ライフサイエンスコーパス: NOX

1 NOX activation occurs at other sites in the cell, where

2 NOX-2-derived oxidative stress mediates inflammasome act

3 NOX-A12, an RNA oligonucleotide in L-configuration (Spie

4 NOX-G15 shows no cross-reactivity with related peptides

5 NOX-rich conditions are typical of the polluted MBL, nea

6 NOX/DUOX family of NADPH oxidases are expressed in diver

7 RV or poly(I.C)-stimulated NADPH oxidase 1 (NOX-1) partially accounts for RV-induced ROS generation.

8 ne dinucleotide phosphate (NADPH) oxidase-2 (NOX-2) expression.

9 ambient air pollutant concentrations (PM2.5, NOX, and black carbon) between examinations and within t

10 DPH oxidase (NOX)-dependent, and apocynin, a NOX inhibitor, protected cells from double-strand breaks

11 orylation in human umbilical vein cells in a NOX-dependent manner, demonstrating a role for reactive

12 ombination of fusing a lipophilic amine to a NOX inhibiting dye shows promise for further pre-clinica

13 does not occur with neutrophils exposed to a NOX inhibitor (Nox2ds) or a NOS-2 inhibitor (1400W) or w

14 does not occur with neutrophils exposed to a NOX inhibitor (Nox2ds), a NOS-2 inhibitor (1400 W), or w

15 Here we show that calcium activated NOX-independent NETosis is fast and mediated by a calciu

16 -mediated mechanism, which in turn activates NOX through Rac1, one of the NOX subunits.

17 llular distribution of the organizer/adapter NOX p47(phox) subunit is altered in PVN dendrites follow

18 Moreover, the increase in NOX 2 and NOX 4 mRNA levels, NADPH oxidase activity, and ROS level

19 e dinucleotide phosphate oxidase (NOX)-2 and NOX-4, respectively.

20 essed for ROS production, Rac1 activity, and NOX gene expression.

21 Antioxidants and NOX inhibitors can prevent HDM-induced DNA damage, revea

22 revealing a novel role for antioxidants and NOX inhibitors in mitigating allergic airway disease.

23 as messenger RNA expression of fibrotic and NOX genes.

24 d IL-1beta and IL-18 production in ileum and NOX-2-dependent oxidative stress.

25 dine residues conserved between the MsrQ and NOX protein families.

26 dels demonstrated that reductions in NO2 and NOX were significantly greater in GMCs compared to reduc

27 oncentrations for nitrogen dioxide (NO2) and NOX in GMCs of 6.4 and 21.7 ppb.

28 on-road ratios of nitrogen dioxide (NO2) and NOX.

29 e inhibition of NOX proteins, p22(phox), and NOX protein knockdowns caused a reduction in ROS, as mea

30 ssociated with increased ROS production, and NOX inhibition does not block LC3 lipidation.

31 both biomass fuel choice scenarios, SO2 and NOX achieve reductions largely through pre-existing rule

32 ntify the associated change in CO2, SO2, and NOX emissions through midcentury.

33 ratures and EGU air emissions (CO2, SO2, and NOX) using historical data.

34 thiobarbituric acid reactive substances and NOX-related genes.

35 e fuel, as a means to comply with sulfur and NOX regulations.

36 n a subchronic model of IL-6-induced anemia, NOX-H94 inhibited the decrease in hemoglobin concentrati

37 specialized ROS-generating enzymes known as NOX/DUOX.

38 oxide production during T1D pathogenesis, as NOX-deficient NOD mice (NOD.Ncf1(m1J) ) were protected a

39 C and concurrently measured two-week average NOX concentrations were 0.6-0.7.

40 es also emitted 2.3 times the route averaged NOX emissions factor at the beginning of each route due

41 explore the contribution of the link between NOX and RyR-mediated Ca(2+) release toward axonal specif

42 ore defined a novel mechanistic link between NOX-derived ROS and macrophage phenotypes, and implicate

43 , suggesting a feedforward mechanism between NOX and RyR.

