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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

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