ライフサイエンスコーパス: NOX2

1 of reactive oxygen species generating enzyme NOX2).

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

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

4 TRPC6 was inversely correlated with that of Nox2.

5 (transported through SGLT1) did not activate 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 fibrosis in the aged is modulated by p52Shc/NOX2.

10 f myofilament proteins via downregulation of NOX2.

11 mposed of two proteins: p22phox and gp91phox/NOX2.

12 rase activity by binding to two sites in the NOX2 3'-UTR.

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

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

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

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

17 The mechanism of Ang II-induced endothelial Nox2 activation in capillary damage was examined using p

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

19 In conclusion, Nox2 activation is an important mechanism in aging-relat

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 Clinical significance of aging-associated Nox2 activation, microgliosis and IL-1beta production wa

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

24 To study NOX2 activation, the interaction of p47(phox) (NOX2 regu

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

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

27 7(phox) phosphorylation, a critical step for NOX2 activation.

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

29 Listeria monocytogenes is able to avoid the NOX2 activity in phagosomes and escape to the cytosol.

30 Elevated Nox2 activity increased phospholamban phosphorylation in

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

32 dysfunction, oxidative stress, and increased Nox2, all of which were induced by Ang II in WT mice.

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

34 Nox2 also stabilizes TRPC3 proteins to enhance TRPC3 cha

35 si-NOX2 and antioxidant N-acetyl cysteine (NAC) reversed si

36 TTP also inhibited NOX2 and decreased the oxidative stress in vivo.

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

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

39 In vitro, recombinant Hhip increased Nox2 and NADPH activity and decreased insulin-positive b

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

41 It consists of two membranous (Nox2 and p22(phox)) and three cytosolic subunits (p40(ph

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

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

44 ng oxidative injury through the induction of NOX2 and the generation of mitochondrial reactive oxygen

45 ver, we find that expression changes in both NOX2 and TRPM8 mRNA predict poor clinical outcome in est

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

47 fold higher gut expression of NADPH oxidase (NOX2) and translocator protein (TSPO).

48 and current (I(Kur)) and F(2)-isoprostanes, NOX2, and PKC-alpha/delta expression and atrial fibrosis

49 hippocampal neuron cell death, and decreased NOX2- and NLRP3 inflammasome-associated neuroinflammatio

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

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

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

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

54 produced by NADPH oxidases (Noxes), such as Nox2, are key components of the macrophage response to i

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

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

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

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

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

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

61 In the absence of Nox2, baseline neurogenesis was unaffected, but the acti

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

63 Activationof NOX2 caused inflammasome activation as shown by NLRP3/AS

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

65 Here we demonstrate that NOX2 collapses the DeltapH of intracellular Salmonella T

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

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

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

69 p52Shc binding to p47(phox) , activating the NOX2 complex, more so at an older age.

70 se cells while use of mice lacking a crucial NOX2 component attenuated inflammatory pathology and red

71 Finally, NOX2 conditional deletion or overexpression respectively

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

73 Training decreased NOX2 content (arterioles P < 0.001; capillaries P < 0.00

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

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

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

77 In this article, we report that NOX2 controls systemic L. monocytogenes spread through m

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

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

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

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

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

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

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

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

86 NOX2 deficiency results in increased expression of IFN-s

87 Nox2 deficiency was associated with declines in the surv

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

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

90 at H(2)O(2) production in wild type (WT) and Nox2-deficient CD19(+) B cells was boosted concomitantly

91 ut a higher rate of proliferation than WT or Nox2-deficient cells.

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

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

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

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

96 We conclude that NOX2 deletion or pharmacological inhibition prevents the

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

98 rophages release IL-6 in an NADPH oxidase 2 (NOX2)-dependent manner, which signals through glycoprote

99 ic stretch to generation of NADPH oxidase 2 (NOX2)-dependent reactive oxygen species (ROS), signals w

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

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

102 Inhibition of Nox2-dependent oxidative stress attenuated the impaired

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

104 In conclusion, Nox2-dependent redox-signalling is crucial in microglial

105 iROS NPCs into proliferation via a transient Nox2-dependent ROS surge.

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

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

108 The clinical significance of Nox2-derived ROS in aging-related loss of cerebral capil

109 on-transgenic (HuNox2Tg) mice to investigate Nox2-derived ROS in brain aging.

110 In this study, we examined Nox2-derived ROS in mediating microglial response to Abe

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

112 2 months) had significantly higher levels of Nox2-derived ROS production, Abeta deposition, microglio

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

114 ther, these data identify leukemia-generated NOX2-derived superoxide as a driver of protumoral p16INK

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

116 or microenvironment is caused by AML-induced NOX2-derived superoxide.

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

118 itical for the activation of the catalytical NOX2 domain, and p47phox is a potential target for thera

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

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

121 ic signaling axis PKC-STAT3-NADPH oxidase 2 (NOX2), enhancing redox signaling as shown by redox prote

122 Microglia express constitutively a Nox2 enzyme that is involved in neuroinflammation by the

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

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

125 ering (si)-TTP RNA upregulated pro-oxidative NOX2 expression and ROS formation, downregulated anti-ox

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

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

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

129 translational modifications (PTMs), elevated NOX2 expression, altered Ca(2+) release dynamics (i.e. C

130 ule network density and properties, elevated NOX2 expression, altered calcium release dynamics, how N

131 2) markedly induced BV2 cell ROS production, Nox2 expression, p47(phox) and ERK1/2 phosphorylation, c

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

133 This is despite low levels of cardiac Nox2 expression.

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

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

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

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

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

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

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

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

142 on by altering islet integrity and promoting Nox2 gene expression in beta cells in response to HDF-me

143 stimulation of sodium palmitate (PA)-BSA on Nox2 gene expression.

