ライフサイエンスコーパス: NAD(P)H oxidase

1 oxygen species (ROS; partially generated by NADPH oxidase).

2 on and assembly of the superoxide-generating NADPH oxidase.

3 primary source is represented by neutrophil NADPH oxidase.

4 ans that was dependent on Dectin-1, Syk, and NADPH oxidase.

5 s superoxide and a nuclear splice variant of NADPH oxidase.

6 re their levels are dynamically regulated by NADPH oxidase.

7 ed tubulointerstitial injury, apoptosis, and NADPH oxidase.

8 phoinositide-dependent protein kinase 1, and NADPH oxidase.

9 r histology, immunoblots, and measurement of NADPH oxidase.

10 cular endothelial cell protein expression of NADPH oxidase.

11 a strategy to inhibit assembly of neutrophil NADPH oxidase.

12 ty, MEMO-1, as a protein that inhibits BLI-3/NADPH oxidase.

13 cy marked by a defect in NOX2, the phagocyte NADPH oxidase.

14 s and activation of the superoxide-producing NADPH-oxidase.

15 ROS originate from mitochondria and NADPH oxidases.

16 damage only via inhibiting the expression of NADPH oxidases.

17 TirA and reactive oxygen species-generating NADPH oxidases.

18 s-tat, a peptide that blocks the activity of NAD(P)H oxidase.

19 ion of FST decreased the expression level of NADPH oxidase 1 (NOX1) and NOX5 as well as the productio

20 NADPH oxidase 1 (NOX1), a membrane-bound flavin dehydrog

21 Activation of Schwann cell TRPA1 evoked NADPH oxidase 1 (NOX1)-dependent H2O2 release, and silen

22 We identified deficiency of NADPH oxidase 2 (NOX2) as the molecular underpinning of

23 Reactive oxygen species (ROS) produced by NADPH oxidase 2 (Nox2) function as key mediators of mech

24 NADPH oxidase 2 (NOX2) generates large amounts of reacti

25 cellular import of H2O2 produced by membrane NADPH oxidase 2 (Nox2) in response to TNF-alpha is facil

26 re, we determine the role of ROS produced by NADPH oxidase 2 (Nox2) in the endothelial-lineage specif

27 NADPH oxidase 2 (Nox2) inhibition, but not Nox4 or Nox1

28 In macrophages, ROS generated by NADPH oxidase 2 (NOX2) was detected in phagolysosomes co

29 fulvene-5, a specific inhibitor of NOX4 and NADPH oxidase 2 (NOX2), decreased their elevated cancer

30 is by forming stably functional complex with NADPH oxidase 2 (Nox2).

31 n species in the heart through activation of NADPH oxidase 2 (NOX2).

32 ase A2 activity of peroxiredoxin 6 modulates NADPH oxidase 2 activation via lysophosphatidic acid rec

33 y inhibiting Akt kinase activities, reducing NADPH oxidase 2 activation, and lowering phagolysosomal

34 (Delta/+) ECs and was suppressed by PI3K and NADPH oxidase 2 inhibitors.

35 de adenine dinucleotide phosphate oxidase 2 (NADPH oxidase 2 or Nox2) is enhanced by angiotensin II (

36 Increased force correlated with reduced NADPH Oxidase 2 protein expression, the major source of

37 supernatant and decreased the expression of NADPH oxidase 2, nitric oxide synthase 2, and nuclear fa

38 in close contact with target T cells release NADPH oxidase 2-containing microvesicles that inhibit TC

39 mannan-induced arthritis in SKG mice and how NADPH oxidase 2-derived reactive oxygen species (ROS) re

40 nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) and their bone marrow chimera, w

41 nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (Nox2)-deficient mice but fail to fully

42 nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-2 (NOX-2) expression.

