ライフサイエンスコーパス: NO

1 NO also appears to function in a cGMP-independent manner

2 NO exposure resulted in immediate and reversible intrace

3 NO formation from thiols occurs from the reaction of RSN

4 NO is a classic non-innocent ligand, and iron nitrosyls

5 NO is a precursor to tropospheric ozone, an air pollutan

6 NO synthetase expression and NO synthesis are linked to

7 NO-induced reduction of cellular viability was demonstra

8 fertilization rates above 100 kg N ha(-1) , NO emissions increased without a concomitant increase in

9 alone (barium chloride; n = 7; Protocol 1); NO (l-NMMA) and PG (ketorolac) inhibition alone, or comb

10 l2 solution of complexes [((R)DDB)Fe(NO)2((*)NO)](+) at 25 degrees C released NO as a neutral radical

11 ic oxide radical to form [((R)DDB)Fe(NO)2((*)NO)](+) was demonstrated and characterized by IR, UV-vis

12 al NO ligand in complex [((Me)DDB)Fe(NO)2((*)NO)](+), the simple addition of MeCN/H2O into CH2Cl2 sol

13 regulation of iNOS protein expression (27%), NO production (20%), ROS (32%) and lipoxygenase inhibiti

14 a low barrier for the pseudopericylic [1,3]-NO shift, calculated to be only 8.4 kcal/mol above 21.

15 A NO delivery platform that directly targets the resistanc

16 combination of sigma receptor moieties and a NO photodonor is reported, providing distinctive ligands

17 M. tuberculosis WhiB1 is a NO-responsive Wbl protein (actinobacterial iron-sulfur p

18 Pharmacologic long-term treatment with a NO-GC stimulator altered auditory nerve responses but di

19 ity and partition between biotic and abiotic NO-producing processes (i.e., chemodenitrification).

20 The remaining six accumulated NO and N2 O to varying degrees and genome sequencing of

21 oxidative stress and activates the alternate NO pathway which may partially account for the nitrite-m

22 d from dietary nitrate, via the 'alternative NO pathway'.

23 Although NO produced by iNOS is thought to have direct bactericid

24 es C after exposure for up to 10 h, although NO and NO2 may have exhibited oxidizing effects (e.g., e

25 O(neutral), with no localized electron in an NO pi* orbital or electron hole in an Fe dpi orbital.

26 Blunted dilatory responses to an NO donor and loss of myogenic tone in KW animals were al

27 e to FIV of mouse mesenteric arteries via an NO-dependent mechanism, whereas Ca(2+) -sensitive K(+) c

28 -sensitive K(+) channels mediate FIV via an NO-independent pathway.

29 involved in restoring GC1 basal activity and NO sensitivity because the Trx/thioredoxin reductase (Tr

30 dinol (SA-2) containing both antioxidant and NO donor functionalities that provide a therapeutic leve

31 SLE, focusing on its regulation of eNOS and NO production in endothelial cells.

32 stimulated in vitro, and iNOS expression and NO production were investigated.

33 NO synthetase expression and NO synthesis are linked to altered metabolism, neoplasti

34 TLRs, B cells, CD4(+) cells, IFN-gamma, and NO, on the level of parasitemia and parasite clearance d

35 GO and NO-GO sequences differed only in that the order of their

36 MC provoked the production of ROS, H2O2, and NO, modulating the PI3K/Akt, MAPK, NFkappaB and Nrf2 pat

37 lial cells; the two gasotransmitters H2S and NO and their interaction may serve as therapeutic target

38 onstitute the best textile-supported H2S and NO detectors reported and the best MOF-based chemiresist

39 NOX4 and matrix protein and whether H2S and NO pathways are integrated.

40 It consists of negative (the Min and NO systems) and positive (Ter signal mediated by MatP/Za

41 rs via two obligate intermediates, NH2OH and NO, necessitating a mediator of the third enzymatic step

42 i) a commercially available photoreactor and NO analyzer were used.

