ライフサイエンスコーパス: IkappaBalpha kinase

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1 sphorylation, acetylation, and activation of IkappaBalpha kinase.

2 sphorylation, acetylation, and activation of IkappaBalpha kinase.

3 ted factor 2, NF-kappaB-inducing kinase, and IkappaBalpha kinase.

4 RAF2 and NIK, suggests that anethole acts on IkappaBalpha kinase.

5 kinase, or pp90(rsk), as a signal-inducible IkappaBalpha kinase.

6 TAK1 activation, which led to suppression of IkappaBalpha kinase, abrogation of IkappaBalpha phosphor

7 This inhibition was due to suppression of IkappaBalpha kinase activation and IkappaBalpha phosphor

8 tion pathway by modifying p65 and inhibiting IkappaBalpha kinase activation and potentiates apoptosis

9 t of NF-kappaB (IkappaBalpha), abrogation of IkappaBalpha kinase activation, and inhibition of NF-kap

10 IkappaBalpha phosphorylation, abrogation of IkappaBalpha kinase activation, and inhibition of NF-kap

11 sphorylation, p65 nuclear translocation, and IkappaBalpha kinase activation, but had no significant e

12 hosphorylation, IkappaBalpha degradation, or IkappaBalpha kinase activation, but it blocked TNF-induc

13 eporter gene expression but had no effect on IkappaBalpha kinase activation, IkappaBalpha phosphoryla

14 ation was mediated through the inhibition of IkappaBalpha kinase activation, IkappaBalpha phosphoryla

15 NF-kappaB to the DNA, but, rather, inhibited IkappaBalpha kinase activation, IkappaBalpha phosphoryla

16 more, AMPK activation significantly enhanced IkappaBalpha kinase activation, NF-kappaB nuclear transl

17 a degradation, IkappaBalpha phosphorylation, IkappaBalpha kinase activation, p65 phosphorylation, p65

18 on of IkappaBalpha through the inhibition of IkappaBalpha kinase activation, thus leading to the supp

19 These results correlated with the IkappaBalpha kinase activation, which is needed for NF-k

20 Simvastatin inhibited TNF-alpha-induced IkappaBalpha kinase activation, which led to inhibition

21 aB) activation correlated with RANKL-induced IkappaBalpha kinase activation.

22 ppaBalpha phosphorylation and degradation or IkappaBalpha kinase activation.

23 factor-kappaB (IkappaBalpha); inhibition of IkappaBalpha kinase activation; and suppression of p65 n

24 s a checkpoint role in the proper control of IkappaBalpha kinase activity in innate and adaptive immu

25 K252a and K252b, suggesting that most of the IkappaBalpha kinase activity in the IKK-1+2 complex may

26 ied HCMV virion extract identified bona fide IkappaBalpha kinase activity in the virion.

27 hypothesized that the HCMV virion contained IkappaBalpha kinase activity, allowing for direct phosph

28 responded with the sequential suppression of IkappaBalpha kinase activity, IkappaBalpha phosphorylati

29 orrelated with sequential suppression of the IkappaBalpha kinase activity, IkappaBalpha phosphorylati

30 responded with the sequential suppression of IkappaBalpha kinase activity, IkappaBalpha phosphorylati

31 bited the pathway leading from activation of IkappaBalpha kinase and IkappaBalpha phosphorylation to

32 results indicate that ursolic acid inhibits IkappaBalpha kinase and p65 phosphorylation, leading to

33 us inflammatory agents through inhibition of IkappaBalpha kinase and p65 phosphorylation.

34 All drugs inhibited IkappaBalpha kinase and suppressed IkappaBalpha degradat

35 ively active NF-kappaB through inhibition of IkappaBalpha kinase and the phosphorylation of IkappaBal

36 enced by 1) phosphorylation of IkappaBalpha, IkappaBalpha kinase, and NFkappaB p65, 2) IkappaBalpha d

37 ociated factor-2, NF-kappaB-inducing kinase, IkappaBalpha kinase, and p65 was also suppressed by thes

38 ssociated factor, NF-kappaB-inducing kinase, IkappaBalpha kinase, and p65.

39 R1, TRADD, TRAF2, NF-kappaB-inducing kinase, IkappaBalpha kinase, and the p65 subunit of NF-kappaB.

40 kinase exists within the cell and that these IkappaBalpha kinases are differentially activated by dif

41 (a) activation of nuclear factor-kappaB and IkappaBalpha kinase, (b) degradation and phosphorylation

42 We discovered that DHA directly inhibits IkappaBalpha kinase beta (IKKbeta) and IKKalpha enzymati

43 ted factor-2, NF-kappaB-inducing kinase, and IkappaBalpha kinase but not by p65.

44 TAK1, receptor-interacting protein, NIK, and IkappaBalpha kinase but not that activated by p65.

45 omain protein, TNFR-associated factor-2, and IkappaBalpha kinase, but not that activated by p65.

