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1 gp91(phox) and p67(phox) (in which "phox" is phagocyte oxidase).
2 g is lacking in the absence of a functioning phagocyte oxidase.
3 e reactive oxygen species generated by NADPH phagocyte oxidase.
4 ofound block in superoxide production by the phagocyte oxidase.
5 etely reversed in mice lacking both iNOS and phagocyte oxidase.
6 gamma-regulated macrophage mechanism-iNOS or phagocyte oxidase.
7 ve oxygen species but was independent of the phagocyte oxidase.
9 d CGD, in which high-level reconstitution of phagocyte oxidase activity may be important for full cor
11 munity help explain an apparent paradox: the phagocyte oxidase and inducible nitric oxide synthase ar
12 n activated primary macrophages lacking both phagocyte oxidase and inducible nitric oxide synthase.
13 eactive oxygen intermediate (ROI)-generating phagocyte oxidase and the reactive nitrogen intermediate
14 regulatory proteins during activation of the phagocyte oxidase, and its translocation to the membrane
15 licited host defense proteins, including the phagocyte oxidase, antimicrobial peptides, and autophagy
17 (iNOS) knockout (KO) and respiratory burst (phagocyte oxidase)-deficient chronic granulomatous disea
22 ella appears to be linked to an active NADPH phagocyte oxidase enzymatic complex, since the flavoprot
23 homologues of the catalytic component of the phagocyte oxidase, gp91phox, were identified in various
24 b1, YOTB/ZK632.12, Vac1, and EEA1) and Vam7p phagocyte oxidase homology domains, which are revealed t
27 stimulated macrophages from mice lacking the phagocyte oxidase inhibited escape from vacuoles by the
30 ctive oxygen species (ROS) produced by NADPH phagocyte oxidase isoform (NOX2) are critical for the el
31 earance of H. pylori from interleukin-10 and phagocyte oxidase mice, provide evidence that severe inf
32 VSMCs) derived from wild-type (p47phox(+/+); phagocyte oxidase) mice with those from mice that lack p
34 lation of the NOX2 component, p47phox (phox: phagocyte oxidase), on its mitogen-activated protein kin
35 glycemia induced Nox4, but not Nox1, and p22 phagocyte oxidase (p22phox) expression and IGF-I stimula
36 Herein, we evaluated humoral immunity in the phagocyte oxidase p47(phox)-deficient model of CGD and f
41 oduction of reactive oxygen intermediates by phagocyte oxidase (phox) and reactive nitrogen intermedi
42 ne that reversibly blocked the activation of phagocyte oxidase (phox) in human neutrophils in respons
43 which is dependent on the respiratory burst phagocyte oxidase (phox) is succeeded by a prolonged nit
48 of the CYBB and NCF2 genes, which encode the phagocyte oxidase proteins gp91(PHOX) and p67(PHOX), res
50 nt in inducible nitric oxide synthase and/or phagocyte oxidase revealed that these two antimicrobial
52 1phox(-/-) mice that lack a functional NADPH phagocyte oxidase, suggesting that sigma(E) plays an imp
53 ologous to gp91(phox) (91-kDa subunit of the phagocyte oxidase), the electron-transporting subunit of
54 cleotide (phosphate) oxidases related to the phagocyte oxidase, the Nox/Duox family, provides additio
55 rget cells but at the same time activate the phagocyte oxidase to generate microbicidal products in i
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