ライフサイエンスコーパス: NOX2

1 bly functional complex with NADPH oxidase 2 (Nox2).

2 ived signal for activation of NADPH oxidase (NOX2).

3 is required for activation of NADPH oxidase (NOX2).

4 of reactive oxygen species generating enzyme NOX2).

5 heart through activation of NADPH oxidase 2 (NOX2).

6 ROS through the superoxide-producing enzyme NOX2.

7 vation mechanism variably involves DUOX1 and NOX2.

8 -dependent phosphorylation and activation of NOX2.

9 ive oxygen species (ROS) due to mutations in NOX2.

10 by modulating buffering by the NADPH oxidase NOX2.

11 TRPC6 was inversely correlated with that of Nox2.

12 (transported through SGLT1) did not activate NOX2.

13 ducing enzyme in microglia, NADPH oxidase 2 (NOX2), a well-known player in the pathogenesis of ALS.

14 Although the role of Nox2, a major ROS-generating enzyme, is well described i

15 structural changes that inhibit endothelial Nox2 activation and oxidative response to tumor necrosis

16 x6-PLA2 We propose that Prdx6-PLA2 modulates NOX2 activation by generation of LPC that is converted t

17 Herein, we show Nox2 activation favors thioredoxin-1 (TRX-1)/p40phox int

18 AngII-induced endothelial NOX2 activation has profound profibrotic effects in the

19 A2AR agonism prevents IR injury by blocking NOX2 activation in iNKT cells.

20 Thus, Prdx6-PLA2 modulates NOX2 activation through generation of LPC for conversion

21 degradation and amplifying Ca(2+)-dependent Nox2 activation through TRPC3-mediated background Ca(2+)

22 SGLT1 deficiency did not prevent HG-induced NOX2 activation, ruling it out in the cellular response

23 show that heart SMIT1 senses HG and triggers NOX2 activation.

24 in skeletal muscle cells is a consequence of Nox2 activation.

25 G, whereas its deletion prevented HG-induced NOX2 activation.

26 7(phox) phosphorylation, a critical step for NOX2 activation.

27 de adenine dinucleotide phosphate oxidase-2 (NOX2) activation causes endothelial dysfunction.

28 These findings suggest that increased NOX2 activity at lipid rafts is an early and major sourc

29 or by 2'-3'-O-(benzoyl-benzoyl) ATP enhanced NOX2 activity in terms of translocation of p67(phox) to

30 Genetic downregulation of Nox2 activity in the mdx mouse decreases reactive oxygen

31 Elevated Nox2 activity increased phospholamban phosphorylation in

32 Ang II-stimulated Nox2 activity increased sarcoplasmic reticulum (SR) Ca(2

33 phagocytosed proteins, we demonstrated that NOX2 activity not only affects levels of phagosomal prot

34 on of Prdx6 with p67(phox) and its effect on NOX2 activity.

35 om blood of CGD patients, who have deficient Nox2 activity.

36 nephrotoxicity showed significantly greater Nox2, alpha-smooth muscle actin and picrosirius levels c

37 Nox2 also stabilizes TRPC3 proteins to enhance TRPC3 cha

38 um, where it directly interacts with nascent NOX2 (also known as gp91(phox) and encoded by Cybb) mono

39 nd there was a mutual dependency between the NOX2 and ERK1/2 pathways.

40 monocyte-derived macrophages (MDM) requires NOX2 and gamma interferon (IFN-gamma) pretreatment.

41 phosphorylation of the p47(phox) subunit of NOX2 and its translocation to the cellular membrane.

42 Inhibition of NOX2 and NOX1 with siRNA or chemical inhibitors signific

43 Both Nox2 and Nox4 contribute to the increase in reactive oxi

44 ta-regulated transcription factor, decreases Nox2 and Nox4 expression, whereas NFAT overexpression in

45 We investigated the role of Nox2 and Nox4 in mediating oxidative stress and myocardi

46 The isoform-specific contribution of Nox2 and Nox4 to ischemia/reperfusion (I/R) injury is po

47 ies were assayed and NADPH oxidase isoforms, Nox2 and Nox4, and antioxidant enzymes were determined b

48 ssion, whereas NFAT overexpression increases Nox2 and Nox4, indicating that the CnAbeta/NFAT pathway

49 dominant-negative Nox, which suppresses both Nox2 and Nox4, than in wild-type or single KO mice.