44 ar benefit in terms of the trade-off between NOX and soot emissions with respect to ULSD and biodiese

45 Despite the differential activation, both NOX-dependent and -independent NETosis require Akt activ

46 a feedforward mechanism that integrates both NOX activity and RyR-mediated Ca(2+) release to support

47 that Mo-DC differentiation was inhibited by NOX inhibitors and reactive oxygen species scavengers.

48 e, specific suppression of ROS production by NOX in endothelium, attainable by Ab-MJ33/IL targeting,

49 acterization of novel anti-hepcidin compound NOX-H94, a structured L-oligoribonucleotide that binds h

50 cell proliferation; however, a comprehensive NOX gene expression analysis is missing for all major mo

51 In contrast, NOX-A12 increased CLL migration underneath a confluent l

52 results suggest a crucial function of early NOX activation in transducing a signal for cellular prot

53 iquitin-Conjugating Enzyme 4a) > Enox2 (Ecto-NOX Disulfide-Thiol Exchanger 2) > Ube2d2 (Ubiquitin-con

54 striatum of HD(140Q/140Q) mice had elevated NOX activity at 3 months of age and a further rise at 6

55 The voltage-gated proton channel Hv1 enables NOX function by compensating cellular loss of electrons

56 gAcrp30 enhanced NOX-2 expression at the plasma membrane, with a concomit

57 ed to the dehydrogenase domain of eukaryotic NOX enzymes, as an efficient cytosolic electron donor to

58 ent protein system related to the eukaryotic NOX family and involved in the reduction of periplasmic

59 Both human and mouse beta-cells express NOX, in particular NOX2.

60 Although the sequences of five NOX genes (nox1, nox2/cybb, nox4, nox5, and duox) have b

61 s, 2.15%/ degrees C +/- 0.29%/ degrees C for NOX emissions, and 1.78%/ degrees C +/- 0.22%/ degrees C

62 oxygen species (ROS), which is essential for NOX-dependent NETosis.

63 independent NETosis, it is not important for NOX-dependent NETosis.

64 sight into previously unknown mechanisms for NOX-independent NETosis.

65 Although mitochondrial ROS is needed for NOX-independent NETosis, it is not important for NOX-dep

66 jury, suggesting a therapeutic potential for NOX-E36 in diabetic nephropathy.

67 Hv1 was required for NOX-dependent ROS generation in brain microglia in situ

68 Mice lacking Hv1 were protected from NOX-mediated neuronal death and brain damage 24 h after

69 Furthermore, NOX-A12 sensitizes CLL cells toward bendamustine and flu

70 e core signaling complex, while the alpha1 H-NOX domain can be removed without a significant effect o

71 l coordination site occupied by zinc in an H-NOX protein.

72 An H-NOX/HisKa regulatory circuit was recently identified in

73 purified the V. cholerae HisKa (HnoK) and H-NOX in its heme-bound (holo) and heme-free (apo) forms.

74 ogs of the sGC heme domain, referred to as H-NOX domains, including those from Nostoc sp. PCC 7120, S

75 binding to sGC from M. sexta and bacterial H-NOX homologs.

76 ical role or signaling output of bacterial H-NOX proteins.

77 The beta1 H-NOX and alpha1 PAS domains are in contact and form the c

78 lves the heme-nitric oxide/oxygen-binding (H-NOX) domain of soluble guanylate cyclase as a selective

79 , which lies adjacent to its heme-binding (H-NOX) domain.

80 signaling helix of the heme-NO/O2 binding (H-NOX) domain.

81 nvolving heme-nitric oxide/oxygen binding (H-NOX) domains as selective NO sensors.

82 Fe(II) form suggested that Vibrio cholerae H-NOX may act as a sensor of the redox state as well as NO

83 nt mechanism for activation of V. cholerae H-NOX that implicates this protein as a dual redox/NO sens

84 Using our previously described H-NOX/diguanylate cyclase functional partners from Shewane

85 nsible for communicating NO occupancy from H-NOX heme to the catalytic domain active site.

