ライフサイエンスコーパス: IKK alpha

1 IKK alpha was not required for RANKL-mediated I kappa B

2 IKK-alpha and IKK-beta formed heterodimers that interact

3 IKK-alpha and IKK-beta isozymes are found in large compl

4 IKK-alpha interacts with CREB-binding protein and in con

5 IKK-alpha was independently discovered as a NF-kappaB-in

6 IKK-alpha, however, does not relocate to the LD but tran

7 Furthermore, caspase-8, IKK-alpha, and NF-kappaB p65 knockdown or dominant negat

8 lts in production of cytokines that activate IKK-alpha and STAT3 in CaP cells to enhance hormone-free

9 polypeptide 3, X-linked (DDX3X) to activate IKK-alpha, which translocates to the nucleus and induces

10 ow that MEKK2 and MEKK3 can in vivo activate IKK-alpha and IKK-beta, induce site-specific IkappaBalph

11 hat DDX3X binds to the HCV 3'UTR, activating IKK-alpha and cellular lipogenesis to facilitate viral a

12 Here, by using a monoclonal antibody against IKK-alpha, we purify the IKK complex to homogeneity from

13 igated the effect of inhibiting the PI3K/AKT/IKK alpha pathway in regulating the inappropriate consti

14 rm of the inhibitor of kappa B kinase alpha (IKK alpha) have mammary gland defects similar to those o

15 entified two proteins, IkappaB kinase alpha (IKK-alpha) and IkappaB kinase beta (IKK-beta), that are

16 IkappaB kinase-alpha (IKK-alpha) and Mitogen- and Stress-activated protein Kin

17 IkappaB kinase-alpha (IKK-alpha) exhibits protein-kinase-dependent and -indepe

18 reen demonstrated that IkappaB kinase-alpha (IKK-alpha) is a crucial host factor for HCV.

19 uclear factor-kappaB (IkappaB) kinase-alpha (IKK-alpha), a protein kinase that is needed for the self

20 ucing kinase (NIK) and IkappaB kinase-alpha (IKK-alpha).

21 but our results suggest that it involves an IKK alpha/IKK beta-independent mechanism.

22 appa B alpha phosphorylation/degradation and IKK alpha/beta and RelA phosphorylation in primary IEC d

23 dent on NF-kappa B-inducing kinase (NIK) and IKK alpha.

24 ed that IKK gamma/NEMO competed with p65 and IKK alpha for binding to the N terminus of CBP, inhibiti

25 ction, the HCV 3'UTR redistributes DDX3X and IKK-alpha to speckle-like cytoplasmic structures shown t

26 tion, the HCV 3'UTR interacts with DDX3X and IKK-alpha, which redistribute to speckle-like cytoplasmi

27 tors of IKK-alpha suppress HCV infection and IKK-alpha-induced lipogenesis, offering a proof-of-conce

28 e therefore examined whether RANKL, RANK and IKK-alpha are also involved in mammary/breast cancer met

29 IkappaB kinase-alpha and -beta (IKK-alpha and IKK-beta), the catalytic subunits of the I

30 composed of IkappaB kinase beta (IKK-beta), IKK-alpha, and IKK-gamma/N, leading to changes in NF-kap

31 her kinase dead (KD) IKK alpha, which blocks IKK alpha kinase activity, KD AKT, which blocks AKT acti

32 Moreover, both IKK-alpha and -beta were activated by hematopoietic prog

33 that MEKK1 can induce the activation of both IKK-alpha and IKK-beta in vivo.

34 d is dependent on phosphorylation of p100 by IKK alpha.

35 s composed of a heterodimer of the catalytic IKK alpha and IKK beta subunits and a presumed regulator

36 In these cells, IKK alpha associates with mTOR, as part of the TORC1 com

37 rted tumor suppressor kinases, such as chk2, IKK-alpha, p38 MAPKs, and DAPK2.

38 ctivating inhibitor of kappaB kinase complex IKK-alpha/beta and active transcription factor NF-kappaB

39 ly controlled by the IkappaB kinase complex (IKK-alpha/beta/gamma).

40 ddition to failed epidermal differentiation, IKK-alpha-deficient mice exhibit abnormal skeletal and c

41 ctivate NF kappa B without activating either IKK alpha or IKK beta.

42 g mouse embryonic fibroblasts lacking either IKK alpha or IKK beta, we found that IKK beta played an

43 dition, dominant negative versions of either IKK-alpha or IKK-beta abolish NF-kappaB activation induc

44 ving dynamic associations with HCV elements, IKK-alpha, SGs, and LDs for its critical role in HCV inf

45 The results indicate a novel role for IKK alpha in controlling mTOR function in cancer cells w

46 However, recent data suggest a role for IKK-alpha in NF-kappaB-dependent gene expression in resp

47 r the levels of phosphorylated c-Jun, c-Fos, IKK-alpha/beta, and p65.

48 ct endogenous IKK complexes, a heterodimeric IKK alpha/beta and a homodimeric IKK beta complex.

49 e nuclear factor kappaB/IkappaB cascade (ie, IKK-alpha,-beta,-gamma/NEMO and CARMA/MALT1/Bcl10 comple

50 lls lacking either catalytic subunit of IKK (IKK-alpha or IKK-beta) fail to induce autophagy in respo

51 uced activation of the IkappaB kinases (IKK) IKK-alpha and IKK-beta is a key step involved in the act

52 gene expression was significantly blunted in IKK alpha(-/-) cells, including osteoclast-specific gene

53 lpha can overcome p100 processing defects in IKK alpha(-/-) cells.

54 ed to directly examine osteoclastogenesis in IKK alpha(-/-) mice.

55 postulated that the morphogenetic defects in IKK-alpha-deficient mice are not caused by reduced NF-ka

56 eless, mouse embryo fibroblasts deficient in IKK-alpha are defective in the induction of NF-kappaB-de

57 LMP1 also induced IKK alpha-mediated p100 processing and p52 nuclear local

58 Interestingly, IKK-alpha and MSK1/2 have also been implicated as histon

59 fic Ikka (also known as Chuk) transgene into IKK-alpha-deficient mice.

60 Inducible expression of either KD IKK alpha or WT PTEN strongly inhibits both the constitu

61 The ability of KD IKK alpha, KD AKT or WT PTEN to decrease beta-catenin-de

62 siently transfecting either kinase dead (KD) IKK alpha, which blocks IKK alpha kinase activity, KD AK

63 omplex, which is composed of the two kinases IKK alpha and IKK beta and the regulatory subunit IKK ga

64 D40 engagement activated the IkappaB kinases IKK-alpha and IKK-beta and stimulated IkappaBalpha phosp

65 rgeted for degradation by I kappa B kinases (IKK alpha and IKK beta).

66 hibitory factor IkappaBs by IkappaB kinases (IKK-alpha and -beta).

67 A clones encoding these two IkappaB kinases, IKK-alpha and IKK-beta.

68 ducing kinase (NIK) and two IkappaB kinases, IKK-alpha and IKK-beta.

69 IKK is made up of two kinases, IKK-alpha and IKK-beta, which phosphorylate I(kappa)B, l

70 Because mice that completely lack IKK alpha have severe skin and skeletal defects that are

71 Mice lacking IKK-alpha in all cell types including bone and cartilage

72 construct with either the dominant negative IKK-alpha or the repressors of NF-kappaB, the IkappaB-al

73 Here we show that Tax binds to neither IKK-alpha nor IKK-beta but instead complexes directly wi

74 ivation of NF-kappa B inducing kinase (NIK)