50 Knockdown of NOX2 and NOX4, using specific siRNA, reduced both basal

51 ression and blocks high glucose induction of Nox2 and Nox4.

52 OX catalytic and regulatory sub-units (NOX1, NOX2 and p47(phox)).

53 rae muscles of 'ligated' rats expressed more Nox2 and p67phox, which are components of NADPH oxidase,

54 ne dinucleotide phosphate (NADPH) oxidase 2 (NOX2) and their bone marrow chimera, we demonstrated tha

55 ne dinucleotide phosphate reduced oxidase 2 (NOX2); and the down-regulation of Sirtuin 1 (Sirt1)/Timp

56 whereas the NADPH oxidase subunits p47phox, Nox2, and Nox4 were upregulated.

57 n this review, we propose that inhibitors of NOX2 are better alternatives than broad-spectrum antioxi

58 Here we report that NOX1 and NOX2 are critical for the differentiation of monocytes t

59 Herein we show that Nrf2 and Nox2 are key regulators of IsoLG modification in pulmona

60 produced by NADPH phagocyte oxidase isoform (NOX2) are critical for the elimination of intracellular

61 tor 1 (FPR1) and neutrophilic NADPH oxidase (NOX2) are required for the rapid depletion of microenvir

62 Together, our data support NOX2 as a critical component of the suppressive machiner

63 so establishes pharmacological inhibition of Nox2 as a novel therapeutic target in insulin resistance

64 This study identifies Nox2 as the central molecule in insulin resistance-media

65 We identified deficiency of NADPH oxidase 2 (NOX2) as the molecular underpinning of CD8 Treg failure

66 hox) subunit of the phagocyte NADPH oxidase (NOX2), as the putative underlying causal variant that dr

67 as dependent on p22phox, and not on gp91phox/NOX2, as shown by the reduced Mo-DC differentiation obse

68 TRPC3 physically interacts with Nox2 at specific C-terminal sites, thereby protecting No

69 ted NADPH oxidase (Nox) 2, and inhibition of Nox2 attenuated mechanical stretch-induced GEF-H1 activa

70 Knockdown of Nox4, but not Nox2, attenuated O(2)(-) production in the nucleus and p

71 TRPC6 could interact with Nox2, but the abundance of TRPC6 was inversely correlate

72 tch pathway components was suppressed in the Nox2(-/-) cells but increased in both WT and Nox2(-/-) m

73 , we implicate Rnf145 in proteostasis of the Nox2 complex by endoplasmic reticulum-associated degrada

74 nction mutations that impair function of the Nox2 complex result in a life-threatening immunodeficien

75 ox2 destabilization through disrupting TRPC3-Nox2 complex underlies attenuation of hyperglycemia-indu

76 ociated with impaired phosphorylation of the NOX2 component, p47phox (phox: phagocyte oxidase), on it

77 Assembly of NOX2 components at lipid rafts requires activation of Ra

78 erentiation 36), which, in turn, activates a Nox2-containing NADPH oxidase, leading to cerebrovascula

79 MICT also reduced microvascular endothelial NOX2 content (P < 0.05) and both increased capillary den

80 content, eNOS serine(1177) phosphorylation, NOX2 content and capillarisation using quantitative immu

81 content, eNOS serine(1177) phosphorylation, NOX2 content and capillarisation using quantitative immu

82 ial eNOS content, while reducing endothelial NOX2 content in microvessels of young obese men.

83 ide of MOG is susceptible to cleavage by the NOX2-controlled cysteine cathepsins L and S in a redox-d

84 short-hairpin RNA-engineered HeLa cells and Nox2(-/-) coronary microvascular endothelial cells.

85 Ca(2+) signaling by platelet and neutrophil NOX2 correlated with differences in the phosphorylation

86 ing the first 2 days of development, whereas nox2/cybb levels remain remarkably stable.

