ライフサイエンスコーパス: ROS

1 ROS are essential for activation of T cells, but how ROS

2 ROS at moderate concentrations have important signaling

3 ROS can cause oxidative damage particularly to proteins.

4 ROS originate from mitochondria and NADPH oxidases.

5 otein expression (27%), NO production (20%), ROS (32%) and lipoxygenase inhibition (IC50=31.24muM) co

6 ess of modulating biochemical reactions as a ROS source to exert cancer death.

7 We constructed a ROS sensor comprising an ascorbic-acid-based hydrogel en

8 ered by culturing cells in the presence of a ROS quencher or in an anaerobic environment.

9 Accordingly, ROS-high NKT cells exhibited increased susceptibility an

10 Genes associated with neutrophil activation, ROS production, intracellular antioxidation, and leukocy

11 In addition, ROS disassembles adherens junctions in epithelial cells

12 ight serve as a protective mechanism against ROS-triggered cytotoxic effects of a cocktail of polluta

13 Although ROS production is typically viewed as a proinflammatory

14 Canli et al. now demonstrate that amplified ROS production specifically by myeloid cells is sufficie

15 pancreatic cells is regulated by Ca(2+) and ROS signaling through Ca(2+)-induced structural changes

16 d a core circuit containing HIF-1, AMPK, and ROS.

17 he Rac GTPases, which control chemotaxis and ROS.

18 show that measuring both DTT consumption and ROS generation in the DTT assay is important to incorpor

19 Approaching the transition, DeltaPsi and ROS increased, and secretory granules disappeared.

20 promoter, and increased Nox1 expression and ROS levels associated with mesenchymal transition in the

21 e increases in fibrotic gene expressions and ROS production but promoted inductions of inflammatory c

22 , normalized the expression of AOE genes and ROS levels, reversed the heightened CB chemosensory refl

23 reover, induction of stress marker genes and ROS-scavenging enzyme genes under various stress conditi

24 hlight the potential of lipid metabolism and ROS as therapeutic targets for reducing tumor recurrence

25 NET and ROS release was monitored after the addition of NADP (NA

26 NET and ROS release, as well as the expression of NET-bound anti

27 the mitochondrial pathways for oxidation and ROS generation, thereby sustaining cancer cell survival

28 , cholangiocellular JNK-phosphorylation, and ROS accumulation in surrounding hepatocytes are present.

29 ts contains its own set of ROS-producing and ROS-scavenging pathways, the steady-state level of ROS,

30 play a role in observed redox reactions and ROS generation.

31 ression and reduced cellular respiration and ROS generation.

32 importance of the crosstalk between RLK and ROS signaling is discussed in the context of stomatal im

33 f the intricate connections between RLKs and ROS signaling and describe the regulatory events that co

34 the pathogenesis of nephrotic syndrome, and ROS formation may be a pathomechanism of COQ2-nephropath

35 Respiratory uncoupling and ROS excess occurred at PCoA > 600 nmol/mg mito prot, in

36 Apoplastic ROS production is a frequent result of RLK signaling in

37 ne H4, DNA-PK, RIP1 and IAPs that attenuates ROS-mediated apoptosis, and targeting this pathway may i

38 show that mutated FLT3-ITD and JAK2 augment ROS production and HR, shifting the cellular milieu towa

39 this proposal remains controversial because ROS scavengers fail to retard mitophagy.

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

41 However, KRIT1 depletion blunted ROS production in response to TNF-alpha.

42 step(s) during OGG1 initiated BER evoked by ROS facilitates NF-kappaB DNA occupancy and gene express

43 tion of Toll/NF-kappaB and EGFR signaling by ROS levels in the PSC/niche controls lymph gland hematop

44 ie through an apoptotic pathway triggered by ROS production.

45 Because cellular ROS status is pivotal to inflammation and bacterial kill

46 egradation of RIP1, accumulation of cellular ROS and degradation of IAPs (cIAP1 and XIAP).

47 kingly, PIKfyve is necessary for chemotaxis, ROS production, and stimulation of the Rac GTPases, whic

48 In contrast, ROS production was stronger and more persistent during r

49 Conversely, ROS were highly elevated in CD4 T cells from mice ectopi

50 rial membrane potential and higher cytosolic ROS production.

51 exposure to stress, four extracts decreased ROS values significantly to 22.5-24.9%.

52 ng through the activation of RBOHD-dependent ROS production.