43 on of Iba1 expression, TNF-alpha release and NO production.

44 further indication for the roles of ROS and NO in atherosclerosis.

45 he NO radical character of coordinated axial NO ligand in complex [((Me)DDB)Fe(NO)2((*)NO)](+), the s

46 A significant positive correlation between NO and ED was also identified.

47 ds to a proatherosclerotic imbalance between NO and superoxide.

48 This suggests a potential interplay between NO and polyamine biosynthesis during drought response.

49 methane monooxygenase, all of which can bind NO and O2.

50 Both NO and TLR9 are important elements of innate immunity to

51 ition of MGDG synthase enzymatic activity by NO.

52 n be explained by the radical consumption by NO as SOx and NOx species share the same radical pool.

53 Our findings indicate that obestatin causes NO-dependent vasodilation in the human circulation.

54 llular viability was demonstrated by in-cell NO detection and total nitrite estimation.

55 energy transfer-based cGMP biosensor cGi500, NO-induced elevation of cGMP was detected in real-time i

56 hypothesis that inhibition of KIR channels, NO and PG synthesis, and Na(+) /K(+) -ATPase would not a

57 ercoming MDR and recent progress of combined NO and drug delivery systems.

58 PG (ketorolac) inhibition alone, or combined NO, PGs, Na(+) /K(+) -ATPase (ouabain) and KIR channel i

59 In contrast, NO-induced Rab11A activation, surface trafficking of bet

60 In contrast, NO-mediated TRAF2 activation in the more aggressive MDA-

61 )(MeCN)](+), effectively reductively couples NO(g) at RT in methanol (MeOH), giving a structurally ch

62 ound that the key products of NOS2 and COX2, NO and prostaglandin E2 (PGE2), respectively, promote fe

63 the NO-sensitive soluble guanylate cyclase (NO-GC, sGC) and triggers intracellular signaling pathway

64 Resulting maps of annual daytime NO, NO2, and black carbon at 30 m-scale reveal stable, p

65 NO in an O2-dependent manner with decreased NO consumption in physiological hypoxia.

66 feedback mechanism controls Ca(2+)-dependent NO synthesis under physiological oxygen.

67 enes including iNOS, and that iNOS-dependent NO production was required for a feedforward loop that m

68 s the main in vivo regulator of O2-dependent NO degradation in smooth muscle remains elusive.

69 ese observations emphasize that eNOS-derived NO can promote angiogenesis.

70 DnrF detects NO via its bound heme cofactor.

71 Endothelial dysfunction/NO bioavailability is associated with worse plasma leaka

72 sent a new method that collects soil-emitted NO through NO conversion to NO2 in excess ozone (O3) and

73 In addition to endogenous NO production from the amino acid l-arginine, via nitric

74 O2 consumption is controlled by endothelial NO in a paracrine, but not intracrine, fashion.

75 xidative stress and inhibited by endothelial NO.

76 ctly phosphorylates and inhibits endothelial NO synthase (eNOS).

77 dative stress and improvement of endothelial NO production represent reasonable therapeutic strategie

78 ced oxidative stress and reduced endothelial NO production is a further indication for the roles of R

79 endothelium, insulin stimulates endothelial NO synthase (eNOS) to generate the antiatherosclerotic s

80 ial of this approach in pregnancy to enhance NO bioactivity, improve uteroplacental vascular function

81 ation was predominantly mediated by enhanced NO activity, because N(G)-monomethyl-l-arginine markedly

82 tly associated with decreased IHVR, enhanced NO bioavailability, HSC deactivation, and reduced intrah

83 This, coupled with enhanced NO bioavailability, underpins differences in NO signalin

84 Exhaled NO was measured, and alveolar concentration and bronchia

85 Exogenous NO in the microenvironment facilitates paracrine signali

86 the diffusion-limited reaction of exogenous NO and endogenous superoxide (O2(*-)) produced in the el

87 udy, we investigated the effect of exogenous NO donor (NaNO2) on corneal wound healing.

