markedly enhances vascular NOS activity and can favorably influence endothelial physiology in the intact and atherosclerotic vessel wall. Paper-1644883.
In addition, the acetylation of nNOS can be expected to potentiate the interaction with CR, eventually leading to the augmented catalytic activity of NOS and expression of the related biological effects. Paper-12780083.
Up-regulation of nNOS expression levels upon hypoxic challenge in APP23tg transgenic animals may therefore reflect a selective vulnerability in these animals even before amyloid deposition. Paper-11402868.
Furthermore, the protein induced osteogenic differentiation, characterized by increased alkaline phosphatase activity, and increased production of type I collagen and gamma-carboxylated osteocalcin in NOS-1 cells. Paper-8557553.
To confirm this hypothesis, we first investigated colocalization of neuronal NO synthase ( nNOS) and AT1 receptors in the hypothalamic magnocellular nuclei of adult male rats by using double immunofluorescence. Paper-13761787.
A scavenger of reactive oxygen species, as well as inhibitors of phosphatidylinositol 3-kinase, ERK, JNK1, and NOS, also blocked PKGIalpha-mediated protection against necrosis and apoptosis. Paper-12350219.
The data are consistent with the hypothesis that PC infiltrates infrequently arising in NOS tumors, as previously inferred for MC, are in response to one or more breast cancer-associated protein tumor antigens. Paper-13340706.
Both radiation and H(2)O(2) protected PTP activity from alkylation by a mechanism reversible by ascorbate and inhibited by NOS inhibitors or expression of a dominant negative mutant of NOS-1. Paper-10771445.
Pre-treatment with TNF-alpha at a low dose (10(-12) M) inhibits insulin-dependent anorexigenic signaling, and this effect is abolished in iNOS but not in nNOS knockout mice. Paper-12176694.
Endothelial NOS and neuronal NOS are constitutively expressed and activated by elevated intracellular calcium, whereas immunologic NOS is inducible with new RNA and protein synthesis upon immune stimulation. Paper-1152934.
MPEP co-infused with morphine not only preserved the analgesia and retarded the development of antinociceptive tolerance, but also partially inhibited the up-regulation of spinal nNOS protein. Paper-12789241.
When added at the apical side, the NOS-inhibitors NMMA and NIL, CAA analogs with a free carboxyl group, markedly inhibited the apical arginine influx and the transepithelial flux of the cationic amino acid. Paper-11097601.
The findings demonstrate that the two types of nNOS cells can be distinguished by antibodies to calbindin, somatostatin and neuropeptide Y, but none of these markers is found exclusively in nNOS cells. Paper-8467596.
Following comments of different switches from apoptosis-death, a new finding of checkpoint (early fluorescence point) of GSNO-initiated thymocyte apoptosis and NOS- GSNOR double control are highlighted. Paper-12590120.
The expression of nNOS protein was observed in the colonic mucosa with or without DSS treatment, while those of iNOS and eNOS were markedly upregulated after DSS treatment. Paper-12879609.
A390V- SNTA1 expressed with SCN5A, nNOS, and PMCA4b in heterologous cells increased peak and late sodium current compared with WT- SNTA1, and the increase was partially inhibited by NOS blockers. Paper-12882738.
In the myenteric plexus, there was a significant increase in the percent of NOS neurons (38% vs. 82% of HuC/D positive neurons) while there was no significant difference in percent of VIP neurons (4% vs. 8%). Paper-13291825.
The nNOS reductase domain is homologous to cytochrome P450 reductase, which contains two conserved clusters of acidic residues in its FMN module that play varied roles in its electron transfer reactions. Paper-1955694.
CONCLUSIONS: The acute decrease of NO after SAH is not determined by reduced constitutive NOS expression and iNOS induction is a consequence of SAH and plays a major role in the pathogenesis of vasospasm. Paper-12460294.
Addition of monomethyl L-arginine monoacetate, competitive inhibitor of NOS, inhibited nitric oxide (NO) production and apoptosis of gammadeltaT lymphocytes induced by hsp60 and hsp70. Paper-12085654.
Neither, the inhibition of NOS by l-NMMA nor the inhibition of COX by indomethacin could revert the effect of ligature on mucin release under unstimulated and isoproterenol-stimulated conditions. Paper-12762416.
Immunohistochemical studies were performed on paraffin-embedded tissue cross sections with neuronal NOS and inducible NOS monoclonal antibody as well as a rabbit polyclonal antibody against the human c-kit receptor. Paper-8489384.
Addition of a NOS inhibitor, after induction of iNOS expression, induced IkappaB-alpha degradation and potenciated the effect of IL-1, indicating that endogenous inducible NO inhibits NF-kappaB activation. Paper-13039498.
Each NOS patient used distinct Hc V-D-J and Lc V-J rearrangements, with her own immune response "footprint," but the overall pattern of gene usage followed that typical of exogenous antigen-induced immune responses. Paper-13340706.
The present study aimed to further examine the specific role for VIP in AVD by using VIP(10-28) to antagonize VIP- mediated dilation in the presence of NO synthase ( NOS) inhibition and an H1 antagonist. Paper-11509554.
The structure of the protein known both as neuronal nitric oxide synthase inhibitory protein, PIN (protein inhibitor of nNOS), and also as the 8 kDa dynein light chain ( LC8) has been solved by X-ray diffraction. Paper-1945519.
Relative quantitative reverse transcriptase-PCR demonstrated that killifish nNOS mRNA is highly expressed in the brain and gill followed by the stomach, kidney, opercular epithelium, intestine and heart. Paper-12159081.
Together, these results indicate sequential inhibition of NO/ NOS, GC, and MAPK pathways by GSPs in mediating the inhibitory signals for cell migration, an essential step in invasion and metastasis. Paper-13535264.
We identified the NOS activated by the peptide as the neuronal isoform: the expression of the C415A neuronal NOS mutant inhibited both CCK- induced stimulation of NOS activity and cell proliferation. Paper-8297061.
The re-expression of p75 neurotrophin receptor and neuronal NOS in motor neurons in parallel with increased NGF secretion by reactive astrocytes may be a mechanism to eliminate critically damaged neurons. Paper-11997966.
Affinity purified anti-M(2) peptide IgG from chagasic sera, while stimulating myocardial M(2) mAChR, it exerts an increase on PGE(2) generation and NOS activity, as well as COX-2/ iNOS isoforms mRNA expression. Paper-13526053.
We compared IL-4 and IFN-gamma serum levels between CLL patients and normal individuals, and determined whether serum IL-4 and IFN-gamma levels correlated with CLL cell CD38 expression and NOS enzyme activity. Paper-10835717.
Prophylactic treatment with pitavastatin also prevented the expression of iNOS and the decrease of eNOS expression and the number of nNOS-positive cells in the hippocampal CA1 sector 5 days after ischemia. Paper-10531592.
Immunohistochemistry was used to identify expressions of bcl-2, bcl-xl, bak, bax, p53, NOS-1, NOS-2, and NOS-3 proteins in 25 EBV positive GCs and in 103 EBV negative GCS. Paper-12197286.
Our studies indicate a tissue-specific program in the ductus arteriosus whereby elevated nNOS expression and NO production regulate the posttranscriptional increase in fibronectin synthesis required for SMC motility. Paper-1950118.