43 Here we discover that NAD(P)H oxidase 4 (NOX4), an enzyme known to catalyse th

44 h factor beta1 (TGFbeta1), endothelin-1, and NAD(P)H oxidase 4 also occur in parallel with Elmo1, as

45 em, 4-HNE elevated the ROS generation enzyme NADPH oxidase 4 (NOX4) and induced the activation of NF-

46 NADPH oxidase 4 (NOX4) enzyme, which catalyzes the reduc

47 d glutathione (GSH) concentration and higher NADPH oxidase 4 (Nox4) expression, consistent with incre

48 High-glucose increases NADPH oxidase 4 (NOX4) expression, reactive oxygen speci

49 NADPH oxidase 4 (Nox4) has been implicated in cardiac re

50 In the present work, we examined the role of NADPH oxidase 4 (Nox4) in LPS-induced TLR4 responses in

51 e, to our knowledge, the first evidence that NADPH oxidase 4 (NOX4) is involved in manifesting A-T di

52 in, and hindlimb that only in the brain does NADPH oxidase 4 (NOX4) lead to ischemic damage.

53 studies showed that hyperglycemia stimulated NADPH oxidase 4 (Nox4) synthesis, and IGF-I facilitated

54 dylinositol-4-phosphate 5-kinase 1alpha, and NADPH oxidase 4 (NOX4) to produce reactive oxygen specie

55 nase 2 (COX2))- and reactive oxygen species (NADPH oxidase 4 (NOX4))-generating enzymes by classical

56 ed macaques and confirmed to directly target NADPH oxidase 4 (NOX4), a reactive oxygen species genera

57 NADPH oxidase 4 (NOX4), a source of cellular superoxide

58 tion of ROS, inhibited ROS generation enzyme NADPH oxidase 4 (NOX4), and increased dual specificity p

59 e reactive oxygen species-generating enzyme, NADPH oxidase 4 (Nox4), regulates a number of physiologi

60 stasis-induced bone destruction, upregulated NADPH oxidase 4 (Nox4), resulting in elevated oxidizatio

61 en peroxide resulting from the activation of NADPH oxidase 4 (NOX4).

62 t and protein expression of all the HIFs and NADPH oxidase 4 seen in PE compared to NT at sea level w

63 nd ankyrin repeat domains 4, interleukin 11, NADPH oxidase 4, and BTB [POZ] domain containing 11) by

64 le factor-1alpha (HIF-1alpha), downstream of NAD(P)H oxidase-4 (NOX4)-derived reactive oxygen species

65 that the reactive oxygen species-generating NADPH oxidase-4 (Nox4) is induced downstream of ATF4, bi

66 renal levels of Bax, cleaved caspase-3, and NADPH oxidase-4 expression and reactive oxygen species (

67 ic PPARalpha(-/-) mice showed more prominent NADPH oxidase-4 overexpression compared with diabetic wi

68 The molecular events that link NADPH oxidase activation and the induction of Toll-like

69 This correlated with deficient NADPH oxidase activation at the plasma membrane in respo

70 ect of LC on angiotensin II (Ang II)-induced NADPH oxidase activation in NRK-52E cells.

71 We hypothesized that in liver, NADPH oxidase activation is key in TLR4 recruitment into

72 had higher levels of Rac1-GTP, required for NADPH oxidase activation, than sham control kidneys, and

73 ed that liver from murine and human NASH had NADPH oxidase activation, which led to the formation of

74 nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation because pretreatment of eosino

75 n hippocampal neurons via diverse effects on NADPH oxidase activity and dendritic spine morphology.

76 Neutrophils displayed an enhanced NADPH oxidase activity and increased reactive oxygen spe

77 ed ROS production functions independently of NADPH oxidase activity and light metabolism but depends

78 ytotoxicity by differentially regulating the NADPH oxidase activity and ROS generation.

79 has been associated with the maintenance of NADPH oxidase activity and the generation of reactive ox

80 with chronic granulomatous disease, who lack NADPH oxidase activity but still develop autoimmunity an

81 Either loss of memo-1 or increasing BLI-3/NADPH oxidase activity by overexpression is sufficient t

82 mately 15% gp91phox expression and increased NADPH oxidase activity in ex vivo-derived neutrophils.

83 ase induced by silica NPs through regulating NADPH oxidase activity in HEK293 cells.

84 H oxidase, while PVAT "senses" the increased NADPH oxidase activity in the underlying vessel and resp

85 The consequences of electrogenic NADPH oxidase activity on both membrane potential and pH

86 Mice in which NADPH oxidase activity was blocked to prevent superoxide

87 horbol 12-myristate 13-acetate (PMA)-induced NADPH oxidase activity were increased in RacET and corre

88 l death), less lipid peroxidation, and lower NADPH oxidase activity, indicating reduced active produc

89 s, and rapid NET formation is independent of NADPH oxidase activity.

