ライフサイエンスコーパス: phox

1 he dimerization domains, but also included a phox-homology domain in the converter region.

2 hanges in expressions of NADPH oxidase gp91 (phox) subunit, alpha-smooth muscle actin (alpha-SMA), an

3 ed PA-induced free-radical production, gp91 (phox) expression, and NFkappaB p65 translocation in HepG

4 gp91(phox-/-) mice presented with higher percentages of healt

5 HMGB1 and genetic ablation of Mac1 and gp91(phox) (the catalytic submit of NADPH oxidase) blocked th

6 burst by downregulating rac1, rac2 and gp91(phox) transcription both in vitro and in vivo.

7 erence was comparable in p47(phox)- and gp91(phox)-deficient subtypes of CGD and independent of risk

8 Wild-type and gp91(phox-/-) mice were treated with the PPARgamma agonist pi

9 In contrast to wild-type animals, gp91(phox-/-) mice exhibited similar defects in MRSA clearanc

10 S3) protein, and (9) coronary arteriole gp91(phox) protein.

11 eracts with nascent NOX2 (also known as gp91(phox) and encoded by Cybb) monomer, one of the membrane-

12 ter protein expression of the catalytic gp91(phox) subunit and the obligate Rac1 protein.

13 , expressed the NADPH oxidase component gp91(phox).

14 ediated gene targeting of a single-copy gp91(phox) therapeutic minigene into one allele of the "safe

15 We sought to investigate how defective gp91(phox) expression in patients with CGD and CGD carriers m

16 ficient mice but not in NOX2-deficient (gp91(phox) (-/-)) mice.

17 NADPH oxidase-deficient (gp91(phox) knockout [KO]), iNOS-deficient (iNOS KO), and C57B

18 donium (DPI) or by genetically deleting gp91(phox), the key enzymatic component of NADPH oxidase, had

19 se model, mice transplanted with either gp91(phox)-deficient or p47(phox)-deficient bone marrow showe

20 A mutation in the CYBB gene encoding gp91(phox) leads to X-linked recessive CGD.

21 AB class M2) AML cells rarely expressed gp91(phox), did not produce ROS, and did not trigger NK or T-

22 species (ROS) generation resulting from gp91(phox) deficiency.

23 anes following infection with OpaD+ Gc. gp91(phox) and p22(phox) were recruited to Gc phagosomes rega

24 e spatially separated between granules (gp91(phox)/p22(phox)) and the cytoplasm (p47(phox), p67(phox)

25 However, gp91(phox) and p22(phox) reduced nicotinamide adenine dinucle

26 scued the accelerated NCGN phenotype in gp91(phox) bone marrow-deficient mice.

27 h) neutrophils early in inflammation in gp91(phox)(-/-) mice led to accelerated development of effero

28 e-1 activity and IL-1beta generation in gp91(phox)-deficient and p47(phox)-deficient monocytes compar

29 r blockade abrogated aggravated NCGN in gp91(phox)-deficient mice.

30 ciency in infection-driven apoptosis in gp91(phox-/-) mice versus WT mice.

31 Pathology in gp91(phox-/-) mice was not associated with alterations in CD4

32 mitochondrial (mt)ROS were deficient in gp91(phox-/-) phagocytes, their restoration with treatment si

33 Only infected gp91(phox) KO mice revealed significant loss of alveolar bone

34 in the murine oral cavities of infected gp91(phox) KO mice than in those of iNOS KO and C57BL/6 mice.

35 ighest loss of bone density in infected gp91(phox) KO mice.

36 nd restored CD95 expression on infected gp91(phox-/-) neutrophils.

37 so attenuated the increased ROS markers gp91(phox), 4-hydroxynonenal, and 3-nitrotyrosine.

38 Toll-like receptor (TLR)4 and Nox2 (gp91(phox)) deficiency prevented monocyte NADPH oxidase activ

39 ting the complex and facilitating Nox2 (gp91(phox)) ubiquitination and degradation.