Interestingly, the inhibitors of calcineurin and PP1/ PP2A could enhance nNOS phosphorylation at Ser847 site at 1 day of reperfusion after ischemia but not at 6 hr of reperfusion. Paper-13002028.
The relative importance of the dopamine transporter and vesicular monoamine transporter knockout is discussed and insights into oxidative mechanisms are described from observations of nNOS knockout and SOD overexpression. Paper-9053622.
However, both Arg-competitive and noncompetitive inhibition of NOS by imidazole has been reported, and optical studies with neuronal NOS provided no evidence for imidazole affecting Arg binding. Paper-9483228.
CONCLUSIONS: These results indicate that atorvastatin upregulates vascular nNOS through Akt/ NF-kappaB pathway, demonstrating a novel nNOS- mediated vascular effect of the statin. Paper-12382279.
The aim of this study was to investigate whether the enhancement of GABA receptor activity could inhibit NMDA receptor- mediated nitric oxide (NO) production by neuronal NO synthase ( nNOS) in brain ischemic injury. Paper-13002028.
This study was performed to verify, by immunohistochemical and biochemical analyses, the presence and expression of nNOS and protein gene product 9.5 ( PGP 9.5) in SSc skin, in different subsets and various phases of the disease. Paper-10822396.
Using an immunohistochemical technique, we studied the expression of NO synthase ( NOS) isoforms NOS1, NOS2, NOS3, and nitrotyrosine, the marker of toxic NO-superoxide pathway, in lung specimens from autopsies. Paper-9854747.
In conclusion, L-arginine can educe the role of pulmonary tissue protection through up-regulating the expression of intra-pulmonary NOS and down -regulating COX2 in pulmonary thromboembolism. Paper-12414365.
In vitro, in the A431 human squamous carcinoma cell line, exogenous and endogenous stimulation of the iNOS pathway led to up-regulation of VEGF-C, which was blocked by the NOS inhibitor L-NNA. Paper-10824702.
Results from CD1 (control), nNOS((-/-)) and eNOS((-/-)) genetic knockout mice were compared.Key results:Smooth muscle of sling and clasp LES displayed unitary membrane potentials of 1- 4 mV. Paper-12720673.
Moreover, although our previous studies showed that the action of HSP90 involves increased Ca(2+)/calmodulin (Ca(2+)/CaM) binding, quantitative measurements of the effect of HSP90 on CaM binding to nNOS have been lacking. Paper-9090071.
In addition to a deficiency in bound heme, neither mutant had any detectable bound tetrahydrobiopterin, as compared to wild-type enzyme, which had a ratio of 0.84 mol of bound pteridine:1 mol of nNOS 160 kDa subunit. Paper-587619.
Structural studies showed that the plasma membrane calcium pump ( PMCA), a sodium-calcium exchanger ( NCX1), and a myogenic nNOS appear to be colocalized with caveolin 1, the main constituent of these caveolae. Paper-12048995.
We also demonstrate that LPS stimulation of the mouse macrophage cell line RAW 264.7 induces the expression of iNOS, but not nNOS or eNOS, at the levels of mRNA transcription and protein expression. Paper-12471035.
In conclusion, the high intensity of NOS1, NOS3, and VEGF were mostly expressed in the titanium group, whereas the low intensity of NOS1, NOS3, and VEGF were mostly expressed in the zirconium oxide group. Paper-11370649.
The objective of the present study was to examine the effects of cardiac NO synthase ( NOS) inhibition on left ventricular (LV) hemodynamics and mechanoenergetics in response to adenylyl cyclase stimulation in human heart failure. Paper-13352787.
The down-regulation of CYP3A after 9 h of stimulation by IL-1beta was attenuated by inhibitors of NO synthase ( NOS) and of the proteasome, showing NO- and proteasome-dependent down-regulation at earlier time points. Paper-13674453.
NMMA blocked completely the somatostatin stimulated increase of cGMP levels and nNOS was detected in rat retina. cGMP immunoreactivity was observed primarily in bipolar cells only of nitroprusside-treated retinas. Paper-11363473.
We found that overexpression of HSP90 significantly increased the shear- stimulated association of HSP90 with eNOS and led to significant increases in NO production and reduced NOS-dependent superoxide generation. Paper-12636759.
Herein, we present results from biochemical, NMR, and crystallographic studies that show that Pak1 (residues 212-222) binds to LC8 along the same groove as canonical LC8 interaction partners (e.g. nNOS and BimL). Paper-13014178.
Beside GABA, these interneurons contain somatostatin, neuropeptide Y, nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) and neuronal NOS, an enzyme which produces NO after the activation of the interneurons. Paper-11830927.
The induction of inducible NO synthase ( NOS) was readily detected in MSCs but not T cells, and a specific inhibitor of NOS reversed the suppression of Stat5 phosphorylation and T-cell proliferation. Paper-12385251.
Histological sections of retina and ONH from animals with normal IOP, with elevated IOP, and elevated IOP treated with timolol, were studied by immunohistochemistry with antibodies to NOS-1, NOS-2, and NOS-3. Paper-12260032.
Protein-protein interactions between CaM and NOS were studied using steady-state fluorescence and spectropolarimetry to monitor the binding of these CaM mutants to nNOS and iNOS CaM-binding domain peptides. Paper-12511995.
The present data indicate that, in addition to its known cAMP signaling pathway, CGRP may act to regulate keratinocyte biology through intracellular NO by modulation of S-nitrosothiol stores and stimulation of NOS activity. Paper-12084472.
Furthermore, inhibitors of prostaglandin synthase or NOS restored the proliferation of T cells, whereas an inhibitor of indoleamine 2,3-dioxygenase and a transforming growth factor-beta-neutralizing antibody had no effect. Paper-12385251.
In particular, one peripheral T-cell lymphoma (not otherwise specified, NOS) with the morphological variant of Lennert lymphoma displayed a chromosomal translocation t(14;19) involving the TCRalpha/delta and the BCL3 loci. Paper-13387973.
Using immunocytochemistry, the number of nNOS- expressing neurons or the optical density of iNOS staining in sections from three coronal levels (bregma 1.0, -0.4, and -2.3mm) were compared between 3-MCPD-treated and control rats. Paper-12721161.
For the first time, sarcolemmal association of sGC and its colocalization with NOS-1 generating the sGC-activator NO and with HO-2 producing the potential sGC upregulator CO have been demonstrated in the present study. Paper-9101556.
We conclude that (1) the variability in CF nasal NO levels are related to naturally occurring variants in the NOS1 gene, and (2) that nasal NOS1-derived NO affects the susceptibility of CF airways to infection with P. aeruginosa. Paper-9198393.
Cultured macrophages, but not VSMCs, expressed inducible NOS (but not neuronal NOS or endothelial NOS) concomitant with activation and secreted 1.51+/-0.3 fmol nitrite per cell, which was blocked by L-NAME (100 micro mol/L). Paper-9564122.
This paper shows the physical interaction between PMCA (isoforms 1 and 4) and alpha-1 syntrophin and proposes a ternary complex of interaction between endogenous PMCA, alpha-1 syntrophin, and NOS-1 in cardiac cells. Paper-12173548.
