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1 e recognition of bacterial cell wall-derived muramyl dipeptide.
2 n of the IL-1 receptor plus the co-stimulant muramyl dipeptide.
3 pon treatment of cells with the NOD2 ligand, muramyl dipeptide.
4 fibroblasts show an increased sensitivity to muramyl dipeptide.
5 owing NOD2-mediated recognition of bacterial muramyl dipeptide.
6 sease were deficient in their recognition of muramyl dipeptide.
7 d to lipopolysaccharide but not to synthetic muramyl dipeptide.
9 tive bacterial cell wall, while NOD2 detects muramyl dipeptide, a ubiquitous cell wall peptidoglycan
10 step mechanism, requiring microbial product, muramyl-dipeptide, a component of peptidoglycan, followe
12 ecular mechanisms that underlie detection of muramyl dipeptide and assembly of NOD2-containing signal
13 ombinant protein is able to bind directly to muramyl dipeptide and can associate with known NOD2-inte
14 39iCstop) are impaired in the recognition of muramyl dipeptide and Enterococcus faecalis, a commensal
18 binding of nucleotide followed by binding of muramyl dipeptide and oligomerization of NOD2 into a sig
19 polymeric form rather than monomers such as muramyl dipeptide and require PGN lysosomal hydrolysis t
20 onstrate that peptidoglycan monomers such as muramyl dipeptide and soluble peptidoglycan fail to indu
21 of a specific bacterial cell wall component, muramyl dipeptide, and activation of Nod2 stimulates an
23 s anthracis lethal toxin, Toxoplasma gondii, muramyl dipeptide, and host intracellular ATP depletion.
24 hypophagic agents, lipopolysaccharide (LPS), muramyl dipeptide, and interleukin-1, when challenged on
25 nges induced by the specific Nod2 activator, muramyl dipeptide, and that the role of NIK occurs in se
27 promiscuous T-cell epitope (ie, MVF) and nor-muramyl-dipeptide as adjuvant emulsified in SEPPIC ISA 7
28 in-containing protein 2 (NOD2) by its ligand muramyl dipeptide, as compared to activation via heterod
29 TZ-injected WT mice received the NOD2 ligand muramyl dipeptide, both hyperglycemia and the proinflamm
31 idoglycan (PGN), a TLR2 ligand that contains muramyl dipeptide, but not other TLR ligands; in contras
32 ptidoglycan are mediated by detection of its muramyl dipeptide component in the cytosol by NOD2, we r
33 lthough Zn(2+) is required for hydrolysis of muramyl dipeptide, disulfide oxidation is not required f
35 caspase recruitment domain (CARD) 15 detects muramyl dipeptide from bacterial peptidoglycans and medi
39 both RIP2 tyrosine phosphorylation and MDP (muramyl dipeptide)-induced cytokine release in a variety
40 The dominant negative form of TAK1 abolished muramyl dipeptide-induced NF-kappaB activation in Nod2-e
43 ty mediated by Nod2 recognition of bacterial muramyl dipeptide is abolished in Nod2-deficient mice.
44 NOD2-dependent recognition of S. aureus and muramyl dipeptide is facilitated by alpha-toxin (alpha-h
47 ty is based on previous studies showing that muramyl dipeptide (MDP) activation of NOD2 negatively re
48 ffectiveness of lipopolysaccharide (LPS) and muramyl dipeptide (MDP) administered into the brain to i
49 n-2 (NOD2) receptor detects bacteria-derived muramyl dipeptide (MDP) and activates the transcription
50 transports small bacterial peptides, such as muramyl dipeptide (MDP) and l-Ala-gamma-D-Glu-meso-diami
51 nts of bacterial peptidoglycan (PGN), namely muramyl dipeptide (MDP) and muramyl tripeptide (MTP).
53 ands similar to the minimal synthetic ligand muramyl dipeptide (MDP) are generated by internalization
54 ling and autophagy activation in response to muramyl dipeptide (MDP) by immunoblot, confocal microsco
56 R4 and Nod2 signaling by exposure to LPS and muramyl dipeptide (MDP) exhibit impaired TNF-alpha and I
57 (P.g.)-induced TNF-alpha can be affected by muramyl dipeptide (MDP) in a biphasic concentration-depe
58 show that activation of Nod2 by its ligand, muramyl dipeptide (MDP) in the bacterial cell wall, indu
59 ase in response to the presence of bacterial muramyl dipeptide (MDP) in the host cell cytoplasm, ther
61 he synergistic effect of IL-32 and synthetic muramyl dipeptide (MDP) on cytokine production was absen
62 ria produce an unusual, glycolylated form of muramyl dipeptide (MDP) that is more potent and efficaci
63 LR), is an intracellular sensor of bacterial muramyl dipeptide (MDP) that was suggested to promote se
64 contrast, ApoE(-/-) mice injected i.p. with Muramyl DiPeptide (MDP) to stimulate NOD2 and given an o
66 n important role in innate immunity to sense muramyl dipeptide (MDP), a component of bacterial cell w
67 n of primary monocyte-derived macrophages by muramyl dipeptide (MDP), a component of bacterial peptid
68 receptor, induces autophagy on detection of muramyl dipeptide (MDP), a component of microbial cell w
70 orm of mycobacterial cell wall component and muramyl dipeptide (MDP), a peptidoglycan derivative resp
72 quently, we determined that the NOD2 ligand, muramyl dipeptide (MDP), activates NF-kappaB in primary
73 Nod2 is required for an immune response to muramyl dipeptide (MDP), an immunostimulatory fragment o
74 components, such as the NOD2 cognate ligand muramyl dipeptide (MDP), and are selectively required fo
75 an intracellular sensor of bacteria-derived muramyl dipeptide (MDP), increase susceptibility to Croh
76 ciated molecular patterns (PAMPs), including muramyl dipeptide (MDP), LPS, and a B-class CpG oligonuc
77 ls were given an intraarticular injection of muramyl dipeptide (MDP), peptidoglycan (PG; a metabolite
80 ion in primary human mononuclear cells, with muramyl dipeptide (MDP), the minimal NOD2/CARD15 activat
82 One such receptor, NOD2, via recognition of muramyl dipeptide (MDP), triggers a distinct network of
83 whole-genome level by microarray analysis of muramyl dipeptide (MDP)-treated Itch(-/-) primary macrop
88 e NOD1 ligand MurNAcTri(DAP) and NOD2 ligand muramyl dipeptide [MDP]) but not bacterial Toll-like rec
90 ochemical and functional analyses identified muramyl dipeptide (MurNAc-L-Ala-D-isoGln) derived from p
91 so specifically bound to agarose-immobilized muramyl dipeptide or GlcNAc-muramyl dipeptide but not to
92 eveloped tolerance to repeated injections of muramyl dipeptide or LPS and were cross-tolerant to S-O-
93 (a metabolite of which is the NOD2 agonist, muramyl dipeptide), or synthetic TLR2/1 and TLR2/6 agoni
96 of the peptidoglycan fragments meso-DAP and muramyl dipeptide, respectively, and drive the activatio
101 soGln for L-isoGln eliminated the ability of muramyl dipeptide to stimulate NOD2, indicating stereose
102 hogen-free facility, were given antibiotics, muramyl dipeptide (to stimulate NOD2), or dextran sodium
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