ライフサイエンスコーパス: RNS

1 RNS produce a variety of DNA lesions in a broad spectrum

2 RNS-induced DNA lesions cause genomic instability in the

3 RNS-induced sensations of pain and increases in systemic

4 RNSs and ROSs may be involved in the presentation of gly

5 genomic boundaries and coding strand of 153 RNS-induced transcripts.

6 (4) also enhanced myeloperoxidase, H(2)O(2,) RNS production, and bacterial killing in K. pneumoniae-i

7 d in niches of the body containing activated RNS- and ROS-generating immune and endothelial cells, po

8 ese data show that capillary dysfunction and RNS generation contribute to tubular injury and suggest

9 thase inhibitor on capillary dysfunction and RNS generation.

10 nging ROS (IC(50) from 1.7 to 108mug/ml) and RNS (IC(50) from 0.05 to 0.59mug/ml), when compared to g

11 gests the formation of hydrogen peroxide and RNS.

12 We detected dose-dependent ROS and RNS activity in the liver within minutes of drug challen

13 and emphasizes interactions between ROS and RNS and the relative roles of cellular ROS/RNS generator

14 lay role in the direct scavenging of ROS and RNS as well as inducing antioxidant defense mechanisms a

15 s capable to efficiently control the ROS and RNS concentrations in the cancer-inhibiting media.

16 +) concentrations and the amounts of ROS and RNS create an amplifying cycle that ultimately triggers

17 Additionally, ROS and RNS deplete cellular defenses and initiate inflammation.

18 ROS and RNS directly oxidize and damage DNA, proteins, and lipid

19 ne assay of biomarkers indicative of ROS and RNS elaboration.

20 cantly advances our understanding of ROS and RNS evasion strategies during infection.

21 time in vivo imaging of drug-induced ROS and RNS for direct evaluation of acute hepatotoxicity.

22 selective and sensitive detection of ROS and RNS in biological systems.

23 and evaluated for susceptibility to ROS and RNS in gamma interferon (IFN-gamma)-activated macrophage

24 the mel2 locus confers resistance to ROS and RNS in laboratory medium, suggesting that this locus mig

25 ortant roles for CXCL1 in generating ROS and RNS in neutrophils and in regulating host immunity again

26 r host defense; however, the role of ROS and RNS in the response to tissue injury is not known.

27 ming to elucidate the involvement of ROS and RNS in transcriptional response to IR.

28 stable and reproducible responses to ROS and RNS in vitro.

29 ly inflict damage on macromolecules, ROS and RNS indirectly induce damage to tissues by activating a

30 To determine ROS and RNS inside macrophages, one needs smaller (i.e., nanomet

31 e used to penetrate cells and detect ROS and RNS inside macrophages.

32 locus plays a role in resistance to ROS and RNS produced by activated macrophages.

33 examined the effects of IFN-gamma on ROS and RNS production by these cells as well as the effects on

34 ssion of the intracellular sites for ROS and RNS production in muscle fibres.

35 genipin against damage stemming from ROS and RNS production in organotypic hippocampal slice cultures

36 y following exposure, requiring both ROS and RNS scavengers.

37 compound, proved to have the highest ROS and RNS scavenging potential.

38 e macrophages produce high levels of ROS and RNS upon activation with gamma interferon (IFN-gamma), w

39 eactive oxygen and nitrogen species (ROS and RNS) is extracellular glutathione peroxidase (eGPx).

40 eactive oxygen and nitrogen species (ROS and RNS) produced by macrophages are essential for protectin

41 eactive oxygen and nitrogen species (ROS and RNS).

42 capacity to scavenge all the studied ROS and RNS, being gum arabic a more potent antioxidant than mal

43 y reactive and short-lived nature of ROS and RNS, combined with limitations of conventional detection

44 dative stress, e.g., scavenging both ROS and RNS, induction of defense mechanisms and alleviating/sup

45 eactive oxygen and nitrogen species (ROS and RNS, respectively), to modulate human neutrophils' oxida

46 gnalling pathways that contribute to ROS and RNS-induced skeletal muscle adaptation to endurance exer

47 ity than skin extract for all tested ROS and RNS.

48 ury with a significant component of ROS- and RNS-mediated damage, such as TBI and stroke, to assess i

49 lts suggest differential effects of ROS- and RNS-rich plasma, and may have a role in optimizing clini

50 ding acetaminophen and kainic acid, known as RNS inducers.

51 Co-localisation was observed between RNS-modified tyrosine residues and the chemokine CCL2 in

52 rsed the capillary perfusion defect, blocked RNS generation, and reduced AKI.