We report here that NADPH analogs such as 2'5'ADP, ATP, and 2'AMP paradoxically activate constitutive calcium/calmodulin regulated nitric oxide synthases (cNOS), including the endothelial isoform ( eNOS) and the neuronal isoform ( nNOS). Paper-11839974.
Two NO donors inhibited activation of neuronal NO synthase ( nNOS) in response to the muscarinic receptor agonist carbachol in Chinese hamster ovary (CHO) cells stably transfected with the M1 muscarinic receptor and nNOS. Paper-1811415.
Cultured MVECs, exposed either to glucose or glucose and varying concentrations of curcumin, were assessed for alterations of NOS expression and activation of nuclear factor-kappaB (NF-kappaB) and activating protein-1 ( AP-1). Paper-12175182.
Two days after the injury, nNOS expression remained high, iNOS and TNF-alpha increased and also GFAP protein expression was observed together with a profusion of reactive astrocytes distributed throughout the SN. Paper-10830031.
Free citrulline metabolism involves three key enzymes: NO synthase ( NOS) and ornithine carbamoyltransferase ( OCT) which produce citrulline, and argininosuccinate synthetase (ASS) that converts it into argininosuccinate. Paper-11486658.
Moreover, the inhibitory effect of L-norvaline was not reversed by the NOS inhibitor L-NAME and L-norvaline did not interfere with TNFalpha-induced activation of NF-kappaB, JNK, p38mapk, while it inhibited p70s6k ( S6K1) activity. Paper-13700163.
The main objectives of this paper were to test the hypothesis that polymorphisms in NOS1 and NOS3 genes associate with ACS in SCD patients and to characterize the association between physician-diagnosed asthma and acute chest syndrome (ACS). Paper-13163808.
Acetyl-CoA carboxylase (ACC)-beta phosphorylation was sensitive to exercise, increasing threefold from rest to low intensity, whereas neuronal NO synthase ( nNOS) micro phosphorylation was only observed at the higher exercise intensities. Paper-9985212.
Moreover, the signals of wt p53, iNOS, p38 kinase, caspase-3 and NOS activity were significantly stronger, whereas, the signals of bcl-2, c-myc and Fas/ FasL were markedly weaker in E2 group than those in C2 group (P<0.05). Paper-11278826.
Six genes ( RGS4, SCA1, GRM4, DPYSL2, NOS1, and GRID1) met this criterion for schizophrenia or schizoaffective disorder; five replicate previous associations, and one, GRID1, shows a novel association with schizophrenia. Paper-11451435.
In addition, AD was associated with significantly increased expression of the p53 pro-apoptosis gene, all 3 isoforms of nitric oxide synthase ( NOS 1-3), and NADPH-oxidase (NOX) 1 and NOX 3, beginning early in the course of disease. Paper-12157139.
To identify modifier genes, we performed family-based association analyses for 10 genes previously associated with asthma and/or COPD, including IL10, TNF, GSTP1, NOS1, NOS3, SERPINA3, SERPINE2, SFTPB, TGFB1, and EPHX1. Paper-12660977.
While mean ELISA IgG EC AAs were higher in autism and PPD- NOS (p < 0.005) compared to HC but not NNI, ELISA IgM EC AAs were higher in children with autism, CDD, PDD-NOS, and epilepsy compared to both HC and NNI (p < 0.0005). Paper-10822336.
The IET rate constant value for the iNOS holoenzyme is similar to that obtained for a CaM- bound neuronal NOS holoenzyme, suggesting that CaM activation effectively removes the inhibitory effect of the unique autoregulatory insert in neuronal NOS. Paper-13491023.
Additionally, immunoreactivity for the NR1 subunit is detectable within nNOS-axons, indicating that NO may be generated in response to axo-axonic interactions with glutamatergic axons in the vicinity and independently of action potential propagation. Paper-1778601.
On the other hand, attenuation of the spinal ERK phosphorylation by the MAPK kinase ( MEK) inhibitor U0126 also could inhibit the increase of nNOS and iNOS expression in the spinal cord of morphine withdrawal rats. Paper-12150566.
In various brain regions, a wide codistribution of NOS- and TH-containing neurons was observed, but real colocalization of nitrergic and catecholaminergic cells was only found in a small neuron population in the posterior tubercle of anuran amphibians. Paper-11464091.
In addition, we employ a software-based differential metabolic profiling method by subtracting LC/ MS data sets derived from samples that contained nNOS from those that did not contain the enzyme to search for products and substrates in complex reaction mixtures. Paper-11523649.
Hematoxylin and eosin-stained sections were subclassified as: 243 adenocarcinoma (ACA), 272 squamous cell carcinoma ( SCC), 35 large cell carcinoma, 32 non-small cell carcinoma NOS, and 6 other ( carcinosarcoma, giant cell carcinoma). Paper-13096420.
Furthermore, we investigated the influence of glucose on the activity of nNOS and the expression of PIN and are able to show that both are increased by glucose stimulation in the beta-cell lines but not in the mouse fibroblastic cell line LTK. Paper-9643137.
Other nitric oxide and reactive oxygen species ( NOS and ROS) donors, as well as reducing conditions were found to be ineffective on TALK-1, TALK-2 and TASK-2 (sin-1, angeli's salt, SNP alone, tBHP, H(2)O(2), and DTT). Paper-10742389.
We find that NOS inhibitors reduce both glutamate- induced p38 activation and the resulting neuronal death, whereas NO donor has effects consistent with NO as an upstream regulator of p38 in glutamate-induced cell death. Paper-10742331.
The results showed a significant increase in the expression levels of AGE (p<0.05), CEL (p<0.001), RAGE (p<0.05), HNE-modified proteins (p<0.01), nNOS, iNOS and eNOS (p<0.01 and p<0.05, respectively), N-tyr (p<0.05), and SOD1 (p<0.05) and SOD2 (p<0.05). Paper-12283989.
We hypothesized that coronary endothelial dysfunction in CHF may be due in part to decreased dimethylarginine dimethylaminohydrolase ( DDAH), the enzyme that degrades endogenous inhibitors of NO synthase ( NOS), including asymmetric dimethylarginine. Paper-10999071.
Whether AT(1) (angiotenin II type 1) receptor blockade can prevent the decrease in conduit artery FMD (flow- mediated dilatation) during NOS (nitric oxide synthase) inhibition by alternative endothelial pathways has not been explored previously in humans. Paper-13131557.
We found the presence of Dp71, beta-dystroglycan, nNOS, beta-sarcoglycan, alpha/beta syntrophin, alpha1-dystrobrevin and beta-dystrobrevin in the nuclear matrix protein fractions and in situ nuclear matrix preparations from HeLa cells. Paper-12206690.
In order to better understand the role of nNOS in the pathogenesis of AD, sections from the EC and hippocampus (HC) of AD and control cases were immunohistochemically analyzed by single- and double-immunolabeling using antibodies against nNOS and PHF-tau. Paper-1369351.
DESIGN: Two HCL, 2 HC-V, 3 MZL of bone marrow (BM), 2 MZL versus B-cell lymphoma, not otherwise specified (BCL, NOS) of BM, and 4 NMZL and 5 extranodal MZL (EMZL) were stained with DBA.44 and TRAP and reviewed for staining pattern/intensity. Paper-12784377.