87 hough the sequences of five NOX genes (nox1, nox2/cybb, nox4, nox5, and duox) have been identified in

88 hybridization to develop a catalog of nox1, nox2/cybb, nox5, and duox expression in zebrafish during

89 cific inhibitor of NOX4 and NADPH oxidase 2 (NOX2), decreased their elevated cancer incidence to that

90 Additionally, it was found that NOX2 deficiency adversely affected the ability of bone m

91 e data provide direct evidence that NOX1 and NOX2 deficiency impairs macrophage differentiation and t

92 nery of CD8 Tregs and suggest that repairing NOX2 deficiency in these cells may protect older individ

93 Nox2 deficiency was associated with declines in the surv

94 hrome b-245, beta polypeptide, also known as NOX2) deficiency in neutrophils impairing ROS production

95 ne dinucleotide phosphate (NADPH) oxidase 2 (Nox2)-deficient mice but fail to fully protect WT animal

96 ating DCs in NOX2-sufficient mice but not in NOX2-deficient (gp91(phox) (-/-)) mice.

97 , Nox2 does not interact with cortactin, and Nox2-deficient hearts were protected from pressure overl

98 Furthermore, Nox2-deficient mice are protected against high-fat diet-

99 Experiments using wild-type and NOX2-deficient myelomonoblastic cells showed that histam

100 Myeloid-specific Nox2 deletion had no effect on angiotensin II-induced hy

101 Unexpectedly, Nox2 deletion in myeloid but not endothelial cells resul

102 ired autophagic flux through activation of a Nox2 dependent Src/PI3K/Akt axis, with a consequent disr

103 ection disrupts the delicate balance between Nox2-dependent antibacterial immunity and inflammation.

104 A deficiency in the NOX2-dependent formation of these antigen storage phagos

105 Furthermore, the NOX2-dependent oxidative burst, produced by macrophages

106 Inhibition of Nox2-dependent oxidative stress attenuated the impaired

107 rt1 and Timp3 in hepatic stellate cells by a NOX2-dependent pathway, and TACE was induced after expos

108 flammatory milieu in bone and that p47(phox)-Nox2-dependent physiological ROS signaling suppresses in

109 ive p53, ectopic expression of NPRL2 induces NOX2-dependent production of reactive oxygen species and

110 ither the NADPH oxidase DUOX1 or the homolog NOX2, depending on the activation mechanism.

111 y potential inhibitors of ONOO(-)formed from Nox2-derived O2 ()and nitric oxide synthase-derived nitr

112 -iso-prostaglandin F2alpha and serum soluble NOX2-derived peptide and the severity of liver steatosis

113 Urinary 8-iso-PGF2alpha and serum soluble NOX2-derived peptide levels were independent from obesit

114 iso- prostaglandin F2alpha and serum soluble NOX2-derived peptide levels.

115 urinary 8-iso-PGF2alpha and of serum soluble NOX2-derived peptide with the severity of steatosis at u

116 urinary 8-iso-PGF2alpha and of serum soluble NOX2-derived peptide, alanine aminotransferase, Cytokera

117 ata highlight the pathogenic role of reduced NOX2-derived ROS levels in autoimmune diseases.

118 d hyperlipidemia stimulate the generation of NOX2-derived ROS through a CD36-PKC pathway and may prom

119 tyrosine phosphorylation of eNOS and excess Nox2-derived superoxide.

120 These results strongly suggest that Nox2 destabilization through disrupting TRPC3-Nox2 compl

121 In contrast, Nox2 does not interact with cortactin, and Nox2-deficien

122 er, we identify tumor-specific dependence on NOX2-driven mitochondrial transfer as a novel therapeuti

123 T) mice, mice deficient in ROS production by NOX2 due to the absence of the gp91 subunit (gp91(phox-/

124 In cultured ECs treated with AngII, NOX2 enhanced EMT as assessed by the relative expression

125 Endothelial NOX2 enhances EMT and has proinflammatory effects.

126 We specifically identified NOX1 and NOX2 enzymes to be responsible for ROS generation.

127 TT allele had significantly lower levels of Nox2 expression and O2 (.-) generation in response to hi

128 d that C242T p22(phox) significantly reduced Nox2 expression but had no significant effect on basal e

129 Higher levels of Nox2 expression increased Notch signaling and arterial E

130 improved endothelial function nor normalized Nox2 expression or RONS production in TTP(-/-) animals.

131 creased in both WT and Nox2(-/-) miPSCs when Nox2 expression was upregulated.