53 tform exhibits high sensitivity and detected ROS generated chemically in solution and in actual cell

54 ant protein peroxiredoxin (AhpC) to detoxify ROS such as hydrogen peroxide, organic hydroperoxide, an

55 Here, we explore the role of different ROS sources arising in obesity and diabetes, and the eff

56 how that NSD substrates are generated during ROS exposure as a result of aggregation of the Sup35 tra

57 Elevated ROS levels result in defective Foxo3(-/-) HSC cycling, a

58 ce of CCs offered no protection, as elevated ROS was accompanied by increased apoptosis of CCs.

59 on of intracellular GSH and ensuing elevated ROS; yet this treatment results in no apparent toxicitie

60 ne aortic arch endothelia exhibited elevated ROS, NOX4, HIF-1alpha, and glycolytic enzyme and PDK1 ex

61 gamma receptor activation, requires elevated ROS production and degranulation and involves EET format

62 TLR4-MD2 complex that triggers endocytosis, ROS generation and increases pro-interleukin-1beta expre

63 homeostasis, including increased endogenous ROS levels and hypersensitivity to oxidizing agents.

64 hyperglycemia and TGF-beta1-induced enhanced ROS production, increased expression of profibrotic and

65 Excessive ROS damages chloroplasts and reduces photosynthesis if n

66 ty and diabetes, and the effect of excessive ROS production on the development of cardiac lipotoxicit

67 dant, significantly eliminated the excessive ROS and suppressed autophagy, indicating that the increa

68 cate balance between needed versus excessive ROS production distinguishes health from an array of dis

69 ts that control and coordinate extracellular ROS production.

70 lation of redox homeostasis is essential for ROS-dependent signaling that does not incur cellular dam

71 x III reduction beyond the optimal range for ROS generation.

72 nce of NADH-related ubiquinone reduction for ROS production under these conditions.

73 lative importance of mitochondrial sites for ROS production, ROS signaling-mediated regulation of cel

74 CD11b(+)F4/80(high) Kupffer cells, generate ROS via dynamin-mediated endocytosis of TLR4 and NOX2, i

75 Most epithelially generated ROS co-localized with polarized mitochondria.

76 ion, normalized the expression of AOE genes, ROS levels, CB chemosensory reflex and BP, and also stab

77 High ROS in the peripheral NKT cells were primarily produced

78 t CD4 or CD8 T cells, have dramatically high ROS in the spleen and liver of mice but not in the thymu

79 This was due to higher ROS production and/or oncogene activation, such as RAS,

80 essential for activation of T cells, but how ROS influence NKT cells is unknown.

81 Defects in ROS-mediated microbe size sensing resulted in large neut

82 y disease stages, and a 45-fold elevation in ROS expression in inflamed ankles compared with the ankl

83 cytokine expression, limited an increase in ROS levels, and reduced cell apoptosis, fibrosis, and hy

84 There was a marked increase in ROS production and augmented GSH reductase and antioxida

85 2 possible, explaining the rapid increase in ROS production provided that site IIf is reduced.

86 Fe(II) is a key player in ROS formation in surrogate lung fluid (SLF) containing a

87 rathecal administration of BzATP resulted in ROS production in the spinal cord and oxidative DNA dama

88 um lycopersicum), we find that ABA-increased ROS is followed by stomatal closure and that both respon

89 d-induced apoptosis accompanied by increased ROS generation, and the stimulation of autophagy by rapa

90 ty acid (FA) oxidation, leading to increased ROS production and apoptosis in hypoxic cancer cells as

91 the treatment of disease, drugs that induce ROS are associated with many side effects and unpleasant

92 They induce ROS-regulated transcripts including for genes implicated

93 e replication, Leishmania is known to induce ROS upon macrophage infection.

94 ion of p66Shc governs its capacity to induce ROS.

95 urther analysis indicate that Zn(2+) induced ROS production, PARP-1 stimulation, increase in the [Ca(

96 remarkably suppressed palmitic acid-induced ROS generation and apoptosis.

97 culated that blockade of Na/K-ATPase-induced ROS amplification with a specific peptide, pNaKtide, mig

98 Palmitate-induced ROS generation in human CD68(low)CD14(high) macrophages

99 own experiments reveal that pathogen-induced ROS activate sod-1 dependent behavioral response non cel

100 PQS induced ROS production in lung epithelial (A549 and NHBE) cells

101 s uncoupling and augmented radiation-induced ROS.