Expression and localization of NOS isoforms are dependent on age and developmental stage, innervation and activity, history of exposure to cytokines and growth factors, and muscle fiber type and species. nNOS in particular may show a fast-twitch muscle predominance. Paper-8689257.
The NMDA receptor antagonist, MK-801, eliminated, and a rather selective nNOS inhibitor, 7-Nitroindazole (7-NI) attenuated, NMDA receptor-evoked enhancement of NOS activity and cGMP level in brain hemispheres and in cerebellum during reperfusion. Paper-1747411.
DESIGN AND PATIENTS: Expression of NOS, angiogenic markers [ vascular endothelial growth factor ( VEGF), angiopoietin-1 and angiopoietin-2] and their receptors was studied in surgical thyroid samples obtained from 22 patients aged 15-68 years. Paper-12014329.
We have further shown in the hypothalamus of ageing BN rats that while the excitatory amino acid receptor content is reduced, nitric oxide synthase ( NOS) activity is increased which is due to increased inducible (iNOS) but not neuronal NOS ( nNOS). Paper-10681464.
Using electron microscopy, we demonstrated the postsynaptic localization of neuronal NOS at symmetrical synapses formed by CB1R-positive axon terminals on pyramidal cell bodies, whereas NO-sGC was found in the presynaptic terminals. Paper-12484669.
A chimera consisting of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding subdomain catalyzed significantly increased rates of cytochrome c reduction in the absence of CaM and of NO synthesis in its presence. Paper-9777495.
Using a semiquantitative RT-PCR analysis, we also showed that up to 12 h of treatment, SNP and N(G)-monomethyl-L-arginine ( L-NMMA, a NOS inhibitor) did not alter mRNA expression of VEGF, FGF2, and their major receptors in OFPAE cells. Paper-11353985.
Thus, estrogen receptor- mediated stimulation of the nNOS/ PSD-95/ NMDA receptor complex assembly is likely to be a critical component of the signaling process by which estradiol facilitates coupling of glutamatergic fluxes for NO production in neurons. Paper-13670844.
The crystal structure of the neuronal NOS ( nNOS) connecting/ FAD binding subdomains reveals that the structure of the nNOS- connecting subdomain diverges from that of CYPOR, implying different alignments of the flavins in the two enzymes. Paper-9777495.
In addition to identifying 36 known CaM-binding proteins, including CaM kinases, calcineurin, nNOS, the IP(3) receptor, and Ca(2+)-ATPase, we identified an ER transmembrane protein, wolframin [the product of the Wolfram syndrome gene ( WFS1)] as interacting. Paper-13751905.
Using a competitive reverse transcription polymerase chain reaction method, endothelial ( eNOS) and inducible ( iNOS), but not neuronal ( nNOS), nitric oxide synthase mRNA expression was detected in isolated fat cells and pieces of adipose tissue. Paper-8379958.
The TAG and underlying corpus cavernosum (CC) were examined histologically and by Western blot analysis for nitric oxide synthase ( NOS), neuronal ( nNOS), endothelial ( eNOS) and inducible ( iNOS) isoforms, and transforming growth factor-beta1 ( TGF-beta1). Paper-13411466.
These results suggest that PMCA4 is tethered to the syntrophin complex as a regulator of NOS-1, but its absence does not cause collapse of the complex, contrary to what has been reported for other proteins within the complex, such as dystrophin. Paper-12173548.
The ciliary muscle (CM) and outflow pathway of normal human eyes were found to be substantially enriched in NADPH-d, the majority of which, by immunological analysis, consisted not of NOS-1 (brain or bNOS) but rather of NOS type 3 ( endothelial cell or ecNOS). Paper-312519.
When rats were pretreated with scutellarin (50 or 75 mg/kg), upregulation of eNOS expression and downregulation of VEGF, bFGF, and iNOS expression was observed, whereas scutellarin had no effect on nNOS expression. Paper-11446386.
The findings suggest that GFAP, MCA-In, S-100, 5-HT, PLP, SP, NOS and SOM may be involved in modulating the physiological functions and maintaining micro-environmental homeostasis of the microcyst in the cochlear nucleus of the gerbil. Paper-12550759.
The results raise the possibility that NMDA receptor activation stimulates two different calmodulin-dependent enzymes ( eEF2 kinase and NOS) reinforcing local NO production by increasing precursor availability together with NOS catalytic activity. Paper-12004991.
CONCLUSIONS: Ad.nNOS, a novel adenoviral vector for gene transfer of NOS, generates high-level nNOS expression in a variety of vascular cell types. nNOS activity in hVSMC is physiologically regulated and of a magnitude comparable to native eNOS activity in HUVEC. Paper-774977.
Together, these data provide substantial evidence that RSK1 associates with and phosphorylates nNOS on Ser847 following mitogen stimulation and suggest a novel role for RSK1 in the regulation of nitric oxide function in brain. Paper-12378501.
We examined, in five human brains, the distribution, through the caudal pons and rostral medulla, of NOS-positive neurons in serial sections stained with NADPH diaphorase for histochemistry, and with antibodies against neuronal NOS peptide for immunohistochemistry. Paper-719904.
These include: (1) NOS/NO levels decreased or altered in the prostate and penile smooth muscle, (2) Autonomic hyperactivity effects on LUTS, prostate growth and ED., (3) increased Rho-kinase activation/ endothelin activity, and (4) prostate and penile ischemia. Paper-10805068.
EGF treatment of HEK-293 (human embryonic kidney) cells, expressing RSK1 and nNOS, led to inhibition of NOS enzyme activity, associated with an increase in phosphorylation of nNOS at Ser847, as is also the case in an in vitro assay. Paper-12378501.
Inhibition of endogenous NO synthesis by a neuronal NOS inhibitor 7-nitroindazole markedly enhanced the histamine-induced hormone secretion, abolished the HTMT-induced response and did not substantially alter the amthamine-evoked ACTH and corticosterone secretion. Paper-10637771.
The cellular distribution of two calcium sensor proteins (VILIP-1 and VILIP-3) and of neuronal NOS immunoreactivity was studied morphometrically in the flocculonodulus, the inferior vermis and the dentate nucleus of 9 schizophrenics, 7 depressive patients and 9 matched controls. Paper-10702158.
In this study, we developed one unique plasmid molecule based on one pMD-18T vector with three exogenous target DNA fragments of Roundup Ready soybean GTS 40-3-2 (RRS), that is, CaMV35S, NOS, and RRS event fragments, plus one fragment of soybean endogenous Lectin gene. Paper-12885172.
In rat pituitary tumor GH3 cells, thyrotropin-releasing hormone (TRH)- stimulated phosphorylation of neuronal NO synthase ( nNOS) at Ser847, being sensitive to an inhibitor of CaM-Ks, KN-93, was enhanced by inhibition of nNOS with 7-nitroindazole (7NI). Paper-12760944.
NOS exists in three distinct isoforms; constitutively ( cNOS) expressed neuronal NOS ( NOS1 or nNOS) and endothelial NOS ( NOS3 or eNOS) or an inducible isoform ( NOS2 or iNOS) capable of high production output of NO during inflammation. Paper-8380925.