132 High fat feeding increased Nox2 expression, superoxide production, and impaired ins

133 This is despite low levels of cardiac Nox2 expression.

134 acrophages lacking the gp91(phox) subunit of NOX2 fail to produce ROS upon FcgammaR ligation, resulti

135 equire reactive oxygen species production by NOX2 for their generation.

136 ir bone marrow chimera, we demonstrated that NOX2 from both hematopoietic and endothelial cells is cr

137 ic ischemia/reperfusion injury revealed that NOX2 from both platelets and neutrophils is required for

138 pecific C-terminal sites, thereby protecting Nox2 from proteasome-dependent degradation and amplifyin

139 Thus, deletion of CD36 or Nox2 from PVM abrogates the deleterious vascular effects

140 heir age-matched wild type controls, loss of Nox2 function in p47(phox-/-) mice resulted in age-relat

141 n species (ROS) produced by NADPH oxidase 2 (Nox2) function as key mediators of mechanotransduction d

142 de adenine dinucleotide phosphate oxidase 2 (NOX2) function cause chronic granulomatous disease (CGD)

143 generated a novel mouse model with a floxed Nox2 gene and used Tie2-Cre, LysM Cre, or Cdh5-CreERT2 d

144 We hypothesized that NOX2 generated ROS is necessary for propagation of downs

145 Furthermore, neutrophil NOX2-generated ROS enhanced the activation and ligand-bi

146 Here we report that in human AML, NOX2 generates superoxide, which stimulates bone marrow

147 NADPH oxidase 2 (NOX2) generates large amounts of reactive oxygen species

148 lex, disrupting the complex and facilitating Nox2 (gp91(phox)) ubiquitination and degradation.

149 CD, six NADPHox-deficient mice on a SCD; (4) NOX2(-/-)/HFD, six NADPHox-deficient mice on a HFD.

150 associated with decreased oxidative stress (Nox2, HIF-1alpha, hydrogen peroxide, hydroxynonenal), an

151 Overexpression of NOX2 in aged CD8 Tregs promptly restored suppressive fun

152 scular levels, but the cell-specific role of Nox2 in BP regulation is unknown.

153 ts identify distinct cell-specific roles for Nox2 in BP regulation.

154 Down-regulation of Nox2 in C2C12 cells by shRNA prevented insulin resistanc

155 kade enabled the activation of NADPH oxidase NOX2 in DCs, which in turn inhibited phagosomal acidific

156 vented by either pharmacologic inhibition of NOX2 in human platelets or genetic ablation of NOX2 in m

157 st-mediated protection entails inhibition of NOX2 in iNKT cells.

158 However, the role of NOX1 and NOX2 in macrophage differentiation and tumor progression

159 X2 in human platelets or genetic ablation of NOX2 in murine platelets.

160 ovascular actions of Abeta and that CD36 and Nox2 in PVM are the molecular substrates of the effect.

161 rved that chemical and genetic inhibition of Nox2 in rats and mice resulted in the prevention of CsA-

162 tial for activation of NADPH oxidase type 2 (NOX2) in pulmonary microvascular endothelial cells (PMVE

163 f H2O2 produced by membrane NADPH oxidase 2 (Nox2) in response to TNF-alpha is facilitated by AQP3 an

164 the role of ROS produced by NADPH oxidase 2 (Nox2) in the endothelial-lineage specification of mouse

165 via dynamin-mediated endocytosis of TLR4 and NOX2, independently from MyD88 and TRIF.

166 cotinamide adenine dinucleotide phosphatase (Nox2)-induced oxidative stress impairs both autophagy an

167 However, Nox2-induced lung damage during coinfection was not asso

168 esis of NASH and is mediated by AGEs through NOX2 induction and down-regulation of Sirt1/Timp3 pathwa

169 affected by BH4 supplementation (10 muM) or NOX2 inhibition ex vivo.

170 ells occurs in response to oxidative stress, NOX2 inhibition had no detectable effect on nonmalignant

171 Nox2 inhibition or conditioned media from Nox2-silenced

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

173 tricts TLR7 signaling, and that an endosomal NOX2 inhibitor decreases viral pathogenicity.