90 ed with an increase in F- actin assembly and NADPH oxidase activity.

91 he ZF domain of VAV1, resulting in decreased NADPH oxidase activity.

92 confirming that the current originates from NADPH oxidase activity.

93 thermore, IL-12-mediated protection required NADPH oxidase activity.

94 nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity in vivo.

95 y has now extended well beyond the phagocyte NADPH oxidase - an industrial strength producer of react

96 reactive oxygen species (ROS) generation by NADPH oxidase and also chromatin decondensation dependen

97 educed Atox1 target proteins such as p47phox NADPH oxidase and cyclin D1 as well as extracellular mat

98 The relationship between NADPH oxidase and HV 1 has become a paradigm that somewh

99 ore, this study aimed to analyze the role of NADPH oxidase and inducible nitric oxide synthase (iNOS)

100 quired for Mtuberculosis to evade killing by NADPH oxidase and LAP.

101 bution to the resistance of Mtuberculosis to NADPH oxidase and LC3 trafficking in vivo.

102 Carbonylation was dependent on NADPH oxidase and myeloperoxidase activity and was inhib

103 of toxic reactive oxygen metabolites by the NADPH oxidase and myeloperoxidase.

104 oxide dismutase and catalase, and suppressed NADPH oxidase and reactive oxygen species (ROS) producti

105 Chemokine-controlled NADPH oxidases and metabolically controlled mitochondria

106 ipheral NKT cells were primarily produced by NADPH oxidases and not mitochondria.

107 lation of beta2-integrin-dependent adhesion, NADPH oxidase, and a subset of protein kinases.

108 tol triphosphate-induced Ca(2+) release, and NADPH oxidase, and pharmacologic inhibition of these rea

109 solic component of the ROS producing enzyme, NADPH oxidase, and the increase in amounts of phosphoryl

110 f reactive chemical species by mitochondria, NADPH oxidase, and type 2 nitric-oxide synthase (NOS-2)

111 nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, antioxidant enzymes, and p38 MAPK activ

112 NOX/DUOX family of NADPH oxidases are expressed in diverse tissues and are

113 avenging rates, in which membrane-associated NADPH oxidases are known to play a crucial role.

114 Apoplastic ROS homeostasis controlled by NADPH oxidases as well as by secreted type III peroxidas

115 ased the generation of superoxide anion from NADPH oxidase, as well as the amount of hydrogen peroxid

116 e granule membrane-associated subunit of the NADPH oxidase at the plasma membrane.

117 was partially restored in mice deficient in NADPH oxidase, Atg5, or Atg7, demonstrating that CpsA ma

118 en substantial progress toward understanding NADPH oxidase, but HV 1 were known only to a tiny handfu

119 n reactive oxygen species (ROS) generated by NADPH oxidase, but Mtuberculosis fails to generate a rob

120 The NADPH oxidase, by generating reactive oxygen species, is

121 hanges during Cd treatment were regulated by NADPH oxidase (C and F)-related ROS production.

122 re Nox2 and p67phox, which are components of NADPH oxidase, compared to triceps surae muscles of 'fre

123 s to this defect in terms of assembly of the NADPH oxidase complex and subsequent ROS production.

124 The NADPH oxidase complex of a sclerotial mycoparasite Conio

125 disease patients, carrying mutations in the NADPH oxidase complex or a MPO-deficient patient were ex

126 ng to p47(phox), a critical component of the NADPH oxidase complex, disrupting the complex and facili

127 ve oxygen species by the NoxR-dependent Nox2 NADPH oxidase complex.

128 utation in the structure and function of the NADPH oxidase complex.

129 bility of the quaternary NCF2/NCF4/VAV1/RAC1 NADPH oxidase complex.

130 ed expression of cytosolic components of the NADPH oxidase complex.

131 nd p38 that are required for assembly of the NADPH oxidase complex.