40 NOX2/gp91(phox) is a catalytic subunit of NOX expressed in phagocy

41 in Nrf2(-/-) mice; whereas, Nrf2(-/-)//gp91(phox-/-) showed prolonged survival.

42 Cryo-immunogold labeling of gp91(phox) and CeCl(3) cytochemistry showed the presence of g

43 ockdown led to decreased recruitment of gp91(phox) and lysosomal-associated membrane protein-1 to pha

44 3) cytochemistry showed the presence of gp91(phox) and oxidant production in numerous small (<100 nm)

45 rts resulted in sustained expression of gp91(phox) and substantially restored neutrophil ROS producti

46 crease in plasma membrane expression of gp91(phox) in TNF-alpha-primed neutrophils, whereas TNF-alpha

47 ients confirmed a greater expression of gp91(phox) mRNA by FAB-M4/M5 AML cells than FAB-M1 cells (P <

48 e lyso-PS (lyso-PS(high)) than those of gp91(phox)(-/-) (lyso-PS(low)) mice.

49 Furthermore, transplantation of gp91(phox)/caspase-1 double-deficient bone marrow rescued the

50 C. glabrata isolates in spleens of gp91(phox-/-) knockout mice with reduced oxidative phagocyte

51 rmine whether pioglitazone treatment of gp91(phox-/-) mice enhanced phagocyte oxidant production and

52 sensing probes, short-term treatment of gp91(phox-/-) mice with pioglitazone enhanced stimulated ROS

53 thesized that pioglitazone treatment of gp91(phox-/-) mice, a murine model of human CGD, would enhanc

54 In vitro infection of gp91(phox-/-) versus WT neutrophils also revealed reduced apo

55 that were deficient in the p47(phox) or gp91(phox) subunits of NOX2 were partially protected from MOG

56 NAD(P)H] oxidase subunits (p47(phox) or gp91(phox)) or indoleamine-pyrrole 2,3-dioxygenase 1 with or

57 or NADPH oxidase 2, and encodes Nox2 or gp91(phox); neutrophil cytosol factor 1 and encodes p47 (phox

58 ared with levels of either wild-type or gp91(phox-/-) mice.

59 adenine dinucleotide phosphate oxidase (gp91(phox) or Nox2) is expressed in the heart.

60 se (CGD) mice that lack the gp91(phox) (gp91(phox-/-)) catalytic subunit show high mortality rates co

61 ressed in mice deficient for p47(phox), gp91(phox), or indoleamine-pyrrole 2,3-dioxygenase 1, suggest

62 AMacs from p47(phox-/-) mice can rescue gp91(phox-/-) mice during primary Lm infection.

63 due to the absence of the gp91 subunit (gp91(phox-/-)) had significantly more severe pathology in the

64 lso observed that NADPH oxidase subunit gp91(phox) was dispensable for stretch-induced cytokine produ

65 We found that gp91(phox)-containing NADPH oxidase activity in macrophages a

66 matous disease (CGD) mice that lack the gp91(phox) (gp91(phox-/-)) catalytic subunit show high mortal

67 th cells from mice lacking NOS-2 or the gp91(phox) component of NOX.

68 Macrophages lacking the gp91(phox) subunit of NOX2 fail to produce ROS upon FcgammaR

69 al that such alterations are related to gp91(phox) expression.

70 Using gp91(phox+/-) mosaic mice, we further demonstrate that influe

71 osomal compartment that co-labeled with gp91(phox), p40(phox), p67(phox), and Rab5, but not with the

72 wild-type mice and immunodeficient gp91(-/-) phox mice and was effective as a live vaccine in wild-ty

73 different genes, was determined in gp91(-/-) phox mice.

74 oxidant enzyme levels, such as iNOS and gp91-phox, thereby decreasing net oxygen radical production b

75 inducible nitric oxide synthase (iNOS), gp91-phox, and 3-nitrotyrosine were detected in ischemic woun

76 HD(140Q/140Q) mice bred to gp91-phox knock-out mice had lower NOX activity in the brain

77 zed at plasma membrane lipid rafts with gp91-phox, a catalytic subunit for the NOX2 isoform.