102 ent fraction based on its ability to inhibit ROS production and the suppression of catabolic markers

103 radiation-induced skin injury by inhibiting ROS production.

104 reactive oxygen species (ROS), intermediate ROS levels between SR-BI(+/+) and nSR-BI(-/-) embryos we

105 Activation and intracellular ROS were measured in healthy neutrophils after treatment

106 ingle-stranded DNA regions and intracellular ROS, and interference with either event protects bacteri

107 ioxidant levels and/or enhance intracellular ROS could disturb the cellular oxidative environment and

108 are a collection of approaches that involve ROS modulation in cells as a strategy to target cancer a

109 For quercetin, 95% of its ROS-scavenging and over 77% of its Folin-Ciocalteau- and

110 acid and accumulation of cytosolic and lipid ROS.

111 those from PLZF haplodeficient mice have low ROS.

112 For maximal ROS production, the rate of NADH generation has to be eq

113 However, measuring ROS (hydrogen peroxide, H2O2) content in vivo is now pos

114 n together, our study shows PKC/NOX-mediated ROS generation and PARP-1 activation as an important mec

115 and functionally regulates SlCipk6-mediated ROS generation.

116 central role of mitochondria in metabolism, ROS regulation, and proteostasis.

117 Cellular and mitochondrial ROS was increased in DJ-1-deficient ((-/-)) BMMs compare

118 ondrial-targeted GCN5L1 blunts mitochondrial ROS, ERK activation and increases FoxO1, gluconeogenic e

119 ssion coincided with increased mitochondrial ROS, as well as increased differentiation, cell death an

120 or protein that contributes to mitochondrial ROS production.

121 ontrols metabolic pathways via mitochondrial ROS mediated ERK activation.

122 increased acetyl-CoA levels, leading to more ROS generation in hypoxic YC-1-treated cells.

123 ary metabolite production, and activation of ROS eliminating processes in response to drought toleran

124 complex III generates significant amounts of ROS in the presence of Mg(2+) and NAD(+) and the absence

125 rf2 pathway activated and the application of ROS scavenger N-acetyl cysteine (NAC) completely blocked

126 ative stress and simultaneous attenuation of ROS-dependent activation of the ATM and CaMKII proapopto

127 d in hUGT1/Car(-/-) neonatal mice because of ROS induction of intestinal UGT1A1.

128 advantage of the spatial-temporal control of ROS generation, the meticulous participation of light, p

129 being prodrugs for intracellular delivery of ROS with the potential to fight cancer.

130 indicating that the increased generation of ROS was associated with the palmitic acid-induced autoph

131 S17 robustly induced generation of ROS with Keap/Nrf2 pathway activated and the application

132 roduction of ATP and increased generation of ROS.

133 our observations identify the importance of ROS in mediating appropriate neutrophil apoptosis and th

134 as found to induce cell death independent of ROS generation, and unlike many natural product based HD

135 The induction of ROS activates the Nrf2-Keap 1 pathway leading to the ind

136 both responses are blocked by inhibitors of ROS-producing respiratory burst oxidase enzymes.

137 avenging pathways, the steady-state level of ROS, as well as the redox state of each compartment, is

138 Low, well-controlled levels of ROS are essential for adaptive signaling pathways, in in

139 mples from REG3A-TG mice had lower levels of ROS than feces from control mice during DSS administrati

140 terestingly, despite having higher levels of ROS, the LEW rat had lower transcript levels for antioxi

141 ay enable precisely targeted manipulation of ROS for effective medical therapies against cancer or im

142 tem reduces the degrees of overproduction of ROS and pro-inflammatory cytokines both in vitro in RAW2

143 to visualize and quantify the production of ROS with spatiotemporal accuracy.

144 Moreover, AMC provoked the production of ROS, H2O2, and NO, modulating the PI3K/Akt, MAPK, NFkapp

145 roglial phenotypes through the production of ROS.

146 Also, reduction of ROS generation in non-cancer cells was achieved with low

147 onstrate that IL-27 is a potent regulator of ROS induction and may be a novel therapeutic target.

148 ical treatment, and the increased release of ROS from cardiac mitochondria and other sources likely c

149 Despite their importance, the role of ROS following infection with the eukaryotic pathogen Lei

150 We addressed the role of ROS in C57BL/6 mice following intradermal infection with

151 e present study, we investigated the role of ROS in NKT cell function.