132 adenine dinucleotide phosphate reduced form (NADPH) oxidase complex and voltage-gated proton channels

133 evels of manganese superoxide dismutase, and NADPH oxidase-complex adaptor cytochrome b-245, alpha-po

134 ac1 GTPase for degradation at Rac1-dependent NADPH oxidase complexes, blocking superoxide generation

135 a/beta leading to reduced phosphorylation of NADPH oxidase components p47 (phox) and p40 (phox) in co

136 Eros is required for expression of the NADPH oxidase components, gp91phox and p22phox Consequen

137 NADPH oxidases contribute to LPS-induced reactive oxygen

138 with Opa- Gc showed limited translocation of NADPH oxidase cytoplasmic subunits to cellular membranes

139 burst caused by decreased phosphorylation of NADPH oxidase cytosolic components that are augmented by

140 far been only observed in patients with the NADPH oxidase deficiency chronic granulomatous disease,

141 Here, we show that NADPH oxidase deficiency enhances the early local releas

142 NADPH oxidase-deficient (gp91(phox) knockout [KO]), iNOS

143 ling and positive feedback between SrcFK and NADPH oxidase dependent ROS production.

144 echanistically, Aspergillus melanin inhibits NADPH oxidase-dependent activation of LAP by excluding t

145 e show that pro-angiogenic stimuli couple to NADPH oxidase-dependent generation of oxidants that cata

146 ase B was increased in hIRECO EC as was Nox2 NADPH oxidase-dependent generation of superoxide, wherea

147 vated during acute infection in a phagocytic NADPH oxidase-dependent manner in myeloid cells.

148 NF-alpha-induced CEC migration by inhibiting NADPH oxidase-dependent NF-kappaB and Rac1 activation an

149 d inflammasome activation, mitochondrial and NADPH-oxidase-dependent production of reactive oxygen sp

150 NADPH oxidase-derived excessive production of reactive o

151 nterleukin-6) were independent predictors of NADPH oxidase-derived O2 (-).

152 PVAT was positively correlated with vascular NADPH oxidase-derived O2 (-).

153 NADPH oxidase-derived oxidative stress plays a key role

154 phagocyte oxidative burst, mediated by Nox2 NADPH oxidase-derived reactive oxygen species, confers h

155 in the malignant microenvironment, including NADPH oxidase-derived reactive oxygen species.

156 ive oxygen species (ROS) and, in particular, NADPH oxidase-derived ROS are a key mediator of CAA-indu

157 Thus, ROS and, in particular, NADPH oxidase-derived ROS are a promising therapeutic ta

158 tely, these data highlight the importance of NADPH oxidase-derived ROS in providing a third signal fo

159 h hypoadiponectinemia and increased vascular NADPH oxidase-derived superoxide anions (O2 (-)).

160 omyocytes is Ca(2+) independent and requires NADPH oxidase-derived superoxide, but not its dismutatio

161 pecific hyporesponsiveness in the absence of NADPH oxidase-derived superoxide.

162 vious findings indicating involvement of the NADPH oxidase dual oxidase 1 (DUOX1) in epithelial wound

163 brafish larvae, activation of the epithelial NADPH oxidase Duox at the wound margin is required early

164 ctive oxygen species (ROSs) generated by the NADPH oxidase Duox in epithelial disc cells.

165 strongly depend on activation of either the NADPH oxidase DUOX1 or the homolog NOX2, depending on th

166 Our results show that IR induces delayed NADPH oxidase DUOX1-dependent H2O2 production in a dose-

167 article, we demonstrate that ROS induced via NADPH oxidase during the early stages of L. amazonensis

168 o-oxidative response to Ang II by modulating NADPH oxidase enzyme via reducing the activity of PKC an

169 protection involves suppression of the NOX3 NADPH oxidase enzyme, a major target of cisplatin-induce

170 .92-7.38] mg/L; P<0.01) and endothelial cell NADPH oxidase expression (P<0.05).

171 alterations and also reverted the changes in NADPH oxidase expression triggered by Ang II.

