ライフサイエンスコーパス: myeloid differentiation factor 88

1 hese outcomes by using the signaling adaptor myeloid differentiation factor 88.

2 hia is completely dependent on expression of myeloid differentiation factor 88.

3 response in murine DCs that is dependent on myeloid differentiation factor 88.

4 TLR/IL-1R domain containing adaptor molecule myeloid differentiation factor 88.

5 GP inhibits independently of TLR2, TLR4, and myeloid differentiation factor 88.

6 ciated death domain through interaction with myeloid differentiation factor 88.

7 ch is blocked by siRNA-mediated knockdown of myeloid differentiation factor 88 adaptor protein but no

8 xpression, but did require expression of the myeloid differentiation factor 88 adaptor protein.

9 Although myeloid differentiation factor 88 an adaptor molecule fo

10 Myeloid differentiation factor 88, an adaptor protein di

11 r p65 translocation, and colocalization with myeloid differentiation factor 88 and calcium-modulating

12 as a scaffold to promote the interaction of myeloid differentiation factor 88 and IL-1R-associated k

13 ndothelial cells that is independent of both myeloid differentiation factor 88 and Toll-like receptor

14 is is dependent on TLR2 and TLR4, as well as myeloid differentiation factor 88 and Toll/IL-1R domain-

15 IRF-8(-/-) DCs expressed TLR9, adaptor myeloid differentiation factor 88, and other signaling m

16 TLR4, TLR2, and myeloid differentiation factor 88 are involved in murine

17 -associated factor 6 function, downstream of myeloid differentiation factor 88, blocked T cell-depend

18 ponses involving the adaptor molecule MyD88 (myeloid differentiation factor 88) but not the TRAM/TRIF

19 Second, Ag-loaded myeloid differentiation factor 88 -deficient dendritic c

20 Myeloid differentiation factor 88-deficient (MyD88(-/-))

21 ll-like receptor 7-deficient (Tlr7(-/-)) and myeloid differentiation factor 88-deficient (Myd88(-/-))

22 Myeloid differentiation factor 88-deficient cells respon

23 erived macrophages, whereas macrophages from myeloid differentiation factor 88-deficient mice display

24 in a Toll-like receptor (TLR)2-dependent and myeloid differentiation factor 88-dependent fashion wher

25 matory response in a Toll-like receptor- and myeloid differentiation factor 88-dependent manner.

26 DC (likely Toll-like) receptors acting in a myeloid differentiation factor 88-dependent manner.

27 maturation and phagosome Ag degradation in a myeloid differentiation factor 88-dependent manner; this

28 on are uncertain, although a role for a TLR4/myeloid differentiation factor 88-dependent pathway lead

29 tosis of bacteria was found to be reliant on myeloid differentiation factor 88-dependent signaling th

30 The effects of the TLR9 agonist CpG are myeloid differentiation factor 88-dependent, whereas the

31 ectly targeted Th17 cells by down-regulating myeloid differentiation factor 88 expression to suppress

32 he other PAMPs); inhibition was dependent on myeloid differentiation factor 88 for MTB and all of the

33 nterleukin; TIR, Toll/IL-1R homology; MyD88, myeloid differentiation factor 88; IFN, interferon; TRIF

34 These effects were largely dependent on myeloid differentiation factor 88, implying a role for T

35 ucing IFN-beta, P. gingivalis utilizes TLR2/ myeloid differentiation factor 88 in modulating osteocla

36 including IL-10; (d) ligands that signal via myeloid differentiation factor 88 induce IL-10, giving a

37 High glucose increased TLR expression, myeloid differentiation factor 88, interleukin-1 recepto

38 xia-induced NSA was nearly ablated in MyD88 (myeloid differentiation factor 88) knock-out mice and in

39 Toll-like receptor signaling through myeloid differentiation factor 88 maintains segregation

40 stimulation of the Toll-like receptor (TLR)-myeloid differentiation factor 88-mediated pathway by mi