174 Use of a selective NOX2 inhibitor prevented increased cytosolic and nuclear

175 KT137831, a NOX1/4 inhibitor, and Phox-I2, a NOX2 inhibitor.

176 cked by the reduced NAD phosphate oxidase 2 (NOX2) inhibitor, gp91ds-tat, and absent in NOX2(-/-) mic

177 regulated ROS production by disrupting TRPC3-Nox2 interaction, without affecting TRPC3-mediated Ca(2+

178 Therefore, endocytosis of TLR4 and NOX2 into macrophages might be a novel therapeutic targe

179 This is the first report to show that Nox2 is a key mediator of insulin resistance in skeletal

180 These studies suggest that Nox2 is a modulator of CsA-induced hypoxia upstream of H

181 ltered in Cdh5-CreERT2 Nox2KO mice (in which Nox2 is deficient only in endothelial cells).

182 Previous studies have shown that NOX2 is essential for killing of G. bethesdensis by neut

183 ctive-oxygen-species-(ROS)-generating-enzyme Nox2 is essential for leukocyte anti-microbial activity.

184 Among these, Nox2 is expressed in multiple cell types, including endo

185 which an essential cytosolic co-activator of Nox2 is lost, to characterize bone metabolism at 6 weeks

186 tide phosphate oxidase 2 (NADPH oxidase 2 or Nox2) is enhanced by angiotensin II (Ang II) and contrib

187 inucleotide phosphate oxidase (gp91(phox) or Nox2) is expressed in the heart.

188 NADPH oxidase (Nox2) is upregulated in the pathogenesis of PD; however,

189 role of NADPH oxidase (Nox) and specifically Nox2 isoform in superoxide generation in two complementa

190 with gp91-phox, a catalytic subunit for the NOX2 isoform.

191 d potential inhibitors of the NADPH oxidase (Nox2) isoform from a small library of bioactive compound

192 ence that activation of the NADPH oxidase 2 (NOX2) isoform of the NADPH oxidase family of ROS-produci

193 Systemic (s) Nox2 knockout (KO), sNox4 KO, and cardiac-specific (c) N

194 When wild-type (WT) and Nox2-knockout (Nox2(-/-)) miPSCs were differentiated int

195 We found that deletion of both NOX1 and NOX2 led to a dramatic decrease in ROS production in mac

196 nhibited tumor necrosis factor-alpha-induced Nox2 maturation, O2 (.-) production, mitogen-activated p

197 our results identify a hitherto unrecognized Nox2-mediated intracellular signaling pathway that contr

198 PD; however, the underlying mechanism(s) of Nox2-mediated oxidative stress in PD pathogenesis are st

199 Recent studies found that Nox2-mediated reactive oxygen species production modulat

200 n together, these observations indicate that Nox2-mediated ROS production promotes arterial EC specif

201 We tested the hypothesis that NOX2 mediates IL-17 production by iNKT cells after IR an

202 y releasing exosomes that carry preassembled NOX2 membrane clusters and are taken up by CD4 T cells.

203 transfer of iNKT cells from p47(phox-/-) or NOX2(-/-) mice to Jalpha18(-/-) (iNKT cell-deficient) mi

204 (NOX2) inhibitor, gp91ds-tat, and absent in NOX2(-/-) mice.

205 or Western diet (WD)-fed wild-type (WT) and NOX2(-/-) mice.

206 in Fisher 344 rats, C57BL/6 J wild type and Nox2-/- mice, and in liver transplant recipients with ch

207 repair, metabolism, and oxidative stress in Nox2-/- mice.

208 ischemic limbs of mice after treatment with Nox2(-/-) miPSC-ECs than WT miPSC-EC treatment.

209 Nox2(-/-) cells but increased in both WT and Nox2(-/-) miPSCs when Nox2 expression was upregulated.

210 When wild-type (WT) and Nox2-knockout (Nox2(-/-)) miPSCs were differentiated into ECs (miPSC-EC

211 Platelet NOX2 modulated intracellular Ca(2+) release but not stor

212 We identified a novel mechanism in which Nox2 modulates cardiomyocyte SR Ca(2+) uptake and contra

213 DPH oxidase 2 (Nox2) resulting from enhanced Nox2 mRNA stability.

214 eactive oxygen species by the NoxR-dependent Nox2 NADPH oxidase complex.

215 al hypomorphic variants in components of the NOX2 NADPH oxidase complex.