88 Rule-in and rule-out uses of FE NO were considered.

89 n this study, the capability of cationic {Fe(NO)2}(9) dinitrosyl iron complexes (DNICs) [((R)DDB)Fe(N

90 nto CH2Cl2 solution of complexes [((R)DDB)Fe(NO)2((*)NO)](+) at 25 degrees C released NO as a neutral

91 bed nitric oxide radical to form [((R)DDB)Fe(NO)2((*)NO)](+) was demonstrated and characterized by IR

92 ated axial NO ligand in complex [((Me)DDB)Fe(NO)2((*)NO)](+), the simple addition of MeCN/H2O into CH

93 initrosyl iron complexes (DNICs) [((R)DDB)Fe(NO)2](+) (R = Me, Et, Iso; (R)DDB = N,N'-bis(2,6-dialkyl

94 mplex 2 is the first example of a [Fe(II){Fe(NO)}(7)] species and is also the first example of a mono

95 nion, with the ferric heme nitrosyl [(OEP)Fe(NO)(5-MeIm)](+) generates a mixture of the C-nitroso der

96 coupling a hydride temporarily stored on Fe(NO)2 (Lewis acid) and a proton accommodated on the expos

97 mes from the large energy gap between the Fe-NO pi-bonding and antibonding molecular orbitals relativ

98 and N-based nucleophiles on synthetic ferric-NO hemes.

99 Along the gradient, we measured field NO emissions, and used chloroform in the laboratory to r

100 se 3 expression and activity is critical for NO-stimulated cGMP production and vasodilation.

101 ppm theoretical limits of detection (LOD for NO = 0.16 ppm and for H2S = 0.23 ppm), these constitute

102 2 MAPKs in BV2 cells, which was required for NO production.

103 with BBMV from Geneva 88 than with BBMV from NO-QAGE, indicating that the ABCC2 mutation also affects

104 duced oligomerization of Cry1Ac in BBMV from NO-QAGE.

105 O3 formation from NO oxidation is several times more efficient than previo

106 te reductase (nap) genes, preventing further NO formation.

107 Thus, H2S recruits iNOS to generate NO to inhibit high glucose-induced NOX4 expression, oxid

108 pounds preserve their capability to generate NO under visible light and possess overall sigma recepto

109 is, therefore, critical to estimating global NO budgets, especially because drylands are expected to

110 results unravel the existence of a novel H2S-NO interaction and identify PYK2 as a crucial target for

111 lear hair cells and preservation of hearing, NO-mediated cascades have both protective and detrimenta

112 OPE also had higher NO, inducible nitric oxide synthase (iNOS) and cyclooxyg

113 tent with a selective role of NO-GC in IHCs, NO-GC beta1 mRNA was found in isolated IHCs but not in O

114 ronic structure is best described as Fe(III)-NO(neutral), with no localized electron in an NO pi* orb

115 NO bioavailability, underpins differences in NO signaling induced by inflammatory and physiologic sti

116 he lower BP was attributable to an increased NO bioavailability that dynamically dilated resistance v

117 te for 10 min caused significantly increased NO production, whereas pulling on syndecan-1, CD44, hyal

118 d eNOS, improved cell viabilities, increased NO generations, and reduced ROS productions in human umb

119 is a primary mechanosensor for shear-induced NO production.

120 res insulin-induced and shear stress-induced NO production.

121 K-1/2 and p65/RelA (NF-kappaB) and inducible NO synthase expression, suggesting that AnxA1 may be inv

122 factors IFN-gamma, TNF-alpha, and inducible NO synthase in the TME merely 4 d postinfection, before

123 ocyte-derived innate TNF-alpha and inducible NO synthase-producing DCs dominated the antibacterial re

124 ase [TDO], arginase [ARG] 1, ARG2, inducible NO synthetase) were evaluated in PBMCs.