152 ion is a further indication for the roles of ROS and NO in atherosclerosis.

153 ompartment in plants contains its own set of ROS-producing and ROS-scavenging pathways, the steady-st

154 time giving rise to a distinct signature of ROS levels at the different compartments of the cell.

155 Critically, our understanding of ROS-mediated PTP oxidation is not yet sufficient to pred

156 ng aerosol chelate Fe(II), but the effect on ROS formation in the presence of lung antioxidants is no

157 e components of the ROS sensing machinery or ROS sensors.

158 drial-targeting antioxidant, showed a potent ROS scavenging efficacy in cultured human skin fibroblas

159 Powdered ROS or PGZ (6-6000muM) was mixed with fat explants and c

160 eted for modulation of NETs while preserving ROS production, an important innate immune defense.

161 psA mutant recruited NADPH oxidase, produced ROS, associated with LC3, and matured into antibacterial

162 e of mitochondrial sites for ROS production, ROS signaling-mediated regulation of cellular stress res

163 o mitochondria, which significantly promoted ROS production by downregulating nicotinamide adenine di

164 s conditions is dependent on the ERF74-RbohD-ROS signal pathway.

165 ities, increased NO generations, and reduced ROS productions in human umbilical vein endothelial cell

166 Abl kinase inhibitor dasatinib: both reduced ROS-induced degradation of beta-catenin/E-cadherin in vi

167 an wild type plants, as indicated by reduced ROS, lowered lipid peroxidation and enhanced photosynthe

168 g mice in vivo with N-acetylcysteine reduces ROS levels, rescues HSC cycling defects, and partially m

169 Sulfide inhibits mitochondria and reduces ROS production.

170 tochlorophyllide to chlorophyllide, reducing ROS production that would otherwise induce cellular dama

171 cells have antioxidant systems that regulate ROS.

172 rome bc family limit the amounts of released ROS to a low, perhaps just signaling, level through an a

173 sensitizing glitazone drugs, rosiglitazone (ROS) and pioglitazone (PGZ) both have anti-proliferative

174 lationship between remaining oil saturation (ROS) and the fraction of micro-pores.

175 are required to maximize malonate-sensitive ROS production by complex II in isolated mitochondria: (

176 Since ROS plays an important role in a variety of inflammation

177 avenge reactive oxygen and nitrogen species (ROS and RNS, respectively), to modulate human neutrophil

178 erived reactive oxygen and nitrogen species (ROS/RNS) are assumed the central biologically active pla

179 mal degradation, reactive oxidative species (ROS) oxidation, extracellular oxidative metabolism (EXOM

180 h the production of reactive oxygen species (ROS) accounts for restriction of parasite replication, L

181 chondrially-derived reactive oxygen species (ROS) activate an adaptive stress response to promote lon

182 system responds to reactive oxygen species (ROS) activated by pathogenic microbes during infection.

183 UVA, FICZ generates reactive oxygen species (ROS) and induces oxidative DNA damage.

184 s the production of reactive oxygen species (ROS) and mitogen-activated protein (MAP) kinase phosphor

185 ation and levels of reactive oxygen species (ROS) and Myc.

186 duced generation of reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) in mouse

187 Liver damage, reactive oxygen species (ROS) and paracrine tumor necrosis factor (Tnf) from Kupf

188 ose deposition, and reactive oxygen species (ROS) and salicylic acid (SA) accumulation.

189 Reactive oxygen species (ROS) and their associated byproducts have been tradition

190 eased production of reactive oxygen species (ROS) and upregulated expression of proinflammatory cytok

191 n hypothesized that reactive oxygen species (ROS) are responsible for the association between chronic

192 ed to the effect of reactive oxygen species (ROS) as a result of both intracellular metabolism and ex

193 rf75 lines lack the reactive oxygen species (ROS) burst in the early stages of various stresses, as a

194 icant generation of Reactive Oxygen Species (ROS) by MCs on co-culture with these species of Leishman

195 eased production of reactive oxygen species (ROS) by the electron transport chain.