78 X31, share with SNX17 next to their obligate phox domain a FERM domain, which may enable them to bind

79 Sorting nexins (SNXs) or phox homology (PX) domain containing proteins are centra

80 p22(phox)-mediated inactivation of tuberin is associated wit

81 We also observed that NOX4 and p22(phox) localize to the nuclear membrane in MV4-11 cells e

82 ogether these data indicate that NOX and p22(phox) mediate the ROS production from FLT3-ITD that sign

83 However, gp91(phox) and p22(phox) reduced nicotinamide adenine dinucleotide phosphat

84 induced through p16-Rb-regulated E2F and p22(phox) was induced by Kras(G12V)-activated NF-kappaB.

85 infection with OpaD+ Gc. gp91(phox) and p22(phox) were recruited to Gc phagosomes regardless of bact

86 a higher protein level of p22(phox) and p22(phox)-interacting NOX isoforms than 32D cells transfecte

87 hat reactive oxygen species, mediated by p22(phox)-based Nox oxidases, are enhanced in VHL-deficient

88 The chronic group, which included C1qB, p22(phox) and galectin-3, showed peak expression at 7 days a

89 is factor-alpha (or high glucose), C242T p22(phox) significantly inhibited tumor necrosis factor-alph

90 ular endothelial cells showed that C242T p22(phox) significantly reduced Nox2 expression but had no s

91 2T single-nucleotide polymorphism causes p22(phox) structural changes that inhibit endothelial Nox2 a

92 e of the 4 genes encoding the components p22(phox), p47(phox), p67(phox), and p40(phox) of the leukoc

93 bligatory NOX dimerization partner Cyba (p22(phox)).

94 translocation of Rac1 and downregulating p22(phox) through a phosphoinositide 3-kinase/Akt-mediated m

95 es (cytochrome b light chain and encodes p22(phox) protein; cytochrome b-245 or NADPH oxidase 2, and

96 phorylation to expose the SH3 pocket for p22(phox) binding.

97 ve, and further defined a novel role for p22(phox)-based Nox oxidases in eIF4E-dependent mRNA transla

98 this adaptor protein within noncanonical p22(phox) or CARD9 complexes that regulate oxidative and cyt

99 FLT3-ITD, have a higher protein level of p22(phox) and p22(phox)-interacting NOX isoforms than 32D ce

100 ral changes in the extracellular loop of p22(phox) and reduces its interaction stability with Nox2 su

101 ly, we find that marked up-regulation of p22(phox) in human renal cell carcinoma correlates with incr

102 ide the first evidence that silencing of p22(phox) reduces HIF-2alpha-dependent gene targeting in vit

103 ) phosphorylation and elevated levels of p22(phox) subunit of the NADPH oxidases (NOXs), and fibrotic

104 in post-translational down-regulation of p22(phox), a small membrane-bound subunit of the NADPH oxida

105 translation and examined the effects of p22(phox)-based Nox oxidases on TORC2 regulation.

106 C13-4 is necessary for the regulation of p22(phox)-expressing granule trafficking to the plasma membr

107 aeruginosa despite normal trafficking of p22(phox)-expressing vesicles toward the phagosome.

108 through transcriptional up-regulation of p22(phox).

109 y separated between granules (gp91(phox)/p22(phox)) and the cytoplasm (p47(phox), p67(phox), and p40(

110 The inhibition of NOX proteins, p22(phox), and NOX protein knockdowns caused a reduction in

111 the NADPH oxidase components e.g. Rac1, p22(phox), p67(phox), and NOXO1 in A549 cells impaired TPA-i

112 and known activators of NOX (Rac1, Rac2, p22(phox), and p47(phox)) contribute to nuclear O(2)(.-) pro

113 hosphate p22 phagocytic oxidase subunit (p22(phox)) cytochrome b alpha gene (CYBA) C242T, crystalliza

114 ch overexpress the NADPH oxidase subunit p22(phox) in smooth muscle, and mice with vascular-specific

115 ation of NOX4 requires catalytic subunit p22(phox), which is upregulated following Kras activation.