125 cent to macrophages that expressed inducible NO synthase, suggesting a potential protective role for

126 for control of M. tuberculosis is inducible NO synthase (iNOS).

127 er, leading to attenuation of host cell iNOS/NO-mediated anti-microbial capacity.

128 Interestingly, NO-GC stimulation exacerbated the loss of auditory nerve

129 ic H2 O2 can oxidize l-Arginine (l-Arg) into NO for enhanced gas therapy.

130 as the most relevant source of intracellular NO during beta-adrenergic stimulation, while no evidence

131 We investigated NO signaling in endothelial cells cultured in physiologi

132 two NO-sensitive guanylate cyclase isoforms [NO-GC1 knockout (KO) or NO-GC2 KO].

133 In the laboratory, NO emission pulses were up to 19x greater in chloroform-

134 at Cavin-2 knockdown cells produce much less NO than WT cells.

135 BdMphi also failed to make NO after stimulation with recombinant badger interferon

136 pulling can be used to activate EGL-mediated NO production and that the heparan sulfate proteoglycan

137 IFN-alpha impairs insulin-mediated NO production, and altered gene expression resulted from

138 in skin cells are the source of UV-mediated NO release.

139 s the rate of NO consumption by metabolizing NO in an O2-dependent manner with decreased NO consumpti

140 Manipulating the interaction between mGluR5, NO production, or MMP-2 and MMP-9 pharmacologically or g

141 provide an effective platform in monitoring NO in biological processes and would have a great potent

142 ne, but not leucine, were increased in NAFLD-NO subjects compared to CTs.

143 f subjects with NAFLD without obesity (NAFLD-NO) compared to those with obesity (NAFLD-Ob) display al

144 g cardiac myocytes, we identified a neuronal NO synthase (nNOS) as the most relevant source of intrac

145 The response to this nitrosative (NO-triggered) stress is controlled by the Crp/Fnr-type t

146 yl radical ([HO2]/[OH]) and increased [NO2]/[NO] with higher levels of RBS and/or RIS.

147 Nootkatone (NO) is a sesquiterpenoid volatile flavor, used in foods,

148 excitation, which yields a remarkable H2 O2 -NO cooperative anticancer effect with minimal adverse ef

149 Accumulation of NO may cause cytotoxic effects.

150 alizing a significant differential amount of NO generated from the normal and stressed rat cardiac ce

151 Analyses of NO-production spectra adds further evidence that nitrite

152 y and locally liberates a controlled dose of NO is reported.

153 out to investigate the metabolic effects of NO in cultured astrocytes from mice by taking advantage

154 The results show that the efficiency of NO conversion to NO2 and subsequent NO2 collection in th

155 Emissions of NO from soils occur primarily during denitrification and

156 We found that Nos2 (-/-) mice incapable of NO-production in immune cells as microbial defence unifo

157 oxide after Mtb infection, and inhibition of NO by N(G)-monomethyl-L-arginine enhanced intracellular

158 , mitochondrial inhibitors, or inhibition of NO formation.

159 Vasodilator responses after inhibition of NO synthase blunted acetylcholine responses in KK and le

160 nalities that provide a therapeutic level of NO necessary to promote angiogenesis and to protect ECs

161 Additionally, salivary levels of NO were significantly associated with better functioning

162 e, this review will discuss the mechanism of NO in overcoming MDR and recent progress of combined NO

163 yzed the response to NO and the mechanism of NO sensing by the DnrF regulator.

164 dilatory capacity in KK to normalization of NO.

165 ocatalytic response towards the oxidation of NO as compared to other control electrodes.

166 atic product resulting from the oxidation of NO by O2 under aerobic conditions.

167 oncentration was observed in the presence of NO and it can be explained by the radical consumption by

168 uncoupling reduces epithelial production of NO and increases oxygen and nitrogen reactive species, a

169 and in vivo, thus reducing the production of NO.