86 esponsive (hno) signaling network involves H-NOX-dependent control of HnoK autophosphorylation and ph

87 owed that holo Fe(III), but not Fe(II)-NO, H-NOX relied heavily upon cysteine for activation.

88 Co-crystallization of 20 with the Ns H-NOX domain revealed that the increased conformational di

89 oxide (NO) binding to the heme cofactor of H-NOX proteins has been implicated as a regulatory mechani

90 ar event during NO-dependent activation of H-NOX proteins is rupture of the heme-histidine bond and f

91 rylation assays of HnoK in the presence of H-NOX show that the holoprotein in the Fe(II)-NO and Fe(II

92 In Shewanella oneidensis, H-NOX-mediated NO sensing increases biofilm formation, whi

93 Heme-nitric oxide/oxygen (H-NOX) binding domains are a recently discovered family of

94 Heme nitric oxide/oxygen (H-NOX)-binding proteins act as nitric oxide (NO) sensors a

95 rved amino acid residues in the regulatory H-NOX domains of GCY-35 and GCY-36, respectively, and appe

96 ure of BAY 58-2667 bound to the Nostoc sp. H-NOX domain was published.

97 Furthermore, interfaces between the H-NOX and catalytic domains were mapped using domain trunc

98 rallel coiled-coil platform upon which the H-NOX and PAS domains are assembled.

99 The H-NOX domain buries surfaces of the alpha1 catalytic domai

100 imerization interface and a segment in the H-NOX domain.

101 changes to assist heme insertion into the H-NOX domain.

102 hich suggested that similar regions in the H-NOX domains of O2 and NO-sensing sGCs are important for

103 The H-NOX family of nitric oxide (NO) sensing proteins has rec

104 sufficient for signal transduction in the H-NOX family.

105 high-resolution crystal structures of the H-NOX protein from Shewanella oneidensis in the unligated,

106 tly identified in Vibrio cholerae, and the H-NOX protein has been spectroscopically characterized.

107 However, the influence of the H-NOX protein on HisKa autophosphorylation has not been ev

108 The H-NOX/NO-responsive (hno) signaling network involves H-NOX

109 These results are broadly applicable to H-NOX-mediated NO signaling in bacteria.

110 s a 150 kDa heterodimeric protein with two H-NOX domains (one with heme, one without), two PAS domain

111 High NOX activity in primary cortical and striatal neurons of

112 For 40 ppb higher NOX, the estimate was 0.2 mum per year (-1.9 to 2.4).

113 f interleukin 6 (IL-6)-induced hypoferremia, NOX-H94 inhibited serum iron reduction completely.

114 aper introduces a new method for identifying NOX emissions hotspots along a bus route using high fide

115 essing autoreactive CD4 T cells deficient in NOX-derived superoxide.

116 Moreover, the increase in NOX 2 and NOX 4 mRNA levels, NADPH oxidase activity, and

117 / degrees C +/- 0.49%/ degrees C increase in NOX emissions, and a 3.32%/ degrees C +/- 0.36%/ degrees

118 developed to identify whether reductions in NOX were greater in GMCs than in other areas, after cont

119 f HD(140Q/140Q) neurons followed the rise in NOX activity and inhibiting only mitochondrial ROS was n

120 te the molecular basis of the variability in NOX activation, we employed genetically encoded fluoresc

121 approximately 112 nmol/min) that inactivates NOX.

122 ent, a few brain regions displayed increased NOX expression levels.

123 ore, both biodiesel fuels produced increased NOX emissions compared to DF.

124 al pathway, we have encapsulated an indirect NOX inhibitor, MJ33, into immunoliposomes (Ab-MJ33/IL) t

125 ed potassium channel is sufficient to induce NOX-independent NETosis.

126 tment strongly inhibited the hypoxia-induced NOX activity in PCa cells (LNCaP, 22Rv1 and PC3) associa

127 together, our results show that LPS-induced NOX-generated ROS production differentially and specific

128 importantly, GPE treatment neither inhibited NOX activity nor showed any cytotoxicity against non-neo

129 prevention of PCa progression via inhibiting NOX activity.