144 of AF, we demonstrate that NADPH oxidase 2 (NOX2) generated oxidative injury causes upregulation of

145 endent mechanoactivation of NADPH oxidase 2 (NOX2)-generated reactive oxygen species (ROS), which act

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

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

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

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

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

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

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

153 These findings show that ROS generated by NOX2 in AML cells promotes glycolysis by activating PFKF

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

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

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

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

158 hway for direct activation of the phagocytic NOX2 in hepatocytes by p52Shc binding and activating the

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

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

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

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

163 Deleting Nox2 in myeloid cells or depleting GP130 in TNBC cells a

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

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

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

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

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

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

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

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

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

173 ted to the control levels in the presence of Nox2 inhibitor or superoxide scavenger.

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 c metabolism to arrhythmia and suggests that NOX2 inhibitors could be a novel therapy for heart rhyth

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

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

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

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

182 s (i.e. Ca(2+) sparks and Ca(2+) waves), how NOX2 is activated by and responds to stretch, and finall

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

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

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

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

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

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

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

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

191 ood, and establishing how the NADPH oxidase (NOX2) kills microbes has proven elusive.

192 ng-related changes were reduced or absent in Nox2 knockout aging mice.

193 knockout mice (NOX4betaKO) (though not from NOX2 knockout mice) and from NOX4-silenced or catalase-o

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

195 This study used littermates of WT and Nox2-knockout (Nox2KO) mice plus endothelial cell-specif

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

197 Thus, despite the established role of NOX2 limiting L. monocytogenes infection in mice, the un

198 TTP affected the NOX2 luciferase activity by binding to two sites in the

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

200 Mechanistically, NOX2 mediated peroxynitrite species were primary to infl

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

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

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

204 1-dependent activities were characterized by NOX2-mediated reactive oxygen species production.

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

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

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

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

209 ters from Duox1(-/-) mice relative to WT and Nox2(-/-) mice, whereas immunization with T cell-depende

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

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

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

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

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

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

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

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

218 t dopaminergic oxidative injury by promoting NOX2 mRNA degradation in the MPP(+) /MPTP model of PD, s

219 In addition, TTP reduced the NOX2 mRNA stability.

220 f TTP to 3'-untranslated regions (3'-UTR) of NOX2 mRNA.

221 The NOX2 NADPH oxidase (NOX2) produces reactive oxygen speci

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

223 Inactivation of NOX2 NADPH oxidase in Pstpip2(cmo) mice did not affect I

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

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

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

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

228 tive oxygen species generation by neutrophil NOX2 NADPH oxidase.

229 yde dehydrogenase 2 was reduced, whereas the NOX2 (NADPH [nicotinamide adenine dinucleotide phosphata

230 blood pressure, glucose, F(2)-isoprostanes, NOX2 (NADPH oxidase 2), and PKC (protein kinase C) were

231 of calcium homeostasis and heart rhythm by a NOX2 (NADPH oxidase 2)-dependent mechanism.

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

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

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

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

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

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

238 ontained higher levels of NOX5-but not NOX1, NOX2, or NOX4-with a bimodal distribution correlating wi

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

240 O) mice plus endothelial cell-specific human Nox2 overexpression-transgenic (HuNox2Tg) mice to invest

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

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

243 ased glucose consumption while inhibition of NOX2 oxidase decreased glucose consumption.

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

245 OS), arising from constitutive activation of NOX2 oxidase, occurs in >60% of patients with AML and th

246 NOX2 oxidative injury (1) underlies the onset, and the m

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

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

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

250 und that ROS production was dependent on the NOX2 phagocyte NADPH oxidase.

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

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

253 acological inhibition or genetic deletion of NOX2 prevented arrhythmogenic abnormalities in vivo duri

254 b39a also increases the levels of Sec22b and NOX2, previously recognized to participate in cross-pres

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

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

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

258 The NOX2 NADPH oxidase (NOX2) produces reactive oxygen species to kill phagosome

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

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

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

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

263 X2 activation, the interaction of p47(phox) (NOX2 regulatory subunit) and p52Shc was evaluated by pro

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

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

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

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

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

269 ignaling and a reduction of NADPH oxidase 2 (NOX2)/ROS production.

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

271 le polymerization by colchicine reduced both NOX2/ROS and oxidized CaMKII, increased S325/S328/S330 p

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

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

274 ce of AF, we performed targeted injection of NOX2 short hairpin RNA (followed by electroporation to f

275 Furthermore, animals treated with NOX2 short hairpin RNA did not develop sustained AF for

276 t of nonsustained AF increased by >5-fold in NOX2 short hairpin RNA-treated dogs.

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

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

279 ) and reduces its interaction stability with Nox2 subunit.

280 2(E62K) retains binding to an NADPH oxidase (NOX2) subunit, p67(phox), and to the RAC-binding domain

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

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

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

284 ndings report a novel antimicrobial role for NOX2 through modulation of type I IFN responses to contr

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

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

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

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

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

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

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

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

293 mRNA expression for the prooxidative enzyme, NOX2, was increased, while mRNA expression for the antio

294 6-3MR mouse model, we show that by targeting NOX2 we reduced BM stromal cell senescence and consequen

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

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

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

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

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

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