41 by the microbiota via Toll-like receptor and myeloid differentiation factor 88-mediated signalling pa

42 fection system, dominant-negative mutants of myeloid differentiation factor 88 (MyD88) and interleuki

43 tor CD14, the intracellular adaptor proteins myeloid differentiation factor 88 (MyD88) and TIR domain

44 timulation through pathways mediated by both myeloid differentiation factor 88 (MyD88) and TIR domain

45 cterium avium or M smegmatis is dependent on myeloid differentiation factor 88 (MyD88) and TLR2 but n

46 ell walls, is driven by the adaptor proteins myeloid differentiation factor 88 (MyD88) and Toll-inter

47 which signals through the adapter molecules myeloid differentiation factor 88 (MyD88) and toll/inter

48 Toll-like receptor (TLR) signaling through myeloid differentiation factor 88 (MyD88) and/or Toll-in

49 t signal through the common adaptor molecule myeloid differentiation factor 88 (MyD88) are essential

50 R4, and TLR9 and the common adaptor molecule myeloid differentiation factor 88 (MyD88) in a Staphyloc

51 ice lacking both Lyn and the adaptor protein myeloid differentiation factor 88 (MyD88) in DCs, specif

52 ial Toll-like receptor (TLR) adaptor protein myeloid differentiation factor 88 (MyD88) in systemic an

53 We describe a role for myeloid differentiation factor 88 (MyD88) in the inducti

54 Myeloid differentiation factor 88 (MyD88) is an adapter

55 Myeloid differentiation factor 88 (MyD88) is an adaptor

56 Myeloid differentiation factor 88 (MyD88) is an essentia

57 Signaling through myeloid differentiation factor 88 (MyD88) is critical fo

58 hrough their key downstream adaptor molecule myeloid differentiation factor 88 (MyD88) is required fo

59 Myeloid differentiation factor 88 (MYD88) L265P somatic

60 The expression of myeloid differentiation factor 88 (MyD88) or TLR5 was st

61 s (TLRs) and the downstream adaptor molecule myeloid differentiation factor 88 (MyD88) play an essent

62 Signaling through the adaptor protein myeloid differentiation factor 88 (MyD88) promotes carci

63 Furthermore, B cell-intrinsic expression of myeloid differentiation factor 88 (MyD88) was required t

64 palmitate rapidly induced the association of myeloid differentiation factor 88 (MyD88) with the TLR2

65 y, and cytokine production were dependent on myeloid differentiation factor 88 (MyD88), a key adapter

66 rs are mediated through the adapter molecule myeloid differentiation factor 88 (MyD88), and mice with

67 lycemia through Toll-like receptor-4 (TLR4), myeloid differentiation factor 88 (MyD88), and nuclear f

68 kin-1 receptor-associated kinase 4 (IRAK-4), myeloid differentiation factor 88 (MyD88), and UNC-93B.

69 , mice deficient in the TLR adaptor molecule myeloid differentiation factor 88 (MyD88), as well as TL

70 sion of the cytoplasmic TLR adapter protein, myeloid differentiation factor 88 (MyD88), but not TLR2

71 of which signal through the adaptor protein myeloid differentiation factor 88 (MyD88), have been sug

72 Comparable levels of mRNA and protein for myeloid differentiation factor 88 (MyD88), IL-1R-associa

73 Here we show that the adaptor molecule, myeloid differentiation factor 88 (MyD88), mediates both

74 Mice deficient in TLR-2, myeloid differentiation factor 88 (MyD88), or NOD-2 and

75 t adapter molecules: the common TLR adapter, myeloid differentiation factor 88 (MyD88), or Toll/inter

76 endent on the signaling pathway intermediary myeloid differentiation factor 88 (MyD88), such that nei

77 tterns and signal through adaptor molecules, myeloid differentiation factor 88 (MyD88), Toll/IL-1 rec