130 owever, less capital is available to install NOX reduction technologies, resulting in an O3 increase.

131 level of p22(phox) and p22(phox)-interacting NOX isoforms than 32D cells transfected with the wild ty

132 The transfer of diabetogenic T cells into NOX-deficient NOD.Rag.Ncf1(m1J) recipients resulted in d

133 fficacy has been shown; inhibiting only late NOX activation does not exhibit such effects.

134 e bred to gp91-phox knock-out mice had lower NOX activity in the brain and in primary neurons, and ne

135 In J774A.1 macrophages, NOX-H94 blocked hepcidin-induced ferroportin degradation

136 arity to the catalytic subunits of mammalian NOX enzymes, only some of which have been functionally a

137 creased expression of the pro-oxidant marker NOX-4.

138 Furthermore, GPE-mediated NOX inhibition was associated with a strong decrease in

139 cardium, accompanied by decreased myocardial NOX-2 levels, reduced nitrosative stress, and lower matr

140 Nitrite accumulation (N-NO2(-)/N-NOX) of 92% was maintained.

141 Unlike NOX-dependent NETosis, NOX-independent NETosis is accompanied by a substantiall

142 mbient concentrations of oxides of nitrogen (NOX; 1999 onwards), predicted via a geographic informati

143 NO2/NOX ratios steadily increased from 0.23 +/- 0.06 in 2009

144 lium-restricted deficiency in the obligatory NOX dimerization partner Cyba (p22(phox)).

145 Administration of NOX-D19, a specific C5a inhibitor, to C3(-/-) recipients

146 O combustion produced the smallest amount of NOX.

147 epresent the first comprehensive analysis of NOX gene expression in the zebrafish and will provide a

148 lacking NOS-2 or the gp91(phox) component of NOX.

149 sociation was linear across the continuum of NOX exposure: per 10-ppb increment in exposure, the 5-ye

150 wnwind ambient based trends in conversion of NOX to NOY from these sources.

151 shes a rationale for clinical development of NOX-A12 in combination with conventional agents in CLL.

152 Here, we examined effects of NOX-A12 on CLL cell migration and drug sensitivity.

153 fy the benefits of reducing the emissions of NOX, SO2, PM2.5, and CO2 that would occur if shore power

154 ociated with a decrease in the expression of NOX catalytic and regulatory sub-units (NOX1, NOX2 and p

155 eveals a previously unrecognized function of NOX in cancer metabolism and suggests that NOX is a pote

156 tudies aimed at determining the functions of NOX enzymes in neurodevelopment and regeneration.

157 These results highlight the importance of NOX-derived superoxide in curbing autoreactivity due, in

158 s can generate phagosomal ROS independent of NOX activity, and we propose that this silica-generated

159 Pharmacological inhibition of NOX activity did not prevent silica-induced phagolysosom

160 The inhibition of NOX proteins, p22(phox), and NOX protein knockdowns caus

161 s of the NOX complex, chemical inhibitors of NOX function, or molecules that scavenge superoxide or R

162 A single injection of NOX-G15 ameliorated glucose excursions in intraperitonea

163 pathways and up-regulation of mRNA level of NOX 2 and NOX4 isoforms in neuronal cells.

164 The liver of NOX(-/-)/HFD mice showed mild steatosis but no non-alcoh

165 Therefore, we hypothesized that loss of NOX-derived superoxide would dampen diabetogenic antivir

166 These data show that overproduction of NOX-derived ROS can promote the proliferation of AML bla

167 idation of benzyl alcohol in the presence of NOX were studied.

168 among participants in the lowest quartile of NOX exposure, decline among those in the highest exposur

169 However, major regulators of NOX-independent NETosis are largely unknown.

170 The role of NOX oxidases in HIF-1-mediated extracellular matrix accu

171 production, suggesting the critical role of NOX-generated ROS in LPS-induced PGD(2) production in BM

172 Then, to address the role of NOX-SOD1-mediated ROS production in HSC activation and l

173 with carbon capture systems, and shifting of NOX emissions in later years from power plants subject t

174 Interestingly, stable silencing of NOX subunits, p22(phox) and p47(phox), in HK-2 cells blo

175 Suppression of NOX by chemical inhibition or genetic knockdown of gene

176 We show that upregulation of NOX is critical to support the elevated glycolysis by pr

177 r conditions by inhibiting the activation of NOXs and the generation of ROS.