170 ng system, efficiently regulates the rate of NO consumption by metabolizing NO in an O2-dependent man

171 angiogenesis is inhibited upon reduction of NO bioactivity both in vitro and in vivo Moreover, genet

172 n(II) complex that mediates the reduction of NO to N2O.

173 ental analysis exhibited higher reduction of NO to nitrogen (N2) comparing to the predictions by the

174 s further utilized to monitor the release of NO from different cells, realizing a significant differe

175 ctivity against M. tuberculosis, the role of NO as a signaling molecule has been poorly characterized

176 oborate current understanding of the role of NO in the metabolism of AOA and suggest that denitrifica

177 Consistent with a selective role of NO-GC in IHCs, NO-GC beta1 mRNA was found in isolated IH

178 ontroversy about the active sites for SCR of NO with NH3 by supported V2O5-WO3/TiO2 catalysts.

179 structure for the electrochemical sensing of NO, which was fabricated via a facile electrochemical al

180 mical reduction in vivo provides a source of NO that exerts beneficial effects upon the cardiovascula

181 ogical coupling-from the potential source of NO, endothelial cells, to the potential beneficiary from

182 l neovasculature requires close titration of NO-Tie2 signalling and localized VEGF induction, suggest

183 enhancing endothelial insulin sensitivity on NO availability is unclear.

184 fficiently fast that, as a result of ongoing NO x emission reductions, autoxidation is now competing

185 t impacting arterial stiffness, FMD, GMD, or NO.

186 te cyclase isoforms [NO-GC1 knockout (KO) or NO-GC2 KO].

187 -seq data, metabolic responses to nitrate or NO and how nitrate and nitrite reduction are coordinated

188 r their analytical response to nitric oxide (NO(*)).

189 Nitric oxide (NO) activates the NO-sensitive soluble guanylate cyclase

190 tics of growth and turnover of nitric oxide (NO) and N2 O at low cell densities of Nitrosomonas europ

191 ough chemical decomposition to nitric oxide (NO) and nitrate.

192 B) emit substantial amounts of nitric oxide (NO) and nitrous oxide (N2O), both of which contribute to

193 nnels (KIR ), and synthesis of nitric oxide (NO) and prostaglandins (PG).

194 h the wound healing effects of nitric oxide (NO) are known, the mechanism by which NO modulates corne

195 n endothelial cells identified nitric oxide (NO) as major mediator of this phenotype in PDX and in pa

196 NTS: In the heart, endothelial nitric oxide (NO) controls oxygen consumption in the working heart thr

197 Nitric oxide (NO) exerts pleiotropic effects on plant development; how

198 oach to investigate sources of nitric oxide (NO) formed in soils.

199 -2 regulates the production of nitric oxide (NO) in endothelial cells by controlling the stability an

200 low-induced vasodilatation via nitric oxide (NO) in mouse mesenteric resistance arteries.

201 xide synthase (iNOS) generates nitric oxide (NO) in myeloid cells that acts as a defense mechanism to

202 Nitric oxide (NO) is a regulatory molecule in the vascular system and

203 Nitric oxide (NO) is able to lower intraocular pressure (IOP); however

204 Nitric oxide (NO) is an intercellular messenger involved in multiple b

205 a respiratory process in which nitric oxide (NO) is an intermediate.

206 Host nitric oxide (NO) is important in controlling TB infection.

207 Nitric oxide (NO) is inactivated by cell-free hemoglobin in a dioxygen

208 The signaling molecule nitric oxide (NO) is synthesized in animals by structurally related NO

209 in cytoglobin (CYGB) regulates nitric oxide (NO) metabolism and cell death.

210 te that bdMphi fail to produce nitric oxide (NO) or upregulate inducible nitric oxide synthase (iNOS)

211 the association of endothelial nitric oxide (NO) pathways with disease severity is unknown.

212 Nitric oxide (NO) produced by endothelial cells in response to cytokin

213 ood pressure, possibly through nitric oxide (NO) production in skin.