172 ilarly, neutrophils with a genetic defect in NADPH oxidase fail to induce either actin and tubulin po

173 a agonism appears to bypass the need for the NADPH oxidase for enhanced mtROS production and partiall

174 In these 3 brothers strongly reduced NADPH oxidase function was found in granulocytes, leadin

175 on of recombinant GM-CSF enhanced neutrophil NADPH oxidase function, conidiacidal activity, and lung

176 autonomic function, platelet activation, and NADPH oxidase gene expression and plasma flavanone metab

177 nicotinamide adenine dinucleotide phosphate (NADPH) oxidase generates reactive oxygen species essenti

178 Functioning independently from NADPH oxidases, glycolate oxidase (GLO) was recently dem

179 dye assay, whereas changes in expressions of NADPH oxidase gp91 (phox) subunit, alpha-smooth muscle a

180 ymorphism, C242T of the p22(phox) subunit of NADPH oxidase, has been reported to be negatively associ

181 the ICAM-1 protein expression and activates NAD(P)H oxidase in MLVECs.

182 f data about the role of the Nox5 isoform of NADPH oxidase in animal models of diabetic nephropathy s

183 Recombinant adiponectin directly inhibited NADPH oxidase in human arteries ex vivo by preventing th

184 We examined the effect of type 2 diabetes on NADPH oxidase in human vessels and explored the mechanis

185 The role of the NADPH oxidase in regulating inflammation driven by nonmi

186 on of sterile inflammation, and identify the NADPH oxidase in regulating the amplitude of the early n

187 phagocyte nicotinamide adenine dinucleotide (NADPH) oxidase in patients with chronic granulomatous di

188 stimulated NET release may arise in part via NADPH oxidase-independent mechanisms.

189 Together, these findings demonstrate that NADPH oxidase-induced redox signaling initiates a transc

190 ocynin or knockdown of p22phox, a subunit of NADPH oxidase, inhibited TNF-alpha-induced ROS generatio

191 ration of the SOD mimetic mito-tempol or the NADPH oxidase inhibitor apocynin attenuated the upregula

192 2X7R agonist, BzATP, and was attenuated by a NADPH oxidase inhibitor apocynin.

193 In addition, NADPH oxidase inhibitor diphenylene iodonium significant

194 The NADPH oxidase inhibitor diphenyleneiodonium (DPI) induce

195 ots with the ROS scavenger ascorbate and the NADPH oxidase inhibitor diphenyliodonium and analysis of

196 that combination treatment of antibiotic and NADPH oxidase inhibitor significantly improved animal su

197 First, the NADPH oxidase inhibitor, apocynin, and the nonspecific R

198 ine, which was normalized by a specific Nox2 NADPH oxidase inhibitor.

199 ine, which was normalized by a specific Nox2 NADPH oxidase inhibitor.

200 by pretreatment with diphenylene iodonium, a NADPH oxidase inhibitor.

201 es superoxide levels in Hace1(-/-) MEFs, and NADPH oxidase inhibitors block the induction of superoxi

202 emonstrate a novel linkage between Atox1 and NADPH oxidase involved in inflammatory neovascularizatio

203 Our results indicate that NADPH oxidase is important to control A. actinomycetemco

204 In many tissues, type 4 NADPH oxidase is induced upon ischemia or hypoxia, conve

205 we identify an ATP-binding motif within the NADPH oxidase isoform, NOX4, and show that ATP directly

206 lucose-induced matrix expression through the NADPH oxidase isoform, NOX4.

207 reactive oxygen species derive from specific NADPH oxidase isoforms remains ill defined.

208 ly and the reactive oxygen species-producing NADPH oxidases, it remains largely unknown how this coor

209 tes expression of Dual oxidase 1 (Duox-1), a NADPH oxidases known to generate H2O2.

210 which, in turn, activates a Nox2-containing NADPH oxidase, leading to cerebrovascular oxidative stre

211 esponse initiated by ROS generation via NOX3 NADPH oxidase, leading to inhibition of STAT1.

212 ropose that strategies to target the myeloid NADPH oxidase may facilitate the development of endogeno

213 The results strongly suggest that NADPH oxidase-mediated peroxynitrite drove TLR4 recruitm

214 We show that inhibition of NADPH oxidase-mediated production of ROS, or scavenging

215 ether, our results establish that phagocytic NADPH oxidase-mediated ROS production by BM myeloid cell

216 oving electrical charge across the membrane: NADPH oxidase moves electrons and HV 1 moves protons.

