ライフサイエンスコーパス: IL-1 receptor-associated kinase

1 We have previously shown that the IL-1 receptor associated kinase 1 (IRAK-1) selectively a

2 itro, reducing levels of the adaptor kinases IL-1 receptor-associated kinase 1 (IRAK-1) and TNF recep

3 guanine nucleotide exchange factor VAV-1 and IL-1 receptor-associated kinase 1 (IRAK-1), respectively

4 at Tbeta4 treatment suppressed expression of IL-1 receptor-associated kinase 1 (IRAK1) and tumor necr

5 S100A7, S100A8, and S100A9 (S100A7/8/9), and IL-1 receptor-associated kinase 1 (IRAK1) establish a re

6 ike receptor (TLR4) signaling first mediates IL-1 receptor-associated kinase 1 (IRAK1) nuclear transl

7 roduction via binding to and phosphorylating IL-1 receptor-associated kinase 1 (IRAK1), leading to IR

8 and TES2-mediated NF-kappaB activations are IL-1 receptor-associated kinase 1 (IRAK1)-dependent.

9 regulation loop involving down-regulation of IL-1 receptor-associated kinase 1 and TNF receptor-assoc

10 R-146a diminished or enhanced, respectively, IL-1 receptor-associated kinase 1 expression and induced

11 actor 7 gene expression and rapidly degraded IL-1 receptor-associated kinase 1 expression in plasmacy

12 of the TNF receptor-associated factor 6 and IL-1 receptor-associated kinase 1 genes, and we found th

13 adaptor protein (TIRAP), and the downstream IL-1 receptor-associated kinase 1, IL-1 receptor-associa

14 ession of IL-25 and IL-33 by upregulation of IL-1 receptor-associated kinase 1, transforming growth f

15 recruitment domain-containing protein 10 and IL-1 receptor-associated kinase 1.

16 tiation factor 88 (MyD88) and interleukin-1 (IL-1) receptor-associated kinase 1 (IRAK-1) (MyD88-TIR a

17 The interleukin-1 (IL-1) receptor-associated kinase 1 (IRAK1) is a member o

18 n of macrophage TLR2 and TLR4 was preserved, IL-1 receptor associated kinase-1 phosphorylation and NF

19 In an alternate pathway, inhibition of IL-1 receptor-associated kinase-1 (IRAK) with AS ODN to

20 timulated macrophages, but failed to inhibit IL-1 receptor-associated kinase-1 activity.

21 -dependent, L type alpha1C subunit (CaV1.2), IL-1 receptor-associated kinase-1 and -2, and IL enhance

22 oid differentiating factor 88 and results in IL-1 receptor-associated kinase-1 phosphorylation.

23 IL-1 receptor-associated kinase 4 (IRAK4) belongs to the

24 t domain adaptor inducing IFN-beta (CARDIF), IL-1 receptor-associated kinase 4 (IRAK4), IkappaB kinas

25 he TLR-signaling pathways (MyD88, TIRAP/MAL, IL-1 receptor-associated kinase 4 [IRAK-4], TLR3, UNC-93

26 D88-dependent signaling molecules, including IL-1 receptor-associated kinase 4 and TNF-receptor assoc

27 ownstream IL-1 receptor-associated kinase 1, IL-1 receptor-associated kinase 4, and TNF receptor-asso

28 IRAK1 (IL-1 receptor associated kinase), a kinase immediately u

29 mDC, with LPS resulted in the activation of IL-1 receptor-associated kinase, an early component in t

30 a/b significantly downregulated interleukin (IL)-1 receptor-associated kinase and TNF receptor-associ

31 MyD88 binds to both IRAK (IL-1 receptor-associated kinase) and the heterocomplex (

32 lyubiquitination of Pelle, an interleukin-1 (IL-1) receptor-associated kinase homolog in the Drosophi

33 ntaining (DD-containing) proteins, MyD88 and IL-1 receptor-associated kinase IRAK.