116 ingly, stable silencing of NOX subunits, p22(phox) and p47(phox), in HK-2 cells blocked TGF-beta1-ind

117 Our data provide the first evidence that p22(phox)-based Nox oxidases maintain HIF-2alpha protein exp

118 le-nucleotide polymorphism, C242T of the p22(phox) subunit of NADPH oxidase, has been reported to be

119 phox) membrane translocation, binding to p22(phox) and endothelial O2(.-) production in response to a

120 42T effects were further confirmed using p22(phox) short-hairpin RNA-engineered HeLa cells and Nox2(-

121 dase genes, e.g., Lpo (lactoperoxidase), p22-phox, p47-phox, and Gp91, in NHK/B0 but their expression

122 NADPH oxidase components p47 (phox) and p40 (phox) in comparison with non-CF MDMs.

123 neutrophil cytosol factor 4 and encodes p40 (phox) protein; and Ras-related C3 botulinum toxin substr

124 dies reveal a role for NADPH oxidase and p40(phox) in skewing epitope selection and T cell recognitio

125 nts p22(phox), p47(phox), p67(phox), and p40(phox) of the leukocyte nicotinamide dinucleotide phospha

126 the cytoplasm (p47(phox), p67(phox), and p40(phox)).

127 strongly dephosphorylated p47(phox) and p40(phox), but not p67(phox), in vitro.

128 ally arising mutations, which compromise p40(phox) function in a chronic granulomatous disease patien

129 etically deficient mice to elucidate how p40(phox), one subunit of the NADPH oxidase complex, functio

130 epitopes from membrane Ag was robust in p40(phox)-deficient B cells.

131 ells with a wild-type, but not a mutant, p40(phox) allele restored exogenous Ag presentation and intr

132 ed in human B cells with reduced oxidase p40(phox) subunit expression.

133 artment that co-labeled with gp91(phox), p40(phox), p67(phox), and Rab5, but not with the secondary g

134 We show that p40(phox) deficiency enhances inflammation in both dextran s

135 We propose that p40(phox) deficiency enhances intestinal inflammation throug

136 ive bioinformatic approach, we show that p40(phox) deficiency leads to upregulation of chemokine rece

137 hase of intestinal inflammation and that p40(phox) expression is necessary for this restitution.

138 phorylation of NADPH oxidase components p47 (phox) and p40 (phox) in comparison with non-CF MDMs.

139 neutrophil cytosol factor 1 and encodes p47 (phox) protein; neutrophil cytosol factor 2 and encodes p

140 p47(phox) C-terminal tail plays a key role in stabilizing in

141 p47(phox) interacts with cytosolic cortactin by coimmunoprec

142 Stable shut down of miR-21, p47(phox) or STAT3 and overexpression of PDCD4 or catalase i

143 Here, we utilized a p47(phox) knock-out mouse model, in which an essential cytos

144 al-regulated kinase 1 (ERK1)/2 abrogated p47(phox) phosphorylation by gAcrp30.

145 nd co-localization between cortactin and p47(phox) at the cell periphery and ROS production, whereas

146 between excessive acute inflammation and p47(phox) deficiency in macrophages.

147 sion, inducible oxidative metabolism and p47(phox) expression.

148 inase-mediated translocation of Rac1 and p47(phox) from the cytosol to the membranes.

149 es the interaction between cortactin and p47(phox) that plays a role in the assembly and activation o

150 -phosphorylated cortactin, MLC, Src, and p47(phox) to caveolin-enriched microdomains (CEM), whereas s

151 ators of NOX (Rac1, Rac2, p22(phox), and p47(phox)) contribute to nuclear O(2)(.-) production in isol

152 and regulatory sub-units (NOX1, NOX2 and p47(phox)).