53 acteria are relatively resistant to ROS, but RNS inhibit growth of, and possibly even kill, mycobacte

54 JNK activation by RNS was abolished in cells lacking functional Fas or fol

55 naling was not involved in JNK activation by RNS.

56 JNK activation and cell death by RNS occurred in a Fas ligand- and caspase-independent ma

57 We demonstrate here that cell death by RNS was caused by c-Jun N-terminal kinase (JNK).

58 While the activation of JNK by RNS or FasL required FADD, the cysteine-rich domain 1 co

59 Activation of JNK by RNS was density dependent and caused mitochondrial depol

60 ns of phoPQ are hypersensitive to killing by RNS generated in vitro.

61 nse involves a specific pathway triggered by RNS.

62 In contrast to PSA degradation by RNSs, dextran depolymerization in the endosome depends o

63 In contrast, RNS induced JNK potently in cells expressing a truncated

64 In contrast, RNS synthesized during high-NO fluxes of gamma interfero

65 agocyte oxidase-derived ROS nor iNOS-derived RNS are essential for resolution of infection, RNS prote

66 in might be mediated by mitochondria-derived RNS, and activation of the c-Src/PI3K pathway might gene

67 ight be mediated by the mitochondria-derived RNS.

68 or simultaneously and differentially detects RNS and ROS using two optically independent channels.

69 of iNOS, Mtb in vivo is likely to encounter RNS by producing nitrite.

70 Thus, this study demonstrates that excess RNS are a nongenetic driving force for Brca2-deficiency-

71 r ROS and IC(50) from 0.04 to 0.12mug/ml for RNS).

72 d with Fas-associated death domain (FADD) in RNS-exposed cells, illustrating that RNS directly target

73 rating a dependence of Fas but not TNF-R1 in RNS-induced signaling to JNK.

74 ynchronizing epidermal/cortical responses in RNS.

75 tial liver grafts, most likely by increasing RNS that leads to mitochondrial damage and dysfunction.

76 S are essential for resolution of infection, RNS protect from chronic chlamydial disease in this mode

77 ucial role for the production of short-lived RNS.

78 Examining the ability of the major RNSs to degrade PSA, we determined that deamination is t

79 In Nox2-/- mice, RNS-mediated protein oxidation, as monitored by protein

80 reless NeuroPace responsive neurostimulator (RNS) and tracked their motion with sub-millimeter precis

81 erable to inactivation by reactive nitrogen (RNS) and oxygen species (ROS) that covalently modify ami

82 NO/RNS at concentrations physiologically relevant to inflam

83 echanism for understanding mutagenesis by NO/RNS.

84 By inhibiting BRCA1 expression, NO/RNS thereby reduces the ability of cells to repair DNA d

85 Moderate NO/RNS concentrations stimulated mutagenesis not directly b

86 thought to be mediated by the effects of NO/RNS in generating DNA damage.

87 tosis, thereby preventing accumulation of NO/RNS-generated mutations.

88 In summary, NO/RNS stimulates genetic instability by inhibiting BRCA1 e

89 esolve infection, produce greater amounts of RNS in vivo, and sustain lower rates of hydrosalpinx for

90 titution protects SsrB against the attack of RNS while preserving its DNA-binding capacity.

91 e formation and abrogate the cytotoxicity of RNS against phoQ Salmonella, presumably by limiting the

92 s used to characterize the lethal effects of RNS on B. burgdorferi.

93 The effects of RNS were quantified by integrating records of the differ

94 Tubular generation of RNS was significantly elevated at 10 h after CLP and was

95 enues aimed at preventing the interaction of RNS with Fas may attenuate tissue damage characteristic

96 eases that are accompanied by high levels of RNS.

97 Interestingly, the majority of RNS-sensitive E. coli proteins differ from E. coli prote

98 (marker of ROS), 3-nitrotyrosine (marker of RNS), poly(adenosine diphosphate-ribose) (PAR, marker of

99 4-HNE) were used as histochemical markers of RNS and ROS formation, respectively.

100 ence was performed to assess the presence of RNS in kidney biopsies.

101 inhibitor, largely blunted the production of RNS, prevented the increase of alanine aminotransferase

102 Suppression of RNS could be an important strategy for pancreatic cancer

103 s that modulate E-selectin expression and/or RNS generation may restore T-cell entry and could potent

104 SPI2) genes are also repressed by high-order RNS (39), we investigated whether the NO-mediated inhibi

105 secretion system is repressed by high-order RNS of IFN-gamma-activated macrophages.

106 generator, and peroxynitrite (PN), a potent RNS.