This LPS-induced Fe(2+)-toxicity enhancement was blocked by trolox, vitamin C, the SOD mimetic MnTBAP, and by the COX-2-specific inhibitor NS398, but not by inhibitors of xanthine oxidase, NADPH oxidase, NOS, and monoamine oxidase. Paper-12194733.
RESULTS: At baseline, 29% of patients had a mental disorder (major depression: 8.4%, minor depression 10.4%, Panic disorder 1.4%, generalized anxiety disorder 2%, anxiety not otherwise specified ( NOS) 11.4%); of these patients, 26% had more than one mental disorder. Paper-13203855.
The expressions of epidermal growth factor receptor ( EGFR), p38 kinase, FAS, FasL and caspase-3 were detected using immunocytochemistry, and the NOS activity and the ratio of differentiated cells/proliferating cells were examined by cytochemistry. Paper-11278826.
METHODS: We examined mRNA ( reverse transcription multiplex polymerase chain reaction) and protein expression ( Western blotting) of i,e and nNOS in enterocytes isolated from the duodenum of patients with untreated CD (n=22) and iron deficiency anaemia ( IDA, n=22). Paper-10742103.
Modulation of ENTs, CATs, and NOS expression and activity in endothelium involves protein kinase C (PKC), mitogen-activated protein kinases p42 and p44 ( p42/44(mapk)), calcium, and phosphatidyl inositol 3 kinase (PI3k), among others. Paper-13099643.
Semiquantitative assessment of numbers of nNOS expressing neurons in different areas of the HC and EC showed a remarkable loss of nNOS expressing neurons in the entorhinal cortex layer II and--less severe--CA1 and CA3 of the hippocampus in patients with AD. Paper-1369351.
Moreover, sCD23 was shown to induce a calcium influx in monocytes, in accordance with an activation of a constitutive NOS through a transient increase in [Ca2+]i. As expected, these events were mimicked by mAbs against CD11b and CD11c, the macrophage receptors for CD23. Paper-1085958.
Although the interflavin electron transfer between FAD and FMN is not strictly regulated in CPR, electron transfer is activated in neuronal NOS reductase domain upon binding calmodulin (CaM), in which the CaM-bound activated form can function by a similar mechanism to that of CPR. Paper-11248266.
We conclude that biglycan is important for the maintenance of muscle cell integrity and plays a direct role in regulating the expression and sarcolemmal localization of the intracellular signaling proteins dystrobrevin-1 and -2, alpha- and beta1-syntrophin and nNOS. Paper-12156205.
All these effects, along with the changes produced in the phosphorylated forms of several MAP kinases and the transcription factor CREB, and the increase in the expression of nNOS and iNOS observed under our experimental conditions, could be involved in the loss of dopaminergic neurons. Paper-13773246.
The amount of TH protein in the brain of Spr-null mice was less than 10% of wild-type, while TH protein in the adrenal, phenylalanine hydroxylase protein in the liver, and nNOS in the brain were not altered. Paper-12724069.
In mucinous carcinoma, the frequency of signet ring cells (62.5%), and background pools of mucin (87.5%) were significantly higher than those of duct cell carcinoma ( NOS), medullary carcinoma, apocrine carcinoma, and papillary carcinoma (P = 0.0408 to < 0.0001). Paper-13313074.
However, the cleavage site on nNOS is a unique leader sequence among the NOS family and this LF- mediated cleavage was not observed in iNOS, a major NOS isoform for anti-bactericidal NO production, even though NO level in LeTx-challenged cells was dramatically reduced. Paper-12760139.
We also found that the NOS inhibitor nitro-l-arginine methyl ester further stimulated the cyclic hypoxia-driven HIF-1alpha accumulation and the associated gain in endothelial cell survival, thereby mirroring the effects of a PI3K/Akt inhibitor. Paper-13566996.
Inducible ( iNOS) and constitutive ( eNOS, nNOS) nitric-oxide synthases differ in their Ca2+-calmodulin (CaM) dependence. iNOS binds CaM irreversibly but eNOS and nNOS, which bind CaM reversibly, have inserts in their reductase domains that regulate electron transfer. Paper-9954572.
Immunohistochemistry localized nNOS to nerve fibers and epithelial cells adjacent to mitochondrion-rich cells (ion transporting cell) in the gill, suggesting that nNOS production of NO may contribute to regulation of vascular tone and/or MRC function in the teleost gill. Paper-12159081.
Antioxidants, NOS inhibitors. and dominant negative, nonphosphorylatable C/ EBP-beta peptides block phosphorylation of C/ EBP-beta within the NLS and its nuclear export as well as rescue the abnormal albumin gene expression, suggesting potential therapeutic interventions. Paper-10767672.
CONCLUSION: These data show that NO production and NOS expression are differentially regulated temporally and in magnitude in the pancreas and lungs in response to cerulein hyperstimulation which suggests differing roles for each NOS isoform. and IAP. Paper-13706432.
OT treatment of these cells induced beating cell colonies that were fully inhibited by N,G-nitro-L-arginine-methyl-ester (L-NAME), an inhibitor of NO synthases ( NOS), partially reduced by 1400W, an inhibitor of inducible NOS, and ODQ, an inhibitor of NO-sensitive guanylyl cyclases. Paper-13136439.
Calmodulin kinase IV directly regulates the activation of the transcription factors CREB ( cyclic AMP response element binding protein) and CREM ( cyclic AMP response element modulator) and, as well, modulates the activity of neuronal NOS. Paper-9441815.
In this report we investigated the effect of 7-nitroindazole (7-NI), a specific neuronal inhibitor of nitric oxide synthase (nNOS) and L-NAME, a nonselective NOS inhibitor upon the adrenergic- and CRH-induced stimulation of the hypothalamic-pituitary-adrenal axis in nonanesthetized rast. Paper-12879612.
RESULTS: The majority of the patients were referred with the tentative diagnosis of ADHD but the most common diagnoses made by child and adolescent psychiatrists at the time of initial evaluation were BPD NOS (61.5%), followed by BPD I (26.9%), and mood disorder NOS (23.1%). Paper-12383310.
Conversely, the exposure of PAECs isolated from fetal lambs to the HSP90 inhibitor radicicol led to significant decreases in eNOS- HSP90 interactions, decreased shear-stimulated NO generation, and increased NOS-dependent superoxide production indicative of eNOS uncoupling. Paper-12636759.
Furthermore, aberrant expression of AGE, CML, CEL, MDAL and HNE, as well as of neuronal, inducible and endothelial nitric oxide synthases ( nNOS, iNOS, eNOS), and superoxide dismutase 2 ( SOD2), was found in muscle fibers containing protein aggregates in myotilinopathies and desminopathies. Paper-12518377.
Gene expression profiling also allows better distinction of PTCL/ NOS from angioimmunoblastic T cell lymphoma, the latter being characterised by follicular T helper lymphocyte derivation and CXCL13, PD1 and vascular endothelial growth factor expression. Paper-13057188.
Previous studies from our laboratory have demonstrated that nNOS production of NO* blocks Ca2+-ionophore- induced activation of ERK1/2 ( extracellular-signal-regulated kinase 1/2) of the mitogen- activated protein kinases through a mechanism involving Ras G-proteins and Raf-1 kinase. Paper-12046639.