178 in decreased ROS generation, a reduction of NOXs (NOX1, 2, 4) and a decrease in inflammatory cytokin

179 se results demonstrate differential roles of NOXs in modulating the redox state in response to differ

180 protein oxidases (diphenylene iododonium) or NOX enzymes (GKT136901).

181 A9, and pharmacologic inhibition of NLRP3 or NOX suppress pyroptosis, ROS generation, and nuclear bet

182 h NOX4 deficiency, renal expression of other NOX isoforms was not altered but NRF2 protein expression

183 we found a pattern of broad and overlapping NOX isoform expression at 1 and 1.5 days post fertilizat

184 C inhibitor, DPI, a NADPH-dependent oxidase (NOX) inhibitor, GKT137831, a NOX1/4 inhibitor, and Phox-

185 choalveolar lavage fluids and NADPH oxidase (NOX) 2 and NOX4 protein expression in lung tissue.

186 n of nitric oxide synthase 2, NADPH oxidase (NOX) 2, NOX4, E-selectin, and monocyte chemotactic prote

187 NADPH oxidase (NOX) activated by pathological mediators including angio

188 ke receptor 4 (TLR4)-mediated NADPH oxidase (NOX) activation.

189 ols, we found brain levels of NADPH oxidase (NOX) activity, which produces reactive oxygen species (R

190 ose stimulated an increase in NADPH oxidase (NOX) and colocalization of G6PD with NOX, which was inhi

191 y of the host epithelial cell NADPH oxidase (NOX) complex and the production of reactive oxygen speci

192 ndispensable component of the NADPH oxidase (NOX) complex comprising the main source of ROS, plays a

193 ROS, mainly sustained by the NADPH oxidase (NOX) complex, promote neuronal development and axonal gr

194 membrane-bound subunit of the NADPH oxidase (NOX) complex.

195 t are mainly sustained by the NADPH oxidase (NOX) complex.

196 Here we report that NADPH oxidase (NOX) expression is directly associated with PCa progress

197 of PTP1B promoted an altered NADPH oxidase (NOX) expression pattern in response to TGF-beta, strongl

198 Phagocytic cell NADPH oxidase (NOX) generates reactive oxygen species (ROS) as part of

199 of the superoxide generating NADPH oxidase (NOX) in AVP-expressing hypothalamic paraventricular nucl

200 , implicating a p47phox-bound NADPH oxidase (NOX) in mediating basal NO production.

201 hosphatase activity following NADPH oxidase (NOX) inhibition.

202 The NADPH oxidase (NOX) isoform NOX4 has been linked with diabetic kidney d

203 oxidase activity, as well as NADPH oxidase (NOX) isoforms 2 and 4 mRNA expression levels and these e

204 These cells with their seven NADPH oxidase (NOX) isoforms provide a vast realm of mechanistic obscur

205 NADPH oxidase (NOX) proteins produce reactive oxygen species (ROS) invo

206 r RNA expression in asthma of NADPH oxidase (NOX) subtype 4.

207 hibition of the ROS generator NADPH oxidase (NOX) using either pharmacologic inhibitors or its p47(ph

208 ecreting cells, expression of NADPH oxidase (NOX), a potent source of ROS, has been reported, along w

209 received apocynin to inhibit NADPH oxidase (NOX), IL-1 receptor antagonist, or IL-18 binding protein

210 9-induced signaling activates NADPH oxidase (NOX), increasing levels of reactive oxygen species (ROS)

211 ges, CD4 T cells also express NADPH oxidase (NOX), the superoxide-generating multisubunit enzyme.

212 Activation of the enzyme NADPH oxidase (NOX), which catalyzes one-electron reduction of O2 to ge

213 e oxygen species derived from NADPH oxidase (NOX)-4 and mitochondrial sources.