217 im of this study was to evaluate the role of NADPH oxidase (NADPHox) in the pathogenesis of oxidative

218 onally interacts with microtubule-associated NADPH oxidase (Nox) 2, and inhibition of Nox2 attenuated

219 cluding Toll-like receptor 4 (TLR4)-mediated NADPH oxidase (NOX) activation.

220 f p22phox, an indispensable component of the NADPH oxidase (NOX) complex comprising the main source o

221 gical levels of ROS, mainly sustained by the NADPH oxidase (NOX) complex, promote neuronal developmen

222 ROS levels that are mainly sustained by the NADPH oxidase (NOX) complex.

223 phox), a small membrane-bound subunit of the NADPH oxidase (NOX) complex.

224 Here we report that NADPH oxidase (NOX) expression is directly associated wi

225 of H2O2 for redox signaling purposes is the NADPH oxidase (Nox) family of enzymes, which were classi

226 ar distribution of the superoxide generating NADPH oxidase (NOX) in AVP-expressing hypothalamic parav

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

228 of endogenous phosphatase activity following NADPH oxidase (NOX) inhibition.

229 The NADPH oxidase (NOX) isoform NOX4 has been linked with di

230 These cells with their seven NADPH oxidase (NOX) isoforms provide a vast realm of mec

231 gulated in fungal strains carrying defective NADPH oxidase (Nox) or the oxidative stress responsive r

232 Previous studies implicate NADPH oxidase (Nox) proteins as important reactive oxyge

233 NADPH oxidase (NOX) proteins produce reactive oxygen spe

234 periments, mice received apocynin to inhibit NADPH oxidase (NOX), IL-1 receptor antagonist, or IL-18

235 utations, S100A9-induced signaling activates NADPH oxidase (NOX), increasing levels of reactive oxyge

236 ls and macrophages, CD4 T cells also express NADPH oxidase (NOX), the superoxide-generating multisubu

237 Activation of the enzyme NADPH oxidase (NOX), which catalyzes one-electron reduct

238 TRAF3 is central in the activation of the NADPH oxidase (Nox)-2 component p40phox and the elevatio

239 tion of reactive oxygen species derived from NADPH oxidase (NOX)-4 and mitochondrial sources.

240 revealed that HDM-induced cellular injury is NADPH oxidase (NOX)-dependent, and apocynin, a NOX inhib

241 ecies (ROS) in T1D, as NOD mice deficient in NADPH oxidase (NOX)-derived superoxide (Ncf1(m1J)) were

242 reviously demonstrated an important role for NADPH oxidase (NOX)-derived superoxide production during

243 tem and reactive oxygen species derived from NADPH oxidase (Nox).

244 te RAC1 to promote proliferative ROS through NADPH oxidase (NOX).

245 ing type 2 nitric-oxide synthase (NOS-2) and NADPH oxidase (NOX).

246 lly, CD47 blockade enabled the activation of NADPH oxidase NOX2 in DCs, which in turn inhibited phago

247 l peptide receptor 1 (FPR1) and neutrophilic NADPH oxidase (NOX2) are required for the rapid depletio

248 NADPH oxidase (Nox2) is upregulated in the pathogenesis

249 e, we identified potential inhibitors of the NADPH oxidase (Nox2) isoform from a small library of bio

250 Stimulated neutrophils activate their NADPH oxidase (NOX2) to generate large amounts of supero

251 oding the p47(phox) subunit of the phagocyte NADPH oxidase (NOX2), as the putative underlying causal

252 ts of histamine, an inhibitor of the myeloid NADPH oxidase/NOX2, on the development of Ag-presenting

253 Furthermore, the NADPH oxidase NOX4 inhibits this transition and therefor

254 TGFbeta-induced expression of the NADPH oxidase Nox4 is essential for fibroblast-myofibrob

255 Within the family of NADPH oxidases, NOX4 is unique as it is predominantly lo

256 NADPH oxidases (Noxes) produce ROS that regulate cell gr

257 NADPH oxidases (NOXs) are involved in inflammation, angi

258 NADPH oxidases (NOXs) are the only enzymes exclusively d

259 elevated levels of p22(phox) subunit of the NADPH oxidases (NOXs), and fibrotic markers, plasminogen

260 SHP2 oxidation requires NADPH oxidases (NOXs), and oxidized SHP2 co-localizes wi

261 Inhibition of NADPH oxidases or knockdown of gp91phox in CD8(+) T cell

262 s as a Cu-dependent transcription factor for NADPH oxidase organizer p47phox, thereby increasing ROS-

263 The described phenomenon was NADPH oxidase, p47phox, and peroxynitrite dependent, as

264 c organisms, and pharmacologic inhibition of NADPH-oxidase partially impairs NET production.