153 scopic dual labeling for vasopressin and p47(phox), a cytoplasmic NADPH oxidase subunit requiring mob

154 Rac1 and p47(phox), cytosolic components of NOX2, translocated to the

155 silencing of NOX subunits, p22(phox) and p47(phox), in HK-2 cells blocked TGF-beta1-induced pATM(Ser1

156 e studies, we treated wild-type (WT) and p47(phox)-deficient mice with LPS to investigate mechanisms

157 a generation in gp91(phox)-deficient and p47(phox)-deficient monocytes compared with wild-type monocy

158 ROS generation in bone marrow cells and p47(phox)-Nox2 signaling in osteoblastic cells, 2-year-old p

159 bserved in p47(phox-/-) macrophages, and p47(phox-/-) mice exhibit increased inflammation and fibrosi

160 y Lm infection were protective in WT and p47(phox-/-) mice that were rechallenged with secondary leth

161 mouse macrophages (C57BL/6, BALB/c, and p47(phox-/-)) and macrophage cell lines (RAW 264.7 and IC21)

162 her in apoE(-/-) compared with apoE(-/-)/p47(phox-/-) mice.

163 gle mutation of S379A completely blocked p47(phox) membrane translocation, binding to p22(phox) and e

164 acute hypoxia-reoxygenation by blocking p47(phox) phosphorylation, a critical step for NOX2 activati

165 s of the protective function provided by p47(phox-/-) AAMacs against Lm infection are enhanced produc

166 In contrast, p47(phox) phosphorylation was inhibited by Acrp30 in associa

167 gp91(phox)/p22(phox)) and the cytoplasm (p47(phox), p67(phox), and p40(phox)).

168 p47(phox) and a decrease in cytoplasmic p47(phox) in PVN AVP dendrites.

169 In contrast, AngII infusion decreased p47(phox) immunolabeling on the plasma membrane (-35.5 +/- 1

170 genes (Lm), whereas p47(phox)-deficient (p47(phox-/-)) CGD mice show survival rates that are similar

171 uctural analysis of the PVN demonstrated p47(phox) immunolabeling in many glial and neuronal profiles

172 purified AcpA strongly dephosphorylated p47(phox) and p40(phox), but not p67(phox), in vitro.

173 icantly suppressed in mice deficient for p47(phox), gp91(phox), or indoleamine-pyrrole 2,3-dioxygenas

174 g II failed to stimulate O. in TALs from p47(phox) -/- mice (p < 0.02).

175 erived macrophages (BMDMs) isolated from p47(phox)(-/-)/HLL mice showed enhanced LPS-stimulated NF-ka

176 re, the adoptive transfer of AAMacs from p47(phox-/-) mice can rescue gp91(phox-/-) mice during prima

177 Notably, anti-serum samples from p47(phox-/-) mice that survived secondary Lm infection were

178 e, adoptive transfer of macrophages from p47(phox-/-) mice, and an isolated perfused lung edema model

179 preparing cortical neuron cultures from p47(phox-/-) mice, which are unable to form a functional NOX

180 re of primary fetal calvarial cells from p47(phox-/-) mice.

181 Adoptive transfer of iNKT cells from p47(phox-/-) or NOX2(-/-) mice to Jalpha18(-/-) (iNKT cell-d

182 mputational structural model of the full p47(phox) protein.

183 Furthermore, p47(phox-/-) DCs pulsed with Lm and adoptively transferred i

184 However, p47(phox)KO hearts showed impaired interaction of cortactin

185 Contrary to our hypothesis, p47(phox)KO mice showed markedly worsened systolic dysfuncti

186 pient mice had a significant increase in p47(phox) immunolabeling on endomembranes just beneath the p

187 in livers from wild-type mice but not in p47(phox) knock-out mice.

188 membrane, with a concomitant increase in p47(phox) phosphorylation.

