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) knockout (KO) and control mice had similar GAS num

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

68 rd the internalized parasite via NOX-2 (gp91-phox) activation.

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

70 compared with WT parasites was lost in gp91-phox (-/-) macrophages, underscoring the role of O(2) (*

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

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

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

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

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

76 Rac1 and p22(phox) knockdown abrogated free radical generation by TGF

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

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

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

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

81 It consists of two membranous (Nox2 and p22(phox)) and three cytosolic subunits (p40(phox), p47(phox

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

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

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

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

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

87 2T single-nucleotide polymorphism causes p22(phox) structural changes that inhibit endothelial Nox2 a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

105 is was also completely bypassed by Rac1, p22(phox), p47(phox), and PAI-1 silencing.

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

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

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

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

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

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

112 42T effects were further confirmed using p22(phox) short-hairpin RNA-engineered HeLa cells and Nox2(-

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

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

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

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

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

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

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

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

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

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

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

124 l chronic granulomatous disease subtype (p40(phox)-deficiency) imply that ROS generated in intracellu

125 p22(phox)) and three cytosolic subunits (p40(phox), p47(phox), and p67(phox)) that undergo structural

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

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

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

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

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

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

132 Expression of Akt3 in p47 (phox-/-) MEFs failed to induce ROS and to inhibit cell p

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

134 p47(phox) interacts with cytosolic cortactin by coimmunoprec

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

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

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

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

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

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

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

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

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

144 prevented translocation of p67(phox) and p47(phox) to the membrane, resulting in decreased NADPH oxid

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 V2 cell ROS production, Nox2 expression, p47(phox) and ERK1/2 phosphorylation, cell proliferation and

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

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

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

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

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

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

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

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

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

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

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

175 s P < 0.001), but there was no change in p47(phox) content (arterioles P = 0.101; capillaries P = 0.3

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

197 the neutrophil cytosolic factor 1 (Ncf1)/p47(phox) gene, which encodes a component of the NADPH oxida

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

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

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

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

202 tudy NOX2 activation, the interaction of p47(phox) (NOX2 regulatory subunit) and p52Shc was evaluated

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

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

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

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

207 ot by the phosphorylation site mutant of p47(phox) In agreement with these observations, Akt3 up-regu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

223 Lastly, an in silico model of p52Shc/p47(phox) interaction using RosettaDock was generated.

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

225 and three cytosolic subunits (p40(phox), p47(phox), and p67(phox)) that undergo structural changes du

226 completely bypassed by Rac1, p22(phox), p47(phox), and PAI-1 silencing.

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

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

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

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

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

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

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

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

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

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

237 phorylation of the NADPH oxidase subunit p47(phox), which results in NADPH oxidase activation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

254 96G>A; p.Arg90His) in NCF1, encoding the p47(phox) subunit of the phagocyte NADPH oxidase (NOX2), as

255 tes by p52Shc binding and activating the p47(phox) subunit that results in redox stress and accelerat

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

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

258 Palmitate-induced p52Shc binding to p47(phox) , activating the NOX2 complex, more so at an older

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

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

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

262 1 inhibited ROS production by binding to p47(phox), a critical component of the NADPH oxidase complex

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

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

265 feration defect was rescued by wild-type p47(phox), but not by the phosphorylation site mutant of p47

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

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

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

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

270 reduced NAD phosphate oxidase component p67 (phox) , activates neutrophil superoxide production, wher

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

272 olic subunits (p40(phox), p47(phox), and p67(phox)) that undergo structural changes during enzyme act

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

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

275 67(phox), and prevented translocation of p67(phox) and p47(phox) to the membrane, resulting in decrea

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

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

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

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

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

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

282 the cytosolic subunit of NADPH oxidase, p67(phox), and prevented translocation of p67(phox) and p47(

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

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

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

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

287 ding to an NADPH oxidase (NOX2) subunit, p67(phox), and to the RAC-binding domain of p21-activated ki

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

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

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

291 Ala mutant of PPE2 did not interact with p67(phox) and thereby did not affect ROS generation.

292 to be critical for its interaction with p67(phox) Trp236Ala mutant of PPE2 did not interact with p67

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

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

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

296 hairpin, which binds a site in the SNX5/SNX6 phox homology domains.

297 -BARs and CI-MPR or IGF1R is mediated by the phox-homology (PX) domain of SNX5 or SNX6 and a bipartit

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

299 ng loop of PCNA interacted directly with the phox homology (PX) domain of the p47phox.

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