216 subset of patients with VEOIBD in which the NOX2 NADPH oxidase genes sequence had been previously an

217 lcholine, which was normalized by a specific Nox2 NADPH oxidase inhibitor.

218 lcholine, which was normalized by a specific Nox2 NADPH oxidase inhibitor.

219 n kinase B was increased in hIRECO EC as was Nox2 NADPH oxidase-dependent generation of superoxide, w

220 The phagocyte oxidative burst, mediated by Nox2 NADPH oxidase-derived reactive oxygen species, conf

221 We report that the Nox2-NoxR complex spatially organizes a heteroligomeric

222 induced by a high fat diet was mitigated in Nox2-null mice compared with wild-type mice after 3 or 9

223 l muscle tissue of wild-type mice but not in Nox2-null mice.

224 to investigate the effects of cardiomyocyte Nox2 on contractile function during increased Ang II act

225 We also found that the involvement of NOX2 on LTP is partially age-dependent, as the activity

226 to which superoxide is released by activated NOX2 on the internalized neutrophil membrane.

227 e, an inhibitor of the myeloid NADPH oxidase/NOX2, on the development of Ag-presenting dendritic cell

228 chrome b-245 or NADPH oxidase 2, and encodes Nox2 or gp91(phox); neutrophil cytosol factor 1 and enco

229 In contrast, the genetic deficiency of Nox2 or its pharmacological inhibition with apocynin (AP

230 eactive oxidative species produced by either Nox2 or Nox4 regulate hypoxia-inducible factor-1alpha an

231 Inhibition of Nox2 or Src kinase reduces oxidative stress and partiall

232 Moreover, ECs lacking either Nox2 or Stim1 failed to trigger store-operated Ca2+ entr

233 and proximity ligation assay, whereas NOX1, NOX2, or NOX5 did not interact with calnexin.

234 Selective knockdown of Nox4, but not Nox2, or selective reduction of ROS in the ER with ER-ta

235 Transgenic mice with endothelial-specific NOX2 overexpression (TG mice) and wild-type littermates

236 erated a mouse model of endothelium-specific Nox2 overexpression and tested the susceptibility to aor

237 patients) due to increased mitochondrial and NOX2 oxidase activity (by 309% and 149%; p=0.002 and p=0

238 how that virus infection activates endosomal NOX2 oxidase and restricts TLR7 signaling, and that an e

239 enzymatic source of reactive oxygen species, NOX2 oxidase, is activated by single stranded RNA and DN

240 In summary, LSS activates the NOX2-p47phox complex to activate eNOS phosphorylation an

241 oduced similar results, indicating a role of NOX2/p47phox-derived hydrogen peroxide in mediating the

242 genetic ablation of receptor activity on the NOX2 pathway.

243 However, inflammatory cell NOX2 per se was not essential for the profibrotic effect

244 ver lines to develop cell-specific models of Nox2 perturbation to investigate its role in BP regulati

245 NOX2 plays a key role in inducing iNKT cell-mediated IL-

246 icotinamide adenosine diphosphate oxidase 2 (Nox2) plays an important role in cyclosporine A (CsA)-in

247 f intracellular hydrogen peroxide or RNAi of NOX2 produced similar results, indicating a role of NOX2

248 Platelet NOX2-produced reactive oxygen species (ROS) regulated P-

249 esults indicate that platelet and neutrophil NOX2-produced ROS are critical for the function of surfa

250 Increased Nox2 reactive oxygen species (ROS) production and sarcol

251 Inhibiting Nox2 reactive oxygen species (ROS) production reduced in

252 Furthermore, we show that inhibition of NOX2 reduces the NMDA receptor function, suggesting a po

253 myeloid cell Nox2, whereas endothelial cell Nox2 regulates angiotensin II-induced hypertension.

254 We propose that Nox2 regulates LPS-mediated Ang2-dependent autocrine ang

255 e that PVM are the cells expressing CD36 and Nox2 responsible for the dysfunction.

256 ith increased expression of NADPH oxidase 2 (Nox2) resulting from enhanced Nox2 mRNA stability.