34 effects of stimulating or inhibiting the TLR/IL-1 receptor-associated kinases IRAK-1 and IRAK-4 in me

35 HCV core and NS3 induced interleukin (IL)-1 receptor-associated kinase (IRAK) activity, phosph

36 ifferentiation primary response gene 88) and IL-1 receptor-associated kinase (IRAK) 1/4 inhibitors, o

37 strated deficient TLR4-induced activation of IL-1 receptor-associated kinase (IRAK) 4, IRAK1, and TAN

38 al modifications and signalosome assembly of IL-1 receptor-associated kinase (IRAK) 4, IRAK1, TNF rec

39 ion of these experiments is that NO inhibits IL-1 receptor-associated kinase (IRAK) activity and atte

40 ability to potently suppress the activity of IL-1 receptor-associated kinase (IRAK) after TLR activat

41 IL-1 receptor-associated kinase (IRAK) is phosphorylated

42 Mutant I1A cells, lacking IL-1 receptor-associated kinase (IRAK) mRNA and protein,

43 ture and signaling, including recruitment of IL-1 receptor-associated kinase (IRAK) to the receptor a

44 se Pelle-like kinase (mPLK, homolog of human IL-1 receptor-associated kinase (IRAK)) participates in

45 LPS-induced activation of the IL-1 receptor-associated kinase (IRAK), and the influenc

46 associate with the IL-1 receptor, including IL-1 receptor-associated kinase (IRAK), MyD88, and TRAF6

47 ive myeloid differentiation protein (MyD88), IL-1 receptor-associated kinase (IRAK), NFkappaB-inducin

48 Mutant A in complementation group I1 lacks IL-1 receptor-associated kinase (IRAK), while the mutant

49 f various innate immune receptors results in IL-1 receptor-associated kinase (IRAK)-1/IRAK-4-mediated

50 elle homologs have been described and termed IL-1 receptor-associated kinase (IRAK).

51 -T6BP complex depends on the presence of the IL-1 receptor-associated kinase (IRAK).

52 is and depends on the TLR-signaling molecule IL-1 receptor-associated kinase (IRAK-1) and its kinase

53 a greatly up-regulated the protein levels of IL-1 receptor-associated kinase (IRAK-1) and tumor-necro

54 The IL-1 receptor-associated kinase (IRAK/mPLK) is linked to

55 Interleukin-1 (IL-1) receptor-associated kinase (IRAK) is phosphorylate

56 hown that the activity of the interleukin-1 (IL-1) receptor-associated kinase (IRAK) is required for

57 The interleukin-1 (IL-1) receptor-associated kinase (IRAK) is required for

58 Interleukin-1 (IL-1) receptor-associated kinase (IRAK) plays an importa

59 d FliC-mediated activation of interleukin-1 (IL-1) receptor-associated kinase (IRAK), a central compo

60 nteractions with TLR4, MyD88, interleukin-1 (IL-1) receptor-associated kinase (IRAK)-2, and tumor nec

61 Interleukin 1 (IL-1) receptor-associated kinase (IRAK)-M is a proximal

62 n IL-1 signaling is the rapid interaction of IL-1 receptor-associated kinases, IRAK and IRAK-2, with

63 The IL-1 receptor-associated kinases (IRAKs) are key regulat

64 Interleukin 1 (IL-1) receptor-associated kinases (IRAKs) are serine/thr

65 that is implicated in the activation of the IL-1-receptor-associated kinase is required for this res

66 IL-1 receptor-associated kinase M (IRAK-M) negatively re

67 nhibitor of NF-kappaB activation 3 (ABIN-3), IL-1 receptor-associated kinase M (IRAK-M), suppressor o

68 sion of the TLR signaling pathway inhibitor, IL-1 receptor associated kinase-M (IRAK-M).

69 er DC expression of toll-like receptor 9 and IL-1 receptor associated kinase-M.

70 IL-1 receptor-associated kinase-M (IRAK-M) is a macropha

71 role of the LPS/TLR4 axis and its inhibitor, IL-1 receptor-associated kinase-M (IRAK-M), in modulatin

72 s potentiation is mediated by a reduction in IL-1 receptor-associated kinase-M, a negative regulator

73 characterize an X chromosome-linked IRAK-1 (IL-1 receptor-associated kinase) polymorphism as an alte

74 onally interact with the recently-identified IL-1-receptor-associated kinase to activate NFkappaB.

75 IGIF signaled through IRAK, IL-1 receptor-associated kinase, to induce nuclear trans

76 mune components such as Toll-like receptors, IL-1 receptor-associated kinase/tumor necrosis factor re

77 The proximal IL-1 signaling molecule IL-1 receptor-associated kinase was not degraded in IL-1

78 A protein kinase designated IRAK (IL-1 receptor-associated kinase) was purified, and its c

79 o Ec-LPS, displayed persisting expression of IL-1 receptor-associated kinase without apparent degrada