189 n of LPS, ROS generation was impaired in p47(phox)(-/-) mice, whereas these mice had increased neutro

190 ited LPS-induced NF-kappaB activation in p47(phox)(-/-)/HLL BMDMs but not in WT/HLL cells.

191 nditions showed increased DNA binding in p47(phox)(-/-)/HLL BMDMs, suggesting that ROS production red

192 factor 1 (Ref-1) levels were present in p47(phox)(-/-)/HLL compared with WT BMDMs, pointing to NADPH

193 This difference was comparable in p47(phox)- and gp91(phox)-deficient subtypes of CGD and inde

194 However, in p47(phox)-deficient cases and in 5 other AR cases with high

195 erved age-related switch of bone mass in p47(phox)-deficient mice occurs through an increased inflamm

196 regulated N-cadherin and beta-catenin in p47(phox)KO hearts but disrupted the actin filament cytoskel

197 mtROS production is also observed in p47(phox-/-) macrophages, and p47(phox-/-) mice exhibit incr

198 type controls, loss of Nox2 function in p47(phox-/-) mice resulted in age-related switch of bone mas

199 higher specific antibody (Ab) titers in p47(phox-/-) mice than wild-type (WT) mice.

200 ed macrophage differentiation program in p47(phox-/-) mice that favors the production of higher level

201 ed with live Lm and sustained in vivo in p47(phox-/-) mice.

202 on is a molecular switch which initiates p47(phox) conformational changes and NADPH oxidase-dependent

203 g either pharmacologic inhibitors or its p47(phox) subunit deficient mouse BMDM also attenuated LPS-i

204 onic hyperglycemia and lack of leukocyte p47(phox) (Akita/Ncf1) bred from C57BL/6-Ins2(Akita)/J (Akit

205 Eight-week-old male p47(phox) null (p47(phox) knockout [KO]), Nox2 null (Nox2KO)

206 including the use of p47(phox-/-) mice, p47(phox-/-) bone marrow chimera mice, adoptive transfer of

207 utation in Ncf1, which encodes the NCF1 (p47(phox)) subunit of NOX2, have defective phagocyte NOX2 ac

208 istribution of the organizer/adapter NOX p47(phox) subunit is altered in PVN dendrites following AngI

209 Eight-week-old male p47(phox) null (p47(phox) knockout [KO]), Nox2 null (Nox2KO), and wild-type

210 h HMGB1 led to membrane translocation of p47(phox) (a cytosolic subunit of NADPH oxidase) and consequ

211 din-1 also stimulated phosphorylation of p47(phox) (an organizer subunit for nicotinamide adenine din

212 henotype with up-regulated expression of p47(phox) , a component of the NOX2 complex critical for rea

213 rc-dependent tyrosine phosphorylation of p47(phox) and cortactin.

214 ed increased intraplatelet expression of p47(phox) and superoxide dismutase-1, suggesting a mechanist

215 e subunits and membrane translocation of p47(phox) are down-regulated, and G6pc3(-/-) macrophages exh

216 e discovered that the C-terminal tail of p47(phox) is critical for stabilizing its autoinhibited stru

217 information, the mechanistic insight of p47(phox) phosphorylation in NADPH oxidase activation remain

218 We showed a novel role of p47(phox) subunit beyond and independent of nicotinamide ade

219 We hypothesized that loss of p47(phox) subunit will result in decreased reactive oxygen s

220 of proinflammatory cytokines in lungs of p47(phox)(-/-)/HLL mice compared with controls.

221 DC) in association with the induction of p47(phox), a cytosolic component of the ROS producing enzyme

222 ith increased cell-surface expression of p47(phox), a cytosolic regulatory subunit of the NADPH oxida

223 low) , and up-regulate the expression of p47(phox).

224 ted mutagenesis and gene transfection of p47(phox-/-) coronary microvascular cells.