196 Reactive oxygen species (ROS) can damage DNA, proteins, and lipids, so cells have

197 Reactive oxygen species (ROS) can induce oxidative stress and are associated with

198 xcess production of reactive oxygen species (ROS) caused by hyperglycemia is a major risk factor for

199 Reactive oxygen species (ROS) contribute to the development of non-alcoholic fatt

200 ne oxidase, a major reactive oxygen species (ROS) contributor during acute inflammation, reduces sulf

201 o produce cytotoxic reactive oxygen species (ROS) diminishes the therapeutic effect in a hypoxic envi

202 cumulates excessive reactive oxygen species (ROS) during the day and is unable to clear it during the

203 s and of generating reactive oxygen species (ROS) from oxygen, peroxides, or ozone.

204 es the potential of reactive oxygen species (ROS) generating activity during differentiation of monoc

205 se-4 expression and reactive oxygen species (ROS) generation after cisplatin treatment.

206 redisposes cells to reactive oxygen species (ROS) generation by electron slippage in the electron tra

207 ation and increased reactive oxygen species (ROS) generation in isolated mitochondria.

208 involved excessive reactive oxygen species (ROS) generation.

209 Reactive oxygen species (ROS) have been suggested as such triggers, but this prop

210 measured levels of reactive oxygen species (ROS) in bacterial cultures and fecal microbiota using 2'

211 eased intracellular reactive oxygen species (ROS) in cultured breast CTCs triggers HBB induction, med

212 e the production of reactive oxygen species (ROS) in lung epithelial cells (A549 and primary normal h

213 ndant production of reactive oxygen species (ROS) in lung tissue.

214 d the production of reactive oxygen species (ROS) in podocytes and that NAC (N-acetyl-cysteine), a po

215 mes also synthesize reactive oxygen species (ROS) in response to light, suggesting the possibility of

216 proteins induced by reactive oxygen species (ROS) in the cytoplasm.

217 eased generation of reactive oxygen species (ROS) in vivo plays a key role in the ageing process has

218 tions decreased and reactive oxygen species (ROS) increased.

219 ors, cytokines, and reactive oxygen species (ROS) influence tumor development from early stages to th

220 lar accumulation of reactive oxygen species (ROS) is associated with a wide range of developmental an

221 nd the elevation of reactive oxygen species (ROS) is essential in apoptosis.

222 evels, and elevated reactive oxygen species (ROS) levels in the CB and adrenal medulla (AM).

223 monstrated enhanced reactive oxygen species (ROS) levels.

224 arch suggested that reactive oxygen species (ROS) mediate the exaggerated EPR associated with PAD.

225 SEP4 could produce reactive oxygen species (ROS) normally.

226 rupt the balance of reactive oxygen species (ROS) often elevated in cancer cells.

227 Reactive oxygen species (ROS) play a critical role in cell signaling and prolifer

228 eine suggested that reactive oxygen species (ROS) play a key role in epigenetic regulation of miR-663

229 exposed to damaging reactive oxygen species (ROS) produced from a variety of sources including chemic

230 panied by increased reactive oxygen species (ROS) production and decreased insulin secretion.

231 bute to LPS-induced reactive oxygen species (ROS) production and modulate TLR responses, but whether

232 n transfer-mediated reactive oxygen species (ROS) production at concentrations (e.g., 50 muM) used to

233 h degranulation and reactive oxygen species (ROS) production, as well as by phagocytosis, which seque

234 Reactive oxygen species (ROS) production, degranulation, and phagocytosis are nor

235 ed to cause reduced reactive oxygen species (ROS) production, predisposes to SLE (odds ratio (OR) = 3

236 sis associated with reactive oxygen species (ROS) production.

237 a and generation of reactive oxygen species (ROS) promote chronic diseases, which have spurred intere

238 a well-established reactive oxygen species (ROS) scavenger.

239 ugh accumulation of reactive oxygen species (ROS) scavenging flavonols has not been established.

240 e identify PML as a reactive oxygen species (ROS) sensor.

241 that mitochondrial reactive oxygen species (ROS) signal to support adipocyte thermogenic identity an

242 Ca(2+) signals into reactive oxygen species (ROS) signaling.

243 idative stress from reactive oxygen species (ROS) than do non-malignant cells because of genetic alte

244 reactive nitrogen (RNS) and oxygen species (ROS) that covalently modify amino acids.

245 tables and generate reactive oxygen species (ROS) that lead to the induction of cytoprotective genes

246 ) and NADPH to form reactive oxygen species (ROS) that oxidize DNA.

247 ction of endogenous reactive oxygen species (ROS) was indicative of bacterial stress.