107 However, Mtb's own ability to produce RNS is rarely considered, perhaps because nitrate reduct

108 rived reactive oxygen species (ROS) regulate RNS during chlamydial urogenital infection in the mouse.

109 e oxygen and reactive nitrogen species (ROS, RNS) formed in the inner ear in response to high-intensi

110 ROS/RNS are often generated by ischemia-induced inflammation

111 In particular, abnormal ROS/RNS ratios are not achievable in discharges since they d

112 city and cytoprotection capacity against ROS/RNS on BAEC.

113 to examine their role in defense against ROS/RNS-mediated microbicidal activity of infected macrophag

114 fibroblasts had increased superoxide and ROS/RNS production (6.2-fold, P < 0.001 and 1.8-fold, P < 0.

115 pression, NF-kappaB/MAPK activation, and ROS/RNS production.

116 olved in the development of cytokine and ROS/RNS resistance may define simplified and specific strate

117 ls are highly resistant to cytokines and ROS/RNS, with no impairment in glucose-stimulated insulin se

118 onential trend was also observed between ROS/RNS and [Formula: see text] for all naphthalene SOA, reg

119 lier time points, methamphetamine caused ROS/RNS generation, which was detected with the fluorigenic

120 d RNS and the relative roles of cellular ROS/RNS generators as amplifiers of the initial ionization e

121 te methamphetamine-induced cytotoxicity, ROS/RNS generation, and dopamine release in cultured cells.

122 ent mitochondria with resulting enhanced ROS/RNS generation.

123 sociated with increased Nox2 expression, ROS/RNS production, and oxidative protein and lipid modifica

124 ability of F. tularensis to resist high ROS/RNS levels, we have hypothesized that additional unknown

125 llenge, KC fibroblasts maintained higher ROS/RNS levels (3.3-fold, P < 0.02), showed higher caspase-3

126 e of iron-containing seed induced higher ROS/RNS production compared to that formed in the presence o

127 nse ROS/RNS are examined in terms of how ROS/RNS modify protein structure and function, for example,

128 cultures showed significant increase in ROS/RNS production (P < 0.001) compared with untreated contr

129 b, significantly attenuated H2O2-induced ROS/RNS accumulation and lipid peroxidation, decreased H2O2-

130 echanisms by MET, may combat age-induced ROS/RNS and protect the myocardium from oxidative stress dis

131 es on the chemistry of radiation-induced ROS/RNS generation and emphasizes interactions between ROS a

132 Radiation-induced ROS/RNS is observed in several cell types with the exception

133 (o) cells show neither radiation-induced ROS/RNS production nor depolarization.

134 Radiation-induced ROS/RNS, depolarization, and calcein fluorescence decrease a

135 oach, simultaneous detection of multiple ROS/RNS products of fluorescent probes, developed in this st

136 amphetamine-induced apoptosis, necrosis, ROS/RNS generation, and dopamine release in NG108-15 cells.

137 neration of reactive oxygen or nitrogen (ROS/RNS), detected with dihydrodichlorofluoroscein by fluore

138 (ROS) and several downstream effects of ROS/RNS (reactive nitrogen species) production such as inhib

139 n) will change type and concentration of ROS/RNS and effectively tune the behavior of human skin cell

140 pressed by pharmacological inhibitors of ROS/RNS and PARP.

141 blasts had increased basal generation of ROS/RNS and were more susceptible to stressful challenges (l

142 high concentrations, moderate levels of ROS/RNS are essential for normal cell function and take part

143 formation, while continued formation of ROS/RNS contributes to the long-term hair cell loss.

144 Weak and very short leaks of ROS/RNS from the vacuoles into the cytoplasm were detected,

145 , we demonstrate real-time monitoring of ROS/RNS in activated macrophages using high-throughput fluor

146 3/7 and caspase-9, and the production of ROS/RNS in ARPE-19 cell cultures.

147 useful in unraveling the complex role of ROS/RNS in redox regulation, cell signaling, and cellular ox

148 The regulation of ROS/RNS is largely attended by peroxiredoxins (Prdxs) and th

149 activation of TLR2 and the generation of ROS/RNS mediates LTA-induced barrier dysfunction in PMEM.

150 In the 1-10 Gy dose range, the amount of ROS/RNS produced/cell is constant, but the percentage of pro

151 d inhibitors confirms the involvement of ROS/RNS signaling and of the importance of transformed cell

152 orrelating with the delayed formation of ROS/RNS, there was a progressive hair cell loss, stabilizing

153 ning the extent of tissue involvement or ROS/RNS-related damage would have a significant clinical imp

154 Cellular mechanisms for regulating ROS/RNS levels are discussed.

155 The mechanisms by which cells sense ROS/RNS are examined in terms of how ROS/RNS modify protein

156 ed reactive oxygen and nitrogen species (ROS/RNS) are assumed the central biologically active plasma

157 Reactive oxygen and nitrogen species (ROS/RNS) are natural byproducts of cellular metabolism.

158 of reactive oxygen and nitrogen species (ROS/RNS) in biological systems.

159 ion of reactive oxygen/nitrogen species (ROS/RNS) in cardiomyocytes, which leads to contractile dysfu

160 of reactive oxygen and nitrogen species (ROS/RNS) on the assembly of TE into elastic fibers.

161 ar reactive oxygen and nitrogen species (ROS/RNS) production was measured for SOA generated from the

162 Reactive oxygen/nitrogen species (ROS/RNS) production was measured with 2',7'-dichlorodihydrof

163 ne and reactive oxygen/nitrogen species (ROS/RNS) signaling.

164 ion of reactive oxygen/nitrogen species (ROS/RNS) was measured with 2',7'-dicholorodihydrofluorescein

165 of reactive oxygen and nitrogen species (ROS/RNS), but are only modestly protected against high conce

166 ing of reactive oxygen/nitrogen species (ROS/RNS).

167 us reactive oxygen and nitrogen species (ROS/RNS).

168 ed reactive oxygen and nitrogen species (ROS/RNS).

169 de and reactive oxygen/nitrogen species (ROS/RNS; hydrogen peroxide, peroxynitrite anions, and peroxy

170 or reactive oxygen and nitrogen species (ROS/RNS; nitroxidative species), including superoxide, perox

171 Radiation-stimulated ROS/RNS is also inhibited by overexpressing the Ca(2+)-bindi

172 These findings establish that ROS/RNS can modify TE and that these modifications affect th

173 The molecular damage that ROS/RNS induce is referred to as nitrooxidative stress.

174 onomethyl arginine citrate inhibited the ROS/RNS fluorescence signal induced by methamphetamine, whic

175 d be reconditioned during EVLP using the ROS/RNS scavenger Mn(III)-tetrakis (4-benzoic acid) porphyri

176 ucts formed from interaction between the ROS/RNS species and the fluorogenic probes, as follows: supe

177 trophil-rich ischemic areas, making this ROS/RNS sensor a novel prognostic indicator.

178 ing intracellular reactive nitrogen species (RNS) accumulation, suppressing the expression of key ele

179 species (ROS) and reactive nitrogen species (RNS) and subsequent oxidative stress.

180 ctive oxygen species (ROS)/nitrogen species (RNS) and the activation of poly(adenosine diphosphate-ri

181 species (ROS) and reactive nitrogen species (RNS) are essential activators of these pathways.

182 species (ROS) and reactive nitrogen species (RNS) are produced, in part, from NADPH oxidase in respon

183 species (ROS) and reactive nitrogen species (RNS) are strongly coupled in liquid-phase reactions: NO3

184 synthase (iNOS), reactive nitrogen species (RNS) can kill Mycobacterium tuberculosis (Mtb).

185 ios and increased reactive nitrogen species (RNS) can lead to AMPK activation.

186 OS expression and reactive nitrogen species (RNS) formation (nitrite and nitrate levels and 3-nitroty

187 Reactive nitrogen species (RNS) function as powerful antimicrobials in host defence

188 e cytotoxicity of reactive nitrogen species (RNS) generated by inducible nitric oxide synthase (iNOS)

189 this pathogen to reactive nitrogen species (RNS) generated from the nitric oxide produced by the ind

190 tify in real time reactive nitrogen species (RNS) generation by renal tubules, and the inducible nitr

191 sodium nitrite, a reactive nitrogen species (RNS) generator, and 0.5 mM paraquat, which produces reac

192 species (ROS) and reactive nitrogen species (RNS) have been implicated in myriad disease etiologies a

193 species (ROS) and reactive nitrogen species (RNS) in aerobic metabolism.

194 species (ROS) and reactive nitrogen species (RNS) in response to bacterial infections.

195 owing exposure to reactive nitrogen species (RNS) is less in co-cultured neurones, compared to neuron

196 ic oxide (NO) and reactive nitrogen species (RNS) may link inflammation to the initiation, promotion,

197 concentrations of reactive nitrogen species (RNS) metabolites.

198 hat GSH scavenges reactive nitrogen species (RNS) other than NO.

199 Reactive nitrogen species (RNS) play an essential role in host defence against Myco

200 species (ROS) and reactive nitrogen species (RNS) play important roles in cell signalling pathways in

201 pecies (ROS), and reactive nitrogen species (RNS) production is unclear, as is the contribution of th

202 uperoxide and ROS/reactive nitrogen species (RNS) productions were determined with an amine-reactive

203 is a highly toxic reactive nitrogen species (RNS) recently discovered as an inflammatory oxidant with

204 species (ROS) and reactive nitrogen species (RNS) that act to further increase resting Ca(2+) concent

205 tentially harmful reactive nitrogen species (RNS) throughout its infective cycle.

206 the production of reactive nitrogen species (RNS) via iNOS protects a significant proportion of mice

207 species (ROS) and reactive nitrogen species (RNS) was determined.

208 species (ROS) and reactive nitrogen species (RNS) was evaluated by in vitro screening assays.

209 l lineO, PN) is a reactive nitrogen species (RNS) which can effect deleterious nitrative or oxidative

210 oxygen (ROS) and reactive nitrogen species (RNS), allowing them to survive and replicate inside thei

211 cies (ROS) and/or reactive nitrogen species (RNS), and antioxidants or ROS scavengers promote cell su

212 species (ROS) and reactive nitrogen species (RNS), and dopamine release were examined in the absence

213 species (ROS) and reactive nitrogen species (RNS), has been proposed as an early unifying event linki

214 Reactive nitrogen species (RNS), in particular nitric oxide (NO), are toxic to bact

215 the generation of reactive nitrogen species (RNS), including peroxynitrite (ONOO).

216 species (ROS) and reactive nitrogen species (RNS), promote diseases such as cancer.

217 nd that excessive reactive nitrogen species (RNS), such as nitrite, are generated in precancerous pan

218 species (ROS) and reactive nitrogen species (RNS), which can alter the biological function of key cel

219 uing dual role in reactive nitrogen species (RNS)-related oxidative stress.

220 species (ROS) and reactive nitrogen species (RNS).

221 of Cys(203) with reactive nitrogen species (RNS).

222 species (ROS) and reactive nitrogen species (RNS).

223 sed generation of reactive nitrogen species (RNS).

224 spite exposure to reactive nitrogen species (RNS).

225 ased detection of reactive nitrogen species (RNS).

226 ker of NO-induced reactive nitrogen species (RNS).

227 of Salmonella to reactive nitrogen species (RNS).

228 xide (NO)-derived reactive nitrogen species (RNSs) and/or superoxide-derived reactive oxygen species

229 Conditioning by remote noxious stimulation (RNS; application of 3 degrees C water to a hand) usually

230 treatment of antioxidant tempol to suppress RNS, not only are DNA lesions significantly reduced, but

231 Root nodule symbioses (RNS) allow plants to acquire atmospheric nitrogen by est

232 ble for activation of root nodule symbiosis (RNS) at both epidermal and cortical levels and is functi

233 These findings illustrate that RNS cause cell death in a Fas- and JNK-dependent manner

234 ADD) in RNS-exposed cells, illustrating that RNS directly targeted Fas.

235 e, an AMPK agonist, these data indicate that RNS generated by metformin is required for AMPK activati

236 O-induced growth inhibition, indicating that RNS-mediated modifications play important physiological

237 The results suggest that RNS may affect particularly those elements of the PSEC e

238 ontribute to tubular injury and suggest that RNS should be considered a potential therapeutic target

239 The RNS-induced effect on the entire PSEC was significantly

240 blood pressure were not correlated with the RNS-induced effects on the different segments of the PSE

241 t to increase resistance of H. capsulatum to RNS in culture.

242 le exhibit increased fitness when exposed to RNS in an NRAMP(R), C3H/HeN murine model of acute oral i

243 nism underlying PhoPQ-mediated resistance to RNS is linked to the coordination of Mg(2+) homeostasis

244 To understand how H. capsulatum responds to RNS, we determined the transcriptional profile of H. cap

245 creased susceptibility of phoQ Salmonella to RNS requires molecular O2 and coincides with the nitroty

246 oxygen species (ROS), were not sensitive to RNS-mediated lipid peroxidation.

247 f Salmonella enterica serovar Typhimurium to RNS in a murine model of systemic salmonellosis.

248 rather than DNA or membrane lipids underlies RNS toxicity in wild-type B. burgdorferi.

249 We now report that higher in vivo RNS production correlates with mouse strain-related inna

250 es the pathways identified here to cope with RNS-induced damage during pathogenesis.

251 t to identify Escherichia coli proteins with RNS-sensitive cysteines.