214 DM-induced cellular injury is NADPH oxidase (NOX)-dependent, and apocynin, a NOX inhibitor, protected

215 T1D, as NOD mice deficient in NADPH oxidase (NOX)-derived superoxide (Ncf1(m1J)) were protected again

216 strated an important role for NADPH oxidase (NOX)-derived superoxide production during T1D pathogenes

217 ote proliferative ROS through NADPH oxidase (NOX).

218 ic-oxide synthase (NOS-2) and NADPH oxidase (NOX).

219 ic-oxide synthase (NOS-2) and NADPH oxidase (NOX).

220 tection and quantification of NAPDH oxidase (NOX) activity in individual phagosomes.

221 mide adenine dinucleotide phosphate oxidase (NOX)-2 and NOX-4, respectively.

222 icotinamide dinucleotide phosphate oxidases (NOX) control various cellular signaling cascades.

223 ide adenine dinucleotide phosphate oxidases (NOX).

224 inucleotide phosphate reduced form oxidases (NOXs) in Mo-DC differentiation.

225 NADPH oxidases (NOXs) are involved in inflammation, angiogenesis, tumor

226 NADPH oxidases (NOXs) are the only enzymes exclusively dedicated to reac

227 of p22(phox) subunit of the NADPH oxidases (NOXs), and fibrotic markers, plasminogen activator inhib

228 SHP2 oxidation requires NADPH oxidases (NOXs), and oxidized SHP2 co-localizes with platelet-deri

229 ditions associated with high nitrogen oxide (NOX = [NO] + [NO2]) concentrations.

230 , sulfur dioxide (SO2), and nitrogen oxides (NOX) associated with energy use in major sectors of the

231 concentrations of PM2.5 and nitrogen oxides (NOX) between 1999 and 2012.

232 gned saturation sampling of nitrogen oxides (NOX) for the counties of Los Angeles and Alameda (San Fr

233 However, nitrogen oxides (NOX) of RME and JME exceeded the Euro III limit value of

234 latform was used to measure nitrogen oxides (NOX), black carbon (BC), and ultrafine particles (UFPs)

235 degrees C, contrasting with nitrogen oxides (NOX).

236 asurements show that emissions of particles, NOX, and CO2 are considerably lower for LNG compared to

237 In particular, NOX-A12 competes with GAGs such as heparin for CXCL12 bi

238 (MCP-1) with the Spiegelmer emapticap pegol (NOX-E36) shows long-lasting albuminuria-reducing effects

239 somes, concomitantly potentiating phagosomal NOX activity.

240 Taken together, our study shows PKC/NOX-mediated ROS generation and PARP-1 activation as an

241 result of reduced investments in power plant NOX controls in earlier years in anticipation of acceler

242 .79, 0.78 for traditional and enhanced PM10, NOX, and NO2 models, respectively.

243 er year (95% CI 1.4-6.8) and for each 40 ppb NOX coronary calcium progressed by 4.8 Agatston units pe

244 5/m(3) and 7.2-139.2 parts per billion (ppb) NOX.

245 Thus, TGF-beta1 promotes NOX-dependent ATM activation leading to p53-mediated fib

246 OS but enhanced by lowering proproliferative NOX-derived ROS.

247 s, which include the NADPH oxidase proteins (NOX/DUOX).

248 ears from power plants subject to a regional NOX cap to those in regions not subject to the cap.

249 t) inhibition, indicating that PRR regulates NOX activity and ROS formation in neuro-2A cells through

250 2050 reference case, but electricity sector NOX increases.

251 ted for diesel trucks and the results showed NOX and BC emissions were reduced by 40% or more between

252 S, valuing changes in emissions of CO2, SO2, NOX, NH3 and particulate matter (PM), including those in

253 tion and plume dilution tracer species (SO2, NOX) emission rates, and an airship was utilized as an a

254 leads to reduced emissions of mobile source NOX, thus reducing O3.