225 mentary methodology including the use of p47(phox-/-) mice, p47(phox-/-) bone marrow chimera mice, ad

226 h increased bone formation in 6-week-old p47(phox-/-) mice but decreased in 2-year-old p47(phox-/-) m

227 naling in osteoblastic cells, 2-year-old p47(phox-/-) mice showed increased senescence-associated sec

228 hox-/-) mice but decreased in 2-year-old p47(phox-/-) mice.

229 nted with either gp91(phox)-deficient or p47(phox)-deficient bone marrow showed accelerated disease w

230 umoral immunity in the phagocyte oxidase p47(phox)-deficient model of CGD and found that UV-inactivat

231 he increase in amounts of phosphorylated p47(phox) upon stimulation.

232 Levels of phosphorylated p47(phox), active Rac1, Nox activity, ROS generation, Jun NH

233 genes encoding the components p22(phox), p47(phox), p67(phox), and p40(phox) of the leukocyte nicotin

234 ignificant increase in near plasmalemmal p47(phox) and a decrease in cytoplasmic p47(phox) in PVN AVP

235 males and males in the near plasmalemmal p47(phox) on AVP dendrites seen in the present study.

236 males and males in the near plasmalemmal p47(phox) on AVP dendrites seen in the present study.

237 ngiotensin II receptor type 1 [AT(1)R]), p47(phox) NADPH oxidase subunit, beta-myosin heavy chain iso

238 ment, platelet isoprostanes, Nox2, Rac1, p47(phox), and protein kinase C, starting 2 hours after admi

239 d thromboxane A(2), platelet Nox2, Rac1, p47(phox), protein kinase C, vasodilator-stimulated phosphop

240 We demonstrate that reduced p47(phox) expression in IC21 macrophages is linked to enhanc

241 idase activation as evidenced by reduced p47(phox) phosphorylation in TLR4 deficient animals.

242 Notably, restoring p47(phox) protein expression levels reverts the p47(phox)-de

243 The observed robust p47(phox-/-) mouse humoral response was recapitulated with l

244 Furthermore, HGF stimulated p47(phox)/Cortactin/Rac1 translocation to lamellipodia and R

245 tory protein expression in Lm-stimulated p47(phox-/-) dendritic cells (DCs) relative to WT DCs.

246 expression of the NADPH oxidase subunit p47(phox), phosphorylated and total p38 mitogen-activated pr

247 de phosphate [NAD(P)H] oxidase subunits (p47(phox) or gp91(phox)) or indoleamine-pyrrole 2,3-dioxygen

248 cultures at low density with GFP-tagged p47(phox) to reconstitute NOX2 activity in widely scattered

249 ivation with apocynin or siRNA targeting p47(phox ) (a subunit of NADPH oxidase) attenuated the incre

250 Our results indicate that p47(phox) is a previously unrecognized regulator for IL-4 si

251 sed inflammatory milieu in bone and that p47(phox)-Nox2-dependent physiological ROS signaling suppres

252 analysis of this process indicates that p47(phox-/-) macrophages are hyperresponsive to IL-4 and sho

253 ubunits to membranes, in particular, the p47(phox) "organizing" subunit, to prevent assembly of the h

254 ever, we observed that deficiency of the p47(phox) component of NADPH oxidase in macrophages was asso

255 The p47(phox) is a key regulatory subunit of NADPH oxidase; howe

256 , I-A(b) mice that were deficient in the p47(phox) or gp91(phox) subunits of NOX2 were partially prot

257 ribe the PI(3,4)P(2) binding mode of the p47(phox) PX domain as identified by a transferred cross-sat

258 The p47(phox) PX domain preferably binds phosphatidylinositol 3,

259 cal phosphoinositide-binding site on the p47(phox) PX domain suggest that different types of phosphoi

260 osphoinositides sequentially bind to the p47(phox) PX domain, allowing the regulation of the multiple

261 n requires membrane translocation of the p47(phox) subunit and is linked to heart failure.