46 death domain, TNFR-associated factor 2, and IkappaBalpha kinase, but not that induced by p65.

47 This mechanism does not appear to require IkappaBalpha kinase-dependent phosphorylation or proteol

48 These data suggest that more than a single IkappaBalpha kinase exists within the cell and that thes

49 ion of nuclear factor-kappaB (NF-kappaB) and IkappaBalpha kinase, IkappaBalpha degradation, p65 phosp

50 or cell, through inhibition of activation of IkappaBalpha kinase, IkappaBalpha phosphorylation, and I

51 necrosis factor (TNF)-induced activation of IkappaBalpha kinase, IkappaBalpha phosphorylation, Ikapp

52 d sequentially the TNF-induced activation of IkappaBalpha kinase, IkappaBalpha phosphorylation, Ikapp

53 as determined by DNA binding, activation of IkappaBalpha kinase, IkappaBalpha phosphorylation, Ikapp

54 lated with the sequential suppression of the IkappaBalpha kinase, IkappaBalpha phosphorylation, Ikapp

55 of the inhibitory subunit of NF-kappaBalpha (IkappaBalpha) kinase, IkappaBalpha phosphorylation, Ikap

56 ctly inhibited tumor necrosis factor-induced IkappaBalpha kinase (IKK) activation and a reducing agen

57 induced NF-kappaB activation was preceded by IkappaBalpha kinase (IKK) activation and IkappaBalpha de

58 ity correlated with sequential inhibition of IkappaBalpha kinase (IKK) activation, IkappaBalpha phosp

59 nd degradation of IkappaBalpha by inhibiting IkappaBalpha kinase (IKK) activation.

60 results in the synergistic activation of the IkappaBalpha kinase (IKK) complex but not of another put

61 lpha through the inhibition of activation of IkappaBalpha kinase (IKK), and this led to suppression o

62 d sequentially the TNF-induced activation of IkappaBalpha kinase (IKK), IkappaBalpha phosphorylation,

63 This FTI suppressed the activation of IkappaBalpha kinase (IKK), thus abrogating the phosphory

64 ity has been undermined by the activation of IkappaBalpha kinase (IKK), which in turn activates nucle

65 of NF-kappaB activation, confirmed that the IkappaBalpha kinase (IKK)-NF-kappaB signaling pathway en

66 ion and ubiquitination and the activation of IkappaBalpha kinase (IKK).

67 ound to be due to constitutive activation of IkappaBalpha kinase (IKK); and this correlated with cons

68 Phosphorylation of cellular IkappaBalpha kinase (IKK)alpha/beta (Ser(176/180)) was e

69 ing 1) PS1145, a small molecule inhibitor of IkappaBalpha kinase (IKK2), 2) antennapedia-linked NF-ka

70 zeta has been shown to be associated with an IkappaBalpha kinase in resting cells.

71 d apoptosis, and suppression of NF-kappaB by IkappaBalpha kinase inhibitors enhanced apoptosis.

72 inases (IKKs) IKK1 and IKK2 are two putative IkappaBalpha kinases involved in NF-kappaB activation.

73 We demonstrate that the PKC-zeta-associated IkappaBalpha kinase is CK2.

74 Although H2O2 activated IkappaBalpha kinase, it did not induce the serine phosph

75 found that picroliv inhibited activation of IkappaBalpha kinase, leading to inhibition of phosphoryl

76 through the inhibition of the activation of IkappaBalpha kinase, leading to sequential suppression o

77 this study was to determine the role of the IkappaBalpha kinase-nuclear factor kappaB (IKK-NF-kappaB

78 se (IKK) complex but not of another putative IkappaBalpha kinase, p90(rsk).

79 kinase ubiquitination, whereas Syk regulates IkappaBalpha kinase phosphorylation.

80 is effect was mediated through inhibition of IkappaBalpha kinase, phosphorylation, ubiquitination, an

81 At present, the identity of the IkappaBalpha kinase(s) that triggers the first step in I

82 paB activation; suppressed the activation of IkappaBalpha kinase that led to abrogation of phosphoryl

83 BA suppressed the activation of IkappaBalpha kinase, thus abrogating the phosphorylation

84 ent signaling events in which CARD9 mediates IkappaBalpha kinase ubiquitination, whereas Syk regulate

85 ssociated factor 2/NF-kappaB-inducing kinase/IkappaBalpha kinase was interrupted at the TNF receptor-

86 Of the putative N-terminal IkappaBalpha kinases, we demonstrated that the Ikappakap

87 ted factor-2, NF-kappaB-inducing kinase, and IkappaBalpha kinase, were all blocked by flavopiridol bu

88 e identification of an additional N-terminal IkappaBalpha kinase which is constitutively active and n

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