255 In-use, spatiotemporal NOX emissions were measured from a conventional powertra

256 c Apoe knockout mice with the mouse-specific NOX-E36 attenuated albuminuria without any change in sys

257 inflammatory phenotype during mouse-specific NOX-E36 treatment.

258 ges resulting in a mixed DNA/RNA-Spiegelmer (NOX-G15) that binds glucagon with a Kd of 3 nm.

259 at NLRX-1 is also required for RV-stimulated NOX-1 expression.

260 In conclusion, the data suggest NOX-G15 as a therapeutic candidate with the potential to

261 th PCa progression in TRAMP mice, suggesting NOX as a potential chemoprevention target in controlling

262 tation of the conserved proline (P117 in SwH-NOX) to alanine, which results in heme flattening, has t

263 erase activity as NO binding to wildtype SwH-NOX.

264 usted analyses (n = 5,708), higher long-term NOX exposure was associated with significantly faster pr

265 We conclude that NOX-H94 protects ferroportin from hepcidin-induced degra

266 ngian hotspot detection, we demonstrate that NOX hotspots occurred at bus stops, during cold starts,

267 These data demonstrate that NOX-A12 effectively interferes with CLL cell migration a

268 ervous system, there is recent evidence that NOX-derived reactive oxygen species (ROS) regulate neuri

269 We provide evidence that NOX-derived ROS contribute to macrophage differentiation

270 Using genetic approaches, we find that NOX activation promotes both axonal development and Rac1

271 We found that NOX-A12 effectively inhibited CXCL12-induced chemotaxis

272 Taken together these data indicate that NOX and p22(phox) mediate the ROS production from FLT3-I

273 Modulation of DAG levels suggested that NOX activation is precluded when phagosomes fail to reac

274 f NOX in cancer metabolism and suggests that NOX is a potential novel target for cancer treatment.

275 Our work suggests that NOX-derived ROS promote axonal growth by regulating Rac1

276 The NOX (nicotinamide adenine dinucleotide phosphate oxidase

277 eductions in the level of H2O2 following the NOX knockdowns were accompanied by a decrease in the num

278 in silico to provide a generic model for the NOX family.

279 ERK activation is essential for the NOX-dependent pathway, whereas its activation is not ess

280 reas its activation is not essential for the NOX-independent pathway.

281 In the monocrotaline model, the NOX-A12-induced reduction of mast cells, CD68(+) macroph

282 iRNAs directed against key components of the NOX complex, chemical inhibitors of NOX function, or mol

283 lectively target the distinct members of the NOX family and interfere with ROS signaling.

284 Of the NOX family members, only NOX4 was expressed in adipocyte

285 t that is common to all seven members of the NOX family.

286 are distinguished from other members of the NOX protein family by the presence of a unique extracell

287 ic induces ROS through p47(phox), one of the NOX subunits that is the key source of arsenic-induced R

288 In addition, Rac1, one of the NOX subunits, was activated after RyR-mediated Ca(2+) re

289 turn activates NOX through Rac1, one of the NOX subunits.

290 g the translational benefit of targeting the NOX/ATM/p53 axis in renal fibrosis.

291 The physiological functions of these NOX enzymes range from defense to specialized oxidative

292 As the role of this NOX in early alcoholic liver injury has not been address

293 s found that the removal efficiency of total NOX(-)-N (NO3(-)-N and NO2(-)-N) in the presence of CuO

294 Unlike NOX-dependent NETosis, NOX-independent NETosis is accomp

295 In vitro, NOX-G15 inhibits glucagon-stimulated cAMP production in

296 Accordingly, we assessed whether NOX activity in PCa cells could be inhibited by Graviola

297 Accordingly, we investigated whether NOX-mediated brain damage in stroke can be inhibited by

298 xidase (NOX) and colocalization of G6PD with NOX, which was inhibited by the PKA inhibitor.

299 ced pulmonary hypertension were treated with NOX-A12 from Day 21 to Day 35 after monocrotaline admini

300 eath were markedly reduced by treatment with NOX inhibitors such as diphenyleneiodonium (DPI), apocyn