257 The lack of Nox2 ROS production protected against decreased in vivo

258 cators of disease pathology, and eliminating Nox2 ROS production reduces aberrant Ca(2+) influx in yo

259 Therefore, we hypothesized that eliminating Nox2 ROS production would decrease calcium influx in adu

260 nd in vivo data demonstrate that eliminating Nox2 ROS protected against aberrant Ca(2+) influx and im

261 In Cos7 cells, which do not express NOX2, ROS was detected in silica-containing phagolysosom

262 tored in macrophages missing LAP components (Nox2, Rubicon, Beclin, Atg5, Atg7, or Atg16L1) but not i

263 w diet (SCD); WT/HFD, six WT mice fed a HFD; NOX2(-/-)/SCD, six NADPHox-deficient mice on a SCD; (4)

264 -specific insulin resistance and deletion of Nox2 showed reduced superoxide production and improved v

265 eneration in bone marrow cells and p47(phox)-Nox2 signaling in osteoblastic cells, 2-year-old p47(pho

266 Nox2 inhibition or conditioned media from Nox2-silenced cells attenuated LPS-induced tube and netw

267 and VEGF-A treatment rescued angiogenesis in Nox2-silenced cells.

268 Nox2 silencing, but not Nox4 or Nox1 silencing, inhibite

269 The role of NOX2, Sirt1, Timp3, and TACE was evaluated in choline-de

270 oscillations are ablated in ECs deficient in Nox2, Stim1, and type II inositol triphosphate receptor

271 ) and reduces its interaction stability with Nox2 subunit.

272 ng immunodeficiency, and genetic variants of Nox2 subunits have been implicated in pathogenesis of in

273 th an increment of tumor-infiltrating DCs in NOX2-sufficient mice but not in NOX2-deficient (gp91(pho

274 eotide phosphate (NADPH) 2 (NADPH oxidase 2; NOX2), termed respiratory burst (RB).

275 we provide evidence that genetic ablation of NOX2 (the prototypical member of NADPH oxidase family of

276 imary immunodeficiency marked by a defect in NOX2, the phagocyte NADPH oxidase.

277 complex, and facilitates the degradation of NOX2 through the endoplasmic-reticulum-associated degrad

278 ed neutrophils activate their NADPH oxidase (NOX2) to generate large amounts of superoxide, which act

279 Nox2 transgenic aortas had increased endothelial ROS pro

280 Nox2 transgenic ECs (but not vascular smooth muscle cell

281 Conditioned media from Nox2 transgenic ECs induced greater Erk1/2 phosphorylati

282 ic increase in endothelial ROS production in Nox2 transgenic mice was sufficient to cause Ang II-medi

283 Using a NOX2 transgenic mouse and a pig model of rapid atrial pa

284 We generated a cardiomyocyte-targeted Nox2-transgenic mouse model and studied the effects of i

285 The Nox2/TRX-1/NF-kappaB intracellular signaling pathway is

286 Moreover, inhibition of NOX2 was able to prevent mitochondrial transfer, increas

287 T, while neither endothelial nor sarcolemmal NOX2 was changed.

288 ated Ca(2+) entry (SOCE), whereas neutrophil NOX2 was crucial for SOCE but not intracellular Ca(2+) r

289 th Tie2-CreNox2 knockout (KO) mice (in which Nox2 was deficient in both endothelial cells and myeloid

290 oid cells) and LysM CreNox2KO mice (in which Nox2 was deficient in myeloid cells) had significantly l

291 crophages, ROS generated by NADPH oxidase 2 (NOX2) was detected in phagolysosomes containing either s

292 As AQP3 associates with Nox2, we propose that this interplay constitutes H2O2-me

293 We further showed that NOX1 and NOX2 were critical for the activation of the MAPKs JNK a

294 Selected hits for Nox2 were further screened for their ability to inhibit

295 t in the p47(phox) or gp91(phox) subunits of NOX2 were partially protected from MOG-induced experimen

296 nized modulation of basal BP by myeloid cell Nox2, whereas endothelial cell Nox2 regulates angiotensi

297 , at resting state, p47phox colocalizes with NOX2, whereas NOXO1 colocalizes with NOX1.

298 The antimicrobial effector NADPH oxidase (NOX2), which generates superoxide within maturing phagos

299 siRNA-mediated knockdown of Nox2, which was specifically elevated in insulin-resista

300 dependent EGFR activation primarily involves NOX2 with a secondary role for DUOX1 and Src.