Our studies show that constitutive expression of the NOS isoforms is differentially regulated and that iNOS and eNOS mRNA levels are dependent on the stage of mucous and squamous differentiation, respectively. bNOS expression was only marginally affected by the RA or differentiation status. Paper-1510445.
Despite their structural similarity, endothelial NOS ( eNOS) has a 6-fold lower NO synthesis activity and 6-16-fold lower cytochrome c reductase activity than neuronal NOS ( nNOS), implying significantly different electron transfer capacities. Paper-12871346.
Emerging data showing co-localisation of xanthine oxidoreductase ( XOR) and nNOS in the sarcoplasmic reticulum of rodents, and increased XOR activity in the nNOS(-/-) myocardium, suggest that nNOS gene deletion may have wider implications on the myocardial redox state. Paper-12317896.
Both the Arg inhibitors N-hydroxy-nor-l-arginine and BEC dose-dependently increased basal contractility in rat myocytes, which was inhibited by both nonspecific and NOS1-specific NOS inhibitors N(G)-nitro-l-arginine methyl ester and S-methyl-l-thiocitrulline, respectively. Paper-11369523.
The concept of endothelium-derived relaxing factor ( EDRF) implies that nitric oxide (NO) produced by NO synthase ( NOS) in the endothelium in response to vasorelaxants such as acetylcholine ( ACh) acts on the underlying vascular smooth muscle cells (VSMC) inducing vascular relaxation. Paper-13093403.
New neuroprotective strategies have been proposed with selective NOS inhibitors for the neuronal (ARL17477) or the inducible (1400 W) isoforms or with compounds combining in one molecule selective nNOS inhibition and antioxidant properties (BN 80933), in experimental ischemia-induced acute neuronal damage. Paper-1959468.
Finally, we demonstrate that Src kinase acts upstream of the PI3K/Akt pathway based on our finding that the selective Src inhibitor, PP2 (10microM), blocked the increases in nNOS phosphorylation levels, NO production, and PI3K/Akt activity induced by ERbeta activation. Paper-12994725.
Nitric oxide (NO), a short-lived gaseous free radical, synthesized from L-arginine by NO synthases ( NOS), is a potent mediator of biologic responses involved in the pathogenesis of autoimmune rheumatic diseases, such as systemic lupus erythematosus ( SLE) and rheumatoid arthritis (RA). Paper-12588690.
The mRNA expression for eNOS and bNOS was induced slightly later than for iNOS, consistent with a temporal increase in calcium-dependent NOS activity that gradually increased up to day 30. mRNA expression for the three NOS isoforms also was found in six of six human fracture callus samples. Paper-2141000.
It was therefore considered worthwhile to investigate the NOS activity in the PMNs, which like neurons, also express neuronal NOS ( nNOS), antioxidant enzyme levels [superoxide dismutase (SOD), catalase and glutathione peroxidase ( Gpx)] and beta-adrenergic receptors in the patients of depression. Paper-9220838.
This process depends on nitric oxide (NO) production by NO synthase ( NOS), matrix metalloproteinase activation, release of hepatocyte growth factor ( HGF) from the extracellular matrix, and presentation of HGF to the c-met receptor as demonstrated by a primary culture and in vivo assays. Paper-13694181.
In this study, the distribution of NOS-containing neurons in mating behavior circuitry of the male Syrian hamster brain was determined using labeling for brain NOS ( bNOS) and reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d). bNOS and NADPH-d labeled equivalent populations of neurons. Paper-781702.
This review article summarizes various types of interesting information obtained from lower organisms (invertebrates, fishes, amphibians, reptiles, and birds) about the properties and distribution of nNOS and eNOS and also the roles of NO produced by the cNOS as an important intercellular signaling molecule. Paper-12607986.
This review article summarizes various types of interesting information obtained from lower organisms (invertebrates, fishes, amphibians, reptiles, and birds) about the properties and distribution of nNOS and eNOS and also the roles of NO produced by the cNOS as an important intercellular signaling molecule. Paper-12416405.
The functionality of the interaction was demonstrated by investigating the inhibition of neuronal nitric-oxide synthase-1 ( NOS-1); PMCA is a negative regulator of NOS-1-dependent NO production, and overexpression of alpha-1 syntrophin and PMCA4 resulted in strongly increased inhibition of NO production. Paper-12173548.
HUVEC from gestational diabetes exhibit reduced SLC29A1 promoter activity when transfected with pGL3-hENT1(-2154) compared with pGL3-hENT1(-1114) constructs, an effect blocked by N(G)-nitro-L-arginine methyl ester (L-NAME, NOS inhibitor), but unaltered by S-nitroso-N-acetyl-L,D-penicillamine (SNAP, NO donor). Paper-12023143.
Characterization of the FMN-depleted mutants showed that bound FMN was essential for reduction of the nNOS heme or cytochrome c, but not for ferricyanide or dichlorophenolindolphenol, and established that the electron transfer path in nNOS is NADPH to FAD to FMN to heme. Paper-1955694.
Analyses by the NADPH-diaphorase reaction, immunocytochemistry, purification with ion-exchange chromatography, Western-blot, and quantitative polymerase chain reaction have revealed the expression of neuronal NOS in the rat intestine and of a 60-kDa subunit of NOS in the enteric nerve plexus of H. pomatia. Paper-13741485.
The present study examined the relationship between an important energy-generating enzyme (cytochrome oxidase; CO), a key energy-consuming enzyme (Na+ K+ ATPase) and neurochemicals associated with excitatory glutamatergic synapses ( NMDAR1 and neuronal nitric oxide synthase, nNOS) in the adult macaque retina. Paper-1488471.
Moreover, the comparison of the nNOS distribution with that of urotensins I and II (UI and UII) suggests that neurosecretory Dahlgren cells belong to two different functional subpopulations: a population of UI/ UII secreting nitrergic neurons and a population of non-nitrergic neurons, which principally secrete UII. Paper-9587897.
F(E)NO was significantly higher in wild-type B6SV129J +/+ mice than in mice with a targeted deletion of type I (neural) NOS ( nNOS, -/-) ( 6.3 +/- 0.9 vs. 3.9 +/- 0.4 parts/billion, P = 0.0345, for +/+ and -/- mice, respectively), indicating that approximately 40% of the NO in expired air in B6SV129 mice is derived from nNOS. Paper-1214946.
MAIN OUTCOME MEASURES: Genotype profiles for GLAST; N-methyl-d-aspartate-receptor subunits NR1, NR2A, and NR2B; MGLUR5; NNOS; PRKG2; CAMK4; the regulatory subunit of PI3K; and CREB were analyzed for association with alcohol dependence using multivariate statistical analysis. Paper-12871682.
Immunoblotting analysis using frontal tissue homogenates at 15, 28, 40 weeks of gestation and 18 months of age revealed single band corresponding to SOD1 molecular weight, observed at all stages examined; a single band compatible with the nNOS molecular mass was detected only at the 28th week of gestation. Paper-9148636.
METHODS: Electrical parameters reflecting trans-epithelial ion transport were measured in Caco-2 cell monolayers mounted in Ussing chambers and exposed to GH and cholera toxin (CT) alone or in combination, in the presence or absence of the NO synthase ( NOS) inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME). Paper-12088080.