214 ed with elevated intracellular nitric oxide (NO) production, which promotes nitrosative stress in met

215 glutamate receptors increases nitric oxide (NO) production, which stimulates matrix metalloprotease-

216 nt inhibitory activity against nitric oxide (NO) production.

217 lasts via mechanisms involving nitric oxide (NO) synthesis and posttranslational modification of prot

218 for the potential function of nitric oxide (NO) to overcome MDR.

219 diated dilation (GMD), urinary nitric oxide (NO), and inflammatory markers were measured before and a

220 pro-inflammatory cytokines and nitric oxide (NO), in response to LPS and alpha-synuclein.

221 nerates the potent vasodilator nitric oxide (NO), is decreased.

222 OS) and its bioactive product, nitric oxide (NO), mediate many endothelial cell functions, including

223 Reactions between nitric oxide (NO), nitrite (NO2-), and unsaturated fatty acids give ri

224 by increased soil emissions of nitric oxide (NO).

225 are subjected to regulation by nitric oxide (NO); in plants, however, it is unknown whether NO affect

226 found that treatment with the physiological NO donor S-nitrosoglutathione (GSNO) increased the abund

227 diatoms, a dominant phylum in phytoplankton, NO was reported to mediate programmed cell death in resp

228 GF WSP possessed NO inhibitory activity, and the strongest was GF121.

229 sterase-5 inhibitor, sildenafil, potentiates NO signaling to inhibit platelet function.

230 xidizing effects (e.g., exposure to 250 ppmv NO/N2 resulted in an 2.4 times increase in surface V2O5

231 he biotic and abiotic processes that produce NO, favoring chemodenitrification during periods when bi

232 he NO reductase genes (norCB), which promote NO consumption.

233 reby identifying genes that display putative NO-regulated histone acetylation.

234 te the antiatherosclerotic signaling radical NO.

235 Reduced NO production under drought conditions in UHb plants was

236 tigated whether the observed drought-related NO changes could involve polyamine pathway.

237 nthesized in animals by structurally related NO synthases (NOSs), which contain NADPH/FAD- and FMN-bi

238 s to quantify the response function relating NO flux to N input rate during the main 2011 and 2012 gr

239 )Fe(NO)2((*)NO)](+) at 25 degrees C released NO as a neutral radical, as demonstrated by the formatio

240 ted dialysis of cytosolic DAF, the remaining NO signals (mostly mitochondrial) were blocked by nNOS d

241 hat single supported Pt atoms are remarkable NO oxidation catalysts.

242 We found that HIF-1alpha function requires NO production, and that HIF-1alpha and iNOS are linked b

243 herapies, an alternative strategy to restore NO-cGMP signaling is via inorganic nitrite.

244 this mechanism by recoupling NOS, restoring NO production and reducing oxidative and nitrosative str

245 The related reaction with [(OEP)Ru(NO)(5-MeIm)](+) generates the (OEP)Ru(PhNO)(5-MeIm) prod

246 l, as demonstrated by the formation of [S5Fe(NO)2](-) from [S5Fe(mu-S)2FeS5](2-).

247 vasodilatation and angiopoietin signalling (NO-Tie-mediated arteriogenesis).

248 ecent years has established that significant NO can be derived from dietary nitrate, via the 'alterna

249 Since NO biosynthesis has been related to polyamine metabolism

250 1/CTLA4 signaling dampened activation of SMX-NO-specific naive and memory T cells, whereas blockade o

251 ming assay and nitroso sulfamethoxazole (SMX-NO) as a model Ag to investigate the activation of speci

252 pes, whereas spectratyping revealed that SMX-NO-specific T cell responses are controlled by public TC

253 e effects of minor flue gas components (SO2, NO, NO2, H2O, and O2) on vanadium at 500-600 degrees C w

254 The results showed that SO2, NO, and NO2 are unlikely to have adsorbed on the surface

255 Reports range from 0 to 67% soil NO emission reductions postbiochar amendment.

256 d understanding of biochar's impacts on soil NO emissions.