265 f reactive oxygen species (ROS) via the NOX3 NADPH oxidase pathway in the cochlea.

266 NADPH oxidase pathway modulators decreased ROS productio

267 se was monitored after the addition of NADP (NADPH) oxidase pathway modulators and inhibitors of Toll

268 ANCA-induced phagocyte NADPH oxidase (Phox) may contribute by generating tissue

269 ) exposure and intrinsic factors such as the NADPH oxidases produce high levels of reactive oxygen sp

270 Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases produce ROS locally in response to vario

271 es containing the DeltacpsA mutant recruited NADPH oxidase, produced ROS, associated with LC3, and ma

272 taining membrane proteins, which include the NADPH oxidase proteins (NOX/DUOX).

273 Mutants of the root-expressed NADPH oxidase RBOH C, but not rbohD, showed enhanced hyd

274 1, followed by direct phosphorylation of the NADPH oxidase RBOHD, resulting in elevated production of

275 Consistently, PLC2 associates with the NADPH oxidase RBOHD, suggesting its potential regulation

276 ires ROS generated by the defense-associated NADPH oxidase, RBOHD.

277 Moreover, CpsA was sufficient to impair NADPH oxidase recruitment to fungal particles that are n

278 vation generates reactive oxygen species via NADPH oxidase, reducing the palmitoylation of receptor-a

279 int specifically regulates septin-dependent, NADPH oxidase-regulated F-actin dynamics to organize the

280 sin or apocynin (inhibitors of alpha1-AR and NADPH oxidase, respectively), but increased vascular per

281 ages on heart rapidly through a ROS-p38 MAPK-NADPH oxidase-ROS positive feedback loop in response to

282 The family prototype PDIA1 regulates NADPH oxidase signaling and cytoskeleton organization, h

283 ion increased endothelial ROS production via NADPH oxidase signaling, up-regulated Nox4 expression, a

284 (tg(sm/p22phox) mice, which overexpress the NADPH oxidase subunit p22(phox) in smooth muscle, and mi

285 The NADPH-oxidase subunit gp91 was significantly increased i

286 h a signaling pathway requiring Src kinases, NADPH oxidase, superoxide radical anion, and hydrogen pe

287 L. amazonensis is impaired by inhibitors of NADPH oxidase, Syk, focal adhesion kinase, and proline-r

288 including the thioredoxin, glutathione, and NADPH-oxidase systems.

289 hich is required to stimulate the phagocytic NADPH-oxidase that generates reactive oxygen species.

290 an enhanced interaction of RHO-1 with BLI-3/NADPH oxidase, thereby stimulating ROS production that s

291 by mutations in the gp91phox subunit of the NADPH oxidase, TI of a gp91phox transgene into AAVS1 res

292 cyte reactive oxygen species produced by the NADPH oxidase to altered inflammatory responses associat

293 dels of IMA/PVAT, the activation of arterial NADPH oxidase triggered a peroxisome proliferator-activa

294 xin 6 (Prdx6) is essential for activation of NADPH oxidase type 2 (NOX2) in pulmonary microvascular e

295 pport the hypothesis that signaling from the NADPH oxidase under normal circumstances governs phagocy

296 ectin-3-induced activation of the neutrophil NADPH oxidase was abrogated by bacterium-derived proteol

297 d the amount of superoxide anion produced by NADPH oxidase was measured by spectrophotometry through

298 We focused on NADPH oxidases, which are specialized ROS-generating enz

299 als with type 2 diabetes stimulates vascular NADPH oxidase, while PVAT "senses" the increased NADPH o

300 (G6PD), an important enzyme from PPP, fuels NADPH oxidase with NADPH to produce superoxide and thus