Although the postsynaptic density protein PSD95 can recruit the calcium-dependent neuronal NO synthase ( nNOS) to the mouth of the calcium-permeable NMDA receptor, and depletion of PSD95 inhibits excitotoxicity, the possibility that selective uncoupling of nNOS from PSD95 might be neuroprotective is unexplored. Paper-10742331.
The mRNA and protein expression of hypoxia-inducible factor-1alpha ( HIF-1alpha), endothelial, neuronal, inducible nitric oxide synthase ( eNOS, nNOS, iNOS), and vascular endothelial growth factor ( VEGF) along with nitric oxide (NO) production and VEGF concentration was up-regulated significantly in hypoxic rats. Paper-12709633.
Diverse apoptotic stimuli activate inducible nitric oxide synthase ( iNOS) or neuronal NOS ( nNOS), with the generated nitric oxide (NO) S-nitrosylating GAPDH, abolishing its catalytic activity and conferring on it the ability to bind to Siah1, an E3-ubiquitin-ligase with a nuclear localization signal (NLS). Paper-12861677.
DESIGN AND METHOD: Concentration- and time-dependent effects of NaN(3) (1-100 mumol/L; 5-60 min incubation) on ADP- and collagen-induced aggregation, NO synthase ( NOS) activity, cGMP synthesis and vasodilator-stimulated phosphoprotein ( VASP) phosphorylation at Ser239 were investigated in platelets from 21 healthy individuals. Paper-12744279.
OBJECTIVES: We aimed to identify the expression profiles of the NOS isoforms endothelial NOS ( eNOS), neuronal NOS ( nNOS) and inducible NOS ( iNOS) and of phosphorylated eNOS and nitrotyrosine within the epidermal and follicular melanin units of normal human haired scalp during the hair growth cycle. Paper-10792145.
Regional expression of cytokines (IL-1alpha, TNF-alpha), inducible nitric oxide synthase ( iNOS) and neuronal NOS ( nNOS) was immunohistochemically investigated in the brains of patients with dementia with Lewy bodies (DLB), compared with those of patients with Alzheimer's disease (AD) and non-demented elderly persons. Paper-9670914.
Antibody microarrayer experiment revealed that pyk2, RAF-1, Mcl-1, syntrophin, calmodulin, isoforms of NOS protein family ( eNOS, nNOS, and iNOS), and synaptotagmin proteins were unambiguously upregulated in the heart of biglycan transgenic mice. Paper-13099847.
We have utilized CaM mutants deficient in binding Ca(2+) with mutations in the N-lobe (CaM(12)), the C-lobe (CaM(34)), or both lobes of CaM (CaM(1234)) to determine their effect on the binding and activation of the Ca(2+)-dependent neuronal ( nNOS) and Ca(2+)-independent inducible NOS ( iNOS) isoforms. Paper-12511995.
Despite their apparent promiscuity, the NOS isoforms support specific signaling because of their subcellular compartmentation with colocalized effectors and limited diffusibility of NO in muscle cells. eNOS and nNOS sustain normal EC coupling and contribute to the early and late phases of the Frank-Starling mechanism of the heart. Paper-11175193.
In the ischemic and failing myocardium, iNOS expression is induced and further contributes to attenuate the inotropic effect of catecholamines, as does eNOS coupled to overexpressed beta3-adrenoceptors. nNOS expression also increases in the aging and ischemic heart, but its role (compensatory or deleterious) remains to be defined. Paper-10737690.
Using intravital microscopy that allows us to visualize the steps of lymphatic metastasis, we show that genetic deletion of eNOS as well as NOS blockade attenuates peritumor lymphatic hyperplasia of VEGF-C-overexpressing T241 fibrosarcomas and decreases the delivery of metastatic tumor cells to the draining lymph nodes. Paper-13697832.
Inhibitors of neuronal NOS ( nNOS) L-NNA, general NOS L-NAME and inducible NOS ( iNOS) aminoguanidine, as well as inhibitors of COX-1, piroxicam, and COX-2, compound NS-398 were administered 15 min prior to carbachol to control or crowded rats (24 rats in cage for 7, during 3 and 7 days). Paper-12265409.
A significant dose trend (P trend = 0.04), however, was observed for total number of putative "at-risk" alleles (Nrf T, NQO1 T, NOS T, and HO-1 LL and LM genotypes), with those carrying three or more at-risk alleles having an odds ratio (OR) of 1.56 [95% confidence interval (95% CI), 0.97-2.51] compared with those having none. Paper-12493034.
Immunohistochemistry with antibodies against the alpha1, beta1 and beta2 sGC subunits showed that the larger part of positivity was present in the sarcolemma region of skeletal muscle fibers and colocalized with NOS-1 mainly in type II myofibers and with HO-2 in type I and type II myofibers. Paper-9101556.
The aim of this study was to determine the possible correlation between parenchymal MCP-1 expression and TAM level by immunohistochemical analysis of 97 invasive ductal breast carcinomas, not otherwise specified ( NOS), and to investigate their relation with tumor size, histological grade, mitotic activity index (MAI) and lymph node status. Paper-10984910.
We have used fluorescence resonance energy transfer (FRET) to examine the conformational transitions of CaM induced by its binding to synthetic nitric oxide synthase ( NOS) CaM- binding domain peptides and full length heme-free constitutive NOS ( cNOS) enzymes over a range of physiologically relevant free Ca (2+) concentrations. Paper-13092589.
RESULTS: The following changes occurred in old rats: (i) an increase of lipofuscin and a decrease in both bNOS-containing neurons and fluorescent adrenergic neurons in the pelvic ganglia; (ii) significantly less expression of NOS mRNA than in young rat penile tissues; and (iii) no significant alteration in adrenoreceptor alpha 1 mRNA expression. Paper-1143001.
Using in vivo microdialysis we infused specific inhibitors of NOS into the BF of rats during SD, and found that an inhibitor of inducible NOS ( iNOS), 1400W, prevented non-rapid eye movement (NREM) recovery, while an inhibitor of neuronal NOS ( nNOS), L-N-propyl-arginine, decreased REM recovery but did not affect NREM recovery. Paper-12237812.
Formation of this ternary complex among NOS-3, globular beta-actin, and Hsp90, in turn, results in an increase in both NOS activity and cyclic guanosine-3',5'-monophosphate, an index of bioactive NO, as well as an increased rate of Hsp90 degradation, thus limiting the duration for which NOS-3 remains activated. Paper-13253365.
These results suggest that Cox-2 expression rescues prostate cancer cells from sanguinarine- induced apoptosis by a mechanism involving inhibition of NOS activity, and that coadministration of Cox-2 inhibitors with sanguinarine may be developed as a strategy for the management of prostate cancer. Paper-11395233.
Our results with mouse and human ES cells demonstrate an increase in Nkx2.5 and myosin light chain ( MLC2) mRNA expression on exposure of cells to NO donors and a decrease in mRNA expression of both cardiac-specific genes with nonspecific NOS inhibitor and a concomitant increase and decrease in the mRNA levels of sGC alpha(1) subunit. Paper-13476186.
Expression of nNOS in the brain and peripheral nervous system is widely determined by staining with NADPH (reduced nicotinamide adenine dinucleotide phosphate) diaphorase or NOS immunoreactivity, and functional roles of NO formed by nNOS are evidenced in the early phylogenetic stages (invertebrates and fishes). Paper-12607986.