257 health cost models to assess how these soil NO reductions could influence U.S. air quality and healt

258 need for quantitative flux analysis to study NO in tumors.

259 In this study, NO donors (SNAP and DETA-NONOate) inhibited DC antigen p

260 acterize heme binding to DnrF and subsequent NO coordination.

261 We conclude that NO can modulate astrocytic energy metabolism in the shor

262 Our results demonstrate that NO plays a key role in cell wall remodelling in trichobl

263 Furthermore, we found that NO inhibits NF-kappaB activity to prevent hyperinflammat

264 We found that NO-mediated angiogenesis was blocked by inhibition of VE

265 These data suggest that NO affects histone acetylation by targeting and inhibiti

266 Nitric oxide (NO) activates the NO-sensitive soluble guanylate cyclase (NO-GC, sGC) and

267 hemia produces superoxide and diminishes the NO bioavailability by forming toxic peroxynitrite anion.

268 However, the NO to HNO conversion mediated by vitamins C, E, and arom

269 opy observes the change in wavenumber of the NO ligand band accompanying the isomerization and associ

270 ry sensitive to the protonation state of the NO moiety.

271 addition, DnrF induced the expression of the NO reductase genes (norCB), which promote NO consumption

272 s strongly diminished in the presence of the NO scavenger 2-4-carboxyphenyl-4,4,5,5-tetramethylimidaz

273 ed to test effects of agents that target the NO pathway in reducing arterial stiffness in HFpEF.

274 Consistent with the NO radical character of coordinated axial NO ligand in c

275 This NO stems from neuronal NOS (nNOS), but not endothelial (

276 r, thereby repressing its expression through NO and p38 MAPK activation.

277 method that collects soil-emitted NO through NO conversion to NO2 in excess ozone (O3) and subsequent

278 AO oxidizes NH2OH by only three electrons to NO under both anaerobic and aerobic conditions.

279 climating system, whereas a long exposure to NO can additionally induce a redirection of carbon to ne

280 h can feed TAG accumulation upon exposure to NO.

281 sensitivity, and limit of detection (LOD) to NO(*).

282 .THF, thiols mediate reduction of nitrite to NO.

283 We analyzed the response to NO and the mechanism of NO sensing by the DnrF regulator

284 E exhibited an excellent selectivity towards NO in the presence of interferences.

285 zene ring are explored using the complex TpW(NO)(PMe3)(eta(2)-PhCF3).

286 Intracellular and transient NO emission acts therefore at the basis of a nitrite-sen

287 lear function of mice lacking one of the two NO-sensitive guanylate cyclase isoforms [NO-GC1 knockout

288 the more recently introduced C60(++) (under NO dosing and with sample cooling) and argon cluster ion

289 ith weight loss, increase in the vasodilator NO, and decrease in lipid oxidation.

290 ctly (via oxygen sensing) or indirectly (via NO sensing downstream of NR activity).

291 onditions, are most vulnerable to N loss via NO as interactions between pH, SOM, and drought stimulat

292 , particularly during summer afternoons when NO levels are low and temperatures are elevated.

293 ); in plants, however, it is unknown whether NO affects histone acetylation.

294 oxide (NO) are known, the mechanism by which NO modulates corneal wound healing remains unclear.

295 The molecular mechanism by which NO operates at the blood-endothelium interface to exert

296 (mesenchymal-like) TNBC cell lines in which NO induced COX2 and PGE2 induced NOS2 proteins.

297 Here, we present a modified method in which NO is oxidized quantitatively to NO2 by chromium trioxid

298 le Fe(+)/ Fe(3+) redox couple activity, with NO detection by oxidation at potentials above +0.45V or

299 of KIR channels alone or in combination with NO, PGs and Na(+) /K(+) -ATPase significantly reduced th

300 (ESI-/ESI+) and red meat intake classes (YES/NO).