262 ile salts induces phosphorylation of the p47(phox) subunit of NOX2 and its translocation to the cellu

263 96G>A; p.Arg90His) in NCF1, encoding the p47(phox) subunit of the phagocyte NADPH oxidase (NOX2), as

264 x) protein expression levels reverts the p47(phox)-dependent AAMac phenotype.

265 ) cells with arsenic induces ROS through p47(phox), one of the NOX subunits that is the key source of

266 Thus ROS and the PKC-zeta to p47(phox) interaction are valid therapeutic targets to block

267 we demonstrate that a novel PKC-zeta to p47(phox) interaction is required for ROS production in canc

268 with TNF-alpha inhibited the PKC-zeta to p47(phox) interaction, inhibited ROS production, degraded PK

269 1 inhibited ROS production by binding to p47(phox), a critical component of the NADPH oxidase complex

270 educed NF-kappaB activity in LPS-treated p47(phox)(-/-)/HLL BMDMs.

271 Compared with wild-type p47(phox) cDNA transfected cells, the single mutation of S37

272 ith Listeria monocytogenes (Lm), whereas p47(phox)-deficient (p47(phox-/-)) CGD mice show survival ra

273 ess or cell death in the nontransfected, p47-phox(-/-) cultures, but did produce oxidative stress and

274 atrial fibrillation showed NADPH oxidase p47-phox subunit protein and mRNA expression 38.4% and 35.7%

275 , e.g., Lpo (lactoperoxidase), p22-phox, p47-phox, and Gp91, in NHK/B0 but their expression was almos

276 sphorylation of the NOX2 component, p47phox (phox: phagocyte oxidase), on its mitogen-activated prote

277 neutrophil cytosol factor 2 and encodes p67 (phox) protein; neutrophil cytosol factor 4 and encodes p

278 activation and 1 membrane-bound Rac1 and p67(phox) subunit.

279 B. p67(phox) terminates the phospholipase A2-derived signal for

280 By isothermal titration calorimetry, p67(phox) bound strongly to phosphoPrdx6 but bound poorly to

281 rylated p47(phox) and p40(phox), but not p67(phox), in vitro.

282 Association of p67(phox) and phosphoPrdx6 in intact MPMVECs after angiotens

283 fic antibodies, coimmunoprecipitation of p67(phox) and phosphorylated Prdx6 was demonstrated with lys

284 X2 activity in terms of translocation of p67(phox) to the membrane and ROS production; this effect wa

285 with angiotensin II; the interaction of p67(phox) with nonphosphorylated Prdx6 was relatively weak.

286 increased by 85% following knockdown of p67(phox) with siRNA.

287 was decreased by >98% in the presence of p67(phox); the calculated dissociation constant (Kd) of the

288 ut bound poorly to Prdx6; phosphorylated p67(phox) did not bind to either Prdx6 or phosphoPrdx6.

289 oxidase components e.g. Rac1, p22(phox), p67(phox), and NOXO1 in A549 cells impaired TPA-induced MnSO

290 ing the components p22(phox), p47(phox), p67(phox), and p40(phox) of the leukocyte nicotinamide dinuc

291 p22(phox)) and the cytoplasm (p47(phox), p67(phox), and p40(phox)).

292 t co-labeled with gp91(phox), p40(phox), p67(phox), and Rab5, but not with the secondary granule mark

293 These data indicate that p67(phox) binds to phosphoPrdx6 and inhibits its PLA2 activi

294 ulated dissociation constant (Kd) of the p67(phox): phosphoPrdx6 complex was 65 nM.

295 vestigated the interaction of Prdx6 with p67(phox) and its effect on NOX2 activity.

296 geted to membranes through an N-terminal PX (phox homology) domain.

297 Although the PX (phox homology) domain alone binds PI3P, we theorized tha

298 Crystal structures of the SNX5 phox-homology (PX) domain in complex with IncE define th

299 ation, which requires the interaction of the phox homology (PX) domain of Tks5 with PI(3,4)P2.

300 Their phox homology (PX) domain acts as a phosphoinositide (PI