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1 aflet of apoptotic cell membranes, and CD14 (LPS-binding protein).
2 ein and accessory proteins, such as CD14 and LPS binding protein.
3 s inhibited by anti-CD14 mAb and enhanced by LPS binding protein.
4 des directly inhibited the binding of LPS to LPS-binding protein.
5 anced by the addition of soluble CD14 and/or LPS-binding protein.
6 ses to LPS, and not to PGN, were enhanced by LPS-binding protein.
7 dependent and was not augmented by exogenous LPS-binding protein.
8 4-70Z/3 cells by H. pylori LPS also requires LPS-binding protein.
9 quires the presence of plasma containing the LPS-binding protein.
10 he 20S proteasome complex were identified as LPS-binding proteins.
11 opology of the "active-site" beta-strands of LPS-binding proteins.
13 nitially bound by transfer proteins, notably LPS binding protein and phospholipid transfer protein, a
14 by competing with E. coli LPS for binding to LPS-binding protein and by directly competing with E. co
15 man SR-BI orthologue, was determined to be a LPS-binding protein and endocytic receptor mediating the
16 and LPS-triggered responses were enhanced by LPS-binding protein and inhibited by an anti-CD14 monocl
18 These data indicate that MD-2 is a genuine LPS-binding protein and strongly suggest that MD-2 could
19 cells to LPS require a plasma protein called LPS-binding protein and the glycosylphosphatidylinositol
20 The structure reveals homology to eukaryotic LPS-binding proteins and allowed for the prediction of a
21 homologous to the LPS binding region of the LPS binding protein, and we demonstrated that two basic
22 no acid conservation, structural analysis of LPS-binding proteins, and MD simulations further confirm
23 d formed monomeric complexes with MD-2 in an LPS-binding protein- and CD14-dependent manner with simi
24 /CD18-transfected CHO-K1, thus implying that LPS-binding protein can also transfer LPS to CD11/CD18.
25 100A8; the acute-phase protein SAA3; and the LPS binding protein CD14 were confirmed by Northern blot
26 rotein and protein-protein interactions with LPS-binding protein, CD14, myeloid differentiation prote
27 assay, suggest that recombinant factor C, an LPS binding protein, competitively inhibits high-density
30 induction of APP, including serum amyloid A, LPS-binding protein, fibrinogen, or ceruloplasmin; in co
31 es demonstrated that these surface expressed LPS-binding proteins had characteristics that were quali
32 lease from the cells, high concentrations of LPS-binding protein have a modest effect, and phospholip
33 easing protein (BPI) and lipopolysaccharide (LPS)-binding protein, have been considered to be members
36 This study addresses the role of CD14 and LPS-binding protein in the cellular response to H. pylor
37 This cross-linker was used to identify the LPS-binding proteins in membranes of the murine-macropha
40 s of microbial translocation, as measured by LPS-binding protein, in PTM correlated with the rate of
41 receptor molecules in HCEP, that one of the LPS binding proteins is galectin-3, and that the outer c
42 that TECs express CD14, a well-characterized LPS-binding protein known to mediate many LPS responses.
50 d plasma levels of lipopolysaccharide (LPS), LPS binding protein (LBP), soluble CD14 (sCD14), and int
58 o closely related endogenous serum proteins, LPS-binding protein (LBP) and bactericidal/permeability-
59 We have investigated the effects of human LPS-binding protein (LBP) and human bactericidal/permeab
60 in, we found that two human plasma proteins, LPS-binding protein (LBP) and phospholipid transfer prot
61 popolysaccharide (LPS)-interactive proteins, LPS-binding protein (LBP) and the bacteridical/permeabil
66 sm(s) remains to be fully defined, the human LPS-binding protein (LBP) is known to regulate responses
68 lycosylphosphatidylinositol-anchored form of LPS-binding protein (LBP), a component of serum that bin
70 onses to LPS are markedly potentiated by the LPS-binding protein (LBP), a lipid-transfer protein that
71 cytokines as well as components of the LPS, LPS-binding protein (LBP), and CD14 system in bronchoalv
72 plex consisting of lipopolysaccharide (LPS), LPS-binding protein (LBP), and the cell surface antigen
73 , TLR4, and MD-2, which, in conjunction with LPS-binding protein (LBP), bind LPS to the virus and aug
74 ormation of the LPS receptor complex by LPS, LPS-binding protein (LBP), CD14, and toll-like receptor
75 by two closely related LPS-binding proteins, LPS-binding protein (LBP), which potentiates LPS' inflam
83 PS)) can be regulated by two closely related LPS-binding proteins, LPS-binding protein (LBP), which p
84 that TLR2 associates with the high-affinity LPS binding protein membrane CD14 to serve as an LPS rec
85 n a CD14-dependent manner, and soluble CD14, LPS binding protein, or their combination potentiated bo
87 contrast, the addition of recombinant human LPS-binding protein (rLBP) had opposing effects on the L
88 els of circulating lipopolysaccharide (LPS), LPS-binding protein, soluble CD14, and fucose-binding le
89 n-induced cytokine production was maximal at LPS-binding protein:soluble CD14 ratios <1, typically ob
90 dividuals with subclinical infection; higher LPS-binding protein:soluble CD14 ratios were inhibitory.
91 ons, in a defined medium containing purified LPS-binding protein, the LPS-deacylating activity of MNC
92 form complexes with a serum protein known as LPS-binding protein; the LPS in this complex is subseque
93 we show that LPS in the presence of serum or LPS binding protein triggers formation of CD14-CR3 compl
97 increasing protein (BPI) are closely related LPS-binding proteins whose binding to LPS has markedly d
98 iginally identified as a lipopolysaccharide (LPS) binding protein with gram-negative bactericidal act
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