78 deficient in the common TLR adaptor protein, myeloid differentiation factor 88 (MyD88), were infected

79 TLR-4, and the cytosolic TLR adapter protein myeloid differentiation factor 88 (MyD88), which are cen

80 d by a constitutively active adapter protein myeloid differentiation factor 88 (MyD88), which interac

81 e that mice deficient in the adaptor protein myeloid differentiation factor 88 (MyD88), which is requ

82 pe I IFN expression proceeded independent of myeloid differentiation factor 88 (MyD88), which is the

83 HIV(+) macrophages, but whether HIV impairs myeloid differentiation factor 88 (MyD88)-dependent and/

84 umbers in a Toll-like receptor 4 (TLR4)- and myeloid differentiation factor 88 (MyD88)-dependent mann

85 ly through a Toll-like receptor (TLR) 7- and myeloid differentiation factor 88 (MyD88)-dependent path

86 r-inducing interferon-beta (TRIF)-dependent, myeloid differentiation factor 88 (MyD88)-independent TL

87 letely dependent on the Toll-like receptor 4/myeloid differentiation factor 88 (MyD88)-mediated pathw

88 ression independently of the adaptor protein myeloid differentiation factor 88 (MyD88).

89 deletion of the inflammatory adaptor protein myeloid differentiation factor 88 (MyD88).

90 or 3 (TLR3), signal via the adaptor molecule myeloid differentiation factor 88 (MyD88).

91 toll-like receptor 4 (TLR4) and its adaptor myeloid differentiation factor 88 (MyD88).

92 LR-4 signaling through the cytosolic adaptor myeloid differentiation factor 88 (MyD88).

93 LR9 are dependent on the common TLR adaptor, myeloid differentiation factor 88 (MyD88).

94 te with several adaptor molecules, including myeloid differentiation factor 88 (MyD88).

95 ecognition and signaling through the adaptor myeloid differentiation factor 88 (MyD88).

96 y on an intracellular adapter protein called myeloid differentiation factor 88 (MyD88).

97 oth TLR3 and TLR4 can directly interact with myeloid differentiation factor 88 (MyD88).

98 Using myeloid differentiation factor 88 (MyD88)/TIR-domain-con

99 r protein inducing interferon beta (TRIF) or myeloid differentiation factor-88 (MyD88) and CX3CR1 kno

100 s for targeted disruption of TLR9, TLR3, and myeloid differentiation factor-88 (MyD88), and most of t

101 sess the role of the common adaptor molecule myeloid differentiation factor-88 (MyD88).

102 a), which in turn activate a well-described, myeloid-differentiation factor 88 (MYD88)-mediated, nucl

103 Knockdown of either myeloid differentiation factor 88 or Toll-like receptor-

104 ts from mice with genetic deletion of MyD88 (myeloid differentiation factor 88) or TLRs (Toll-like re

105 y several Toll-like receptor ligands through myeloid differentiation factor 88- or TRIF-dependent pat

106 s) in vitro via the Toll-like receptor (TLR)-myeloid differentiation factor 88 pathway.

107 and -18R, as a result of genetic ablation of myeloid differentiation factor 88 promotes the acceptanc

108 by triggering the Toll-like receptor (TLR)2-myeloid differentiation factor 88 signaling pathway, thu

109 of NF-kappa B, but rather depended on a TLR2-myeloid differentiation factor 88 signaling pathway.

110 ammatory cytokines that was dependent on the myeloid differentiation factor 88 signaling pathway.

111 tion of the cytoplasmic TLR-adapter molecule myeloid differentiation factor 88, suggesting the involv

112 nt of Toll-like receptor 4 signaling and the myeloid differentiation factor 88 Toll-like receptor sig

113 -like receptor 4, MD2, Toll-like receptor 9, myeloid differentiation factor 88, Toll/IL-1R domain-con

114 on the IRF-3 kinase, TBK1, and IRF-3 but was myeloid differentiation factor 88-, Toll-interleukin 1 r