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1 (TLR4) and LPS and is a critical part of the LPS receptor.
2 nly two signalling pathways emanate from the LPS receptor.
3 R4 carbohydrates in LPS cross-linking to the LPS receptor.
4 logical activity, appears to be a functional LPS receptor.
5 a 55-kDa protein, has been identified as an LPS receptor.
6 ugh membrane CD14 (mCD14), a proinflammatory LPS receptor.
7 ike protein was previously known to bind the LPS receptor.
8 3 (polyinosinic-polycytidylic acid) or TLR4 (LPS) receptor.
9 ophages through the CD14 lipopolysaccharide (LPS) receptor.
10 fy components of the putatively shared Taxol/LPS receptor, a novel, photoactivatable Taxol analogue w
11 lthough CD14 has been identified as the main LPS receptor, accumulating evidence has suggested the po
15 receptor 4 (Tlr4) is the lipopolysaccharide (LPS) receptor and biochemical evidence that Tlr4 confers
16 eracts with ligand-binding protein and CD14 (LPS receptor) and activates expression of inflammatory g
18 the patient's monocytes expressed CD14, the LPS receptor, and bound LPS in a specific manner, but fa
19 uman neutrophils occurs via CD14, a proposed LPS receptor, and requires the presence of plasma contai
20 l. report that caspases 4/5/11 are cytosolic LPS receptors, becoming activated through oligomerizatio
21 h requires the cytosolic lipopolysaccharide (LPS) receptor caspase-11 and antagonizes IFN-I productio
23 a high affinity to monocytes but not to the LPS receptor CD14, and experiments performed at 4 degree
26 ing expression of either lipopolysaccharide (LPS) receptor CD14 or myeloid differentiation protein-88
28 by overexpression of the lipopolysaccharide (LPS) receptors CD14 and TLR4, which antagonize each othe
29 if LPS stimulation was mediated through the LPS receptor, CD14, surface receptors on HGF were assess
31 showed that monocytic TM interacted with the LPS receptors, CD14 and TLR4/myeloid differentiation fac
34 anscription factors, is the formation of the LPS receptor complex by LPS, LPS-binding protein (LBP),
35 TLR4.myeloid differentiation factor 2 (MD-2) LPS receptor complex is strongly activated by hexa-acyla
36 t that a signal transduction molecule in the LPS receptor complex may belong to the IL-1 receptor/tol
37 ding the function and biology of the corneal LPS receptor complex may lead to novel therapies for the
38 lls are capable of expressing the functional LPS receptor complex proteins, CD14 and Toll-like recept
40 ctions as the transmembrane component of the LPS receptor complex, an unduplicated pathway for the de
41 binding protein membrane CD14 to serve as an LPS receptor complex, and that LPS treatment enhances th
42 luable tools to characterize elements in the LPS receptor complex, as well as to activate or inhibit
43 ith decreased cell surface expression of the LPS receptor complex, Toll-like receptor 4 (TLR4)/MD-2.
49 uggests that the functional integrity of the LPS receptor depends both on the surface expression of a
51 e deletions essentially ablated soluble CD14 LPS receptor function, whereas only two of the deletions
57 (TLR4) is an important lipo-polysaccharide (LPS) receptor in gastric epithelial cell signaling trans
61 e receptor 4 (Tlr4), the lipopolysaccharide (LPS) receptor, is sufficient to induce nuclear factor ka
62 either lacking or expressing human CD14 (the LPS receptor), it was observed that expression of human
63 smic LptD beta-taco domain that functions as LPS receptor, LptM intercalates the lateral gate of the
64 binding to the O-antigen lipopolysaccharide (LPS) receptor of Salmonella were examined at high temper
66 l half of the membrane CD14 was a functional LPS receptor on the cell membrane, we engineered a chime
67 een LPS responsiveness and the expression of LPS receptors or factors regulating LPS responsiveness o
68 colitis and in humans certain alleles of the LPS receptor protein TLR4 increase inflammatory bowel di
72 al epithelial cells expressed the functional LPS receptor-signaling protein TLR4, which was also augm
74 Mechanistically, Toll-like receptor 4 (TLR4, LPS receptor)-sphingosine kinase 1 (SphK1) signaling und
76 mmatory responses, such as those lacking the LPS receptor TLR4 (Toll-like receptor 4), are resistant
77 study, we investigated the importance of the LPS receptor TLR4 and MyD88, an adaptor molecule involve
78 of VEGF, NRP-1 directly interacted with the LPS receptor TLR4 and suppressed downstream signaling th
79 argeting of multiple elements, including the LPS receptor TLR4 and the key adaptor/signaling proteins
80 ry cytokines, along with upregulation of the LPS receptor TLR4 in lung tissue and increased activatio
81 velopment in mice requires activation of the LPS receptor TLR4 on the intestinal epithelium, through
82 with a global or conditional mutation of the LPS receptor TLR4 with this CMA microbiota induced expre
85 ecific, dependent on the lipopolysaccharide (LPS) receptor TLR4, and can be recapitulated by mimickin
86 t mice, we demonstrated that the presence of LPS receptor (TLR4) is not required on hematogenous immu
88 ve demonstrated that the lipopolysaccharide (LPS) receptor (TLR4) is expressed in TRPV1 containing tr
89 -driven suicide gene, we discovered that the LPS receptor Toll-like receptor 4 (TLR4) is specifically
90 culture, we demonstrate that hRetn binds the LPS receptor Toll-like receptor 4 (TLR4) through its N t
92 at regulates signals transduced by the major LPS receptor Toll-like receptor 4 on the surface of mous
93 LPS without affecting the expression of the LPS receptor Toll-like receptor 4, demonstrating that RI
94 which acute lung inflammation depends on the LPS receptor (Toll-like receptor 4, TLR-4), the loss of
95 C3HHeJ, which has a mutation in the primary LPS receptor, Toll-like receptor 4 (TLR4), is extremely
98 Endotoxin-mediated down-regulation of the LPS receptor, Toll-like receptor 4, has been suggested a
104 is the signal transduction component of the LPS receptor, whereas MD-2 is the endotoxin-binding unit