Finally, we consider whether the proposed migration of nNOS from the SR to the sarcolemma in the failing heart may have consequences for the nitrosative vs. oxidative balance at the level of the RyR2, and whether this may contribute to an increased diastolic Ca(2+) leak, depleted SR Ca(2+) store, and reduced contractility in heart failure. Paper-12708716.
In these caspase-3-containing fibers, DNA fragmentation, dystrophin breakdown, increased immunolabeling of mu-calpain, decreased cytochrome c, cathepsin-D effusion from the lysosomes and increased lipid peroxidation were observed, while no changes in active caspase-12, eNOS or nNOS immunolabeling were seen. Paper-13071728.
RESULTS: All isoforms of NOS, especially iNOS expression, was significantly upregulated in company with NR2A/B expression, not only in declining neuronal cells but also in reactive astrocytes in the tissue, with hemosiderin deposits, adjacent to CA and moreover the degree of iNOS expression was significantly correlated with seizure frequency. Paper-12596356.
Penile tissue sections were subjected to Masson trichrome staining for SMC and collagen, and immunodetection for alpha smooth muscle actin, iNOS, neuronal NOS ( nNOS), endothelial NOS ( eNOS), proliferating cell nuclear antigen ( PCNA), and terminal transferase dUTP nick end labeling ( TUNEL). Paper-13615023.
We measured expression of mRNA encoding ET-1, nitric oxide synthase-1, 2, 3 ( NOS1, 2, 3), haeme oxygenase-1, 2 ( HO-1, 2), adrenomedullin ( ADM), calcitonin gene-related peptide, vasoactive intestinal peptide, and prostacyclin synthase in whole lung using real-time reverse transcriptase-polymerase chain reaction. Paper-12702304.
These results suggest that genipin induces neurite outgrowth through an NO-cGMP-PKG signaling pathway followed by MAPK phosphorylation without TrkA activation in Neuro2a cells and that PKG downstream to NOSs, which may be mainly nNOS, is very important for the signaling molecule to induce neuritogenesis by genipin. Paper-12734487.
Both processes, nNOS phosphorylation and iNOS expression induced by LPS + IFNgamma, are regulated by Janus Kinase/Signal Transducer and Activator of Transcription ( JAK/ STAT) pathway, as IFNgamma increases (727)STAT-3 phosphorylation and specific inhibitors of JAK/ STAT pathway, such as AG490, inhibited both processes. Paper-13609796.
Employing immunocytochemical labeling, Western blotting and RT-PCR, we found that, in contrast to the most commonly accepted view, neuronal NOS was not restricted to the sarcolemma and that muscles of DMD and BMD patients retained all three NOS isoforms with an up-regulation of the inducible NOS isoform, CREB and nitrotyrosine. Paper-12110793.
Neither pathway depended on L-type Ca(2+) channels, in contrast with GluR6 kainate receptor action.1 Immunohistochemistry confirmed the presence of GluR4 and GluR5 clustered at the surface of myelinated axons; GluR5 coimmunoprecipitated with nNOS and often colocalized with neuronal nitric oxide synthase clusters on the internodal axon. Paper-13652137.
We then demonstrated that intracerebroventricular administration of nNOS inhibitor N-omega-nitro-l-arginine methyl ester further enhanced upregulation of AVP mRNA level but totally abolished upregulation of nNOS mRNA level in the paraventricular and supraoptic nuclei of anesthetized rats induced by a prior administration of Ang II. Paper-13761787.
The levels of different transcripts coding for molecules involved in nuclear condensation [ Prm-1 ( protamine 1) and Prm-2], capacitation [ eNOS (endothelial nitric oxide synthase), nNOS (neuronal nitric oxide synthase), c-myc], motility and sperm survival ( aromatase) have been assessed using semi-quantitative RT (reverse transcriptase)-PCR. Paper-13246473.
Of particular significance is that NOS overexpression stimulates the transcription and translation of a range of extracellular matrix genes important to the structure of connective tissues such as tendons, including collagen Ialpha1, collagen IIIalpha1, collagen IValpha5, biglycan, decorin, laminin, and matrix metalloproteinase 10 ( MMP10). Paper-12201529.
These include NMDA ( GRIN1, GRIN2A, GRIN2B) and metabotropic ( GRM3, GRM4) glutamate receptors, growth factors ( BDNF, NRG1), and many of their downstream signaling components or accomplices ( AKT1, DAO, DAOA, DISC1, DTNBP1, DPYSL2, IMPA2, NCAM1, NOS1, NOS1AP, PIK3C3, PIP5K2A, PDLIM5, RGS4, YWHAH). Paper-12584524.
In this study we show that biglycan directly or indirectly activates proteins involved in cardiac remodeling ( TGF-beta, pyk2), signal transduction ( RAF-1, Mcl-1, syntrophin, calmodulin, nNOS p38MAPK and MAP kinases), cardioprotection ( NOS family, TGF-beta) and Ca++ signaling ( connexin, calmodulin, synaptotagmin). Paper-13099847.
We report that in endothelial cells, the angiogenic effect of 17beta-estradiol ( E2) is inhibited by the estrogen receptor ( ER) antagonist ICI or the NO synthase ( NOS) inhibitor 7-nitroindazole via downregulation of hTERT, the telomerase catalytic subunit, suggesting that E2 and NO are involved in controlling hTERT transcription. Paper-12865318.
The mRNA levels of 13 genes including CD147 (receptor for CypA), PDGF-BB, endothelin-1 ( ET-1), vascular endothelial growth factor receptor-1 ( VEGFR-1), VEGFR-2, VEGFR-3, neuropilin-1 ( NRP-1), NRP-2, eNOS, iNOS, nNOS, ICAM-1, and PECAM-1 were semiquantitatively determined by real time RT-PCR as standardized with a house keeping gene beta-actin. Paper-11218801.
These synonyms are used for gene NOS1 (nitric oxide synthase 1 (neuronal)): NOS type I, NOS, N-NOS, nNOS, Nitric-oxide synthase, brain, Neuronal NOS, NC-NOS, IHPS1, Constitutive NOS, bNOS.
These accession numbers are used for gene NOS1: B3VK56 (UNIPROT__AC), A8MYP2 (UNIPROT__AC).
NOS1 is a homologue of NOS1 (nitric oxide synthase 1 (neuronal)) from Canis familiaris.
NOS1 is a homologue of NOS1 (nitric oxide synthase 1 (neuronal)) from Bos taurus.
NOS1 is a homologue of NOS1 (nitric oxide synthase 1 (neuronal)) from Gallus gallus.
NOS1 is a homologue of Nos1 (nitric oxide synthase 1, neuronal) from Mus musculus.
NOS1 is a homologue of Nos1 (nitric oxide synthase 1, neuronal) from Rattus norvegicus.
NOS1 is a homologue of nos1 (nitric oxide synthase 1 (neuronal)) from Danio rerio.
NOS1 is a homologue of Nos (Nitric oxide synthase) from Drosophila melanogaster.
NOS1 is a homologue of AgaP_AGAP008255 (AGAP008255-PA) from Anopheles gambiae str. PEST.
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