248 te higher levels of reactive oxygen species (ROS) when presented with planktonic organisms, and pharm

249 MTT, cell cycle and reactive oxygen species (ROS)) were evaluated in Colombian coffee (2 ground and 4

250 i), cell viability, reactive oxygen species (ROS), and secretory granules were assessed with paramete

251 Reactive oxygen species (ROS), generated both endogenously and in response to exo

252 s and production of reactive oxygen species (ROS), in a manner mediated by the co-stimulatory recepto

253 lized production of reactive oxygen species (ROS), in the developing brain, consistent with excitotox

254 had high levels of reactive oxygen species (ROS), intermediate ROS levels between SR-BI(+/+) and nSR

255 lity, mitochondrial reactive oxygen species (ROS), membrane damage, mitochondrial DNA (mtDNA) integri

256 inhibition elevates reactive oxygen species (ROS), p53 levels and cell death in androgen-deprived CRP

257 A bases modified by reactive oxygen species (ROS), primarily as 7, 8-dihydro-8-oxo-2'-deoxyguanosine

258 on but have reduced reactive oxygen species (ROS)-dependent responses such as callose deposition and

259 etting of hyperoxia/reactive oxygen species (ROS)-induced lung injury.

260 more susceptible to reactive oxygen species (ROS)-induced stress.

261 receptor-activated reactive oxygen species (ROS).

262 and accumulation of reactive oxygen species (ROS).

263 se-4 (NOX4)-derived reactive oxygen species (ROS).

264 e and production of reactive oxygen species (ROS).

265 - and extracellular reactive oxygen species (ROS).

266 and the emission of reactive oxygen species (ROS).

267 e PDT by generating reactive oxygen species (ROS).

268 the accumulation of reactive oxygen species (ROS).

269 master regulator of reactive oxygen species (ROS).

270 drial production of reactive oxygen species (ROS).

271 and homeostasis of reactive oxygen species (ROS).

272 eased production of reactive oxygen species (ROS).

273 rophyllide produces reactive oxygen species (ROS).

274 e the production of reactive oxygen species (ROS); 2) decrease succinate dehydrogenase activity (comp

275 reducing lipopolysaccharide (LPS)-stimulated ROS, nitric oxide and TNFalpha production, which transla

276 stigations showed that SQ-CDDP NP stimulated ROS production, expression of heavy metal-inducible and

277 ltured human melanocytes with UVB stimulated ROS production, which was reduced in cells treated with

278 n to mitochondria, presumably by stimulating ROS generation.

279 or-specific (1) O2 generation and subsequent ROS mediated mechanism.

280 protein parvalbumin significantly suppressed ROS production and the ability of HCC metastasis.

281 reported that activation of the Dectin-1/Syk/ROS/NLRP3 pathway during L. amazonensis phagocytosis is

282 We conclude that ROS contribute to TLD by converting single-stranded DNA

283 Here we demonstrate that ROS generated by FICZ/UVA combinations also cause extens

284 We found that ROS induced a robust expression of FOXD3-AS1 in mouse lu

285 Together, our data indicate that ROS signaling is critical for the loss of barrier functi

286 udy provide further evidence indicating that ROS mediates the exaggeration of EPR in rats with simula

287 charge is capable to efficiently control the ROS and RNS concentrations in the cancer-inhibiting medi

288 Q > 1,2-NQ approximately PQ > 1,4-NQ) in the ROS generation.

289 d to provide a more inclusive picture of the ROS activity of ambient PM.

290 hat specific RLKs could be components of the ROS sensing machinery or ROS sensors.

291 dation, contributes almost negligibly to the ROS generation.

292 Pretreatment with the ROS scavenger N-acetyl-L-cysteine, the ERK1/2 inhibitor

293 lE-LacZ lethality shares attributes with the ROS-dependent component of antibiotic lethality.

294 Small microbes triggered ROS intracellularly, suppressing IL-1beta expression to

295 The sensing mechanism is based upon ROS-induced oxidation of the ascorbic acid units within

296 However, when ROS generation exceeds endogenous antioxidant capacity,

297 mice, plasma H2S levels were decreased while ROS and expression of its modulator (ROMO1) were increas

298 ma production; the latter is correlated with ROS generation.

299 nditioned media from the culture of fat with ROS or PGZ on i) platelet-derived growth factor-BB (PDGF

300 members of the NOX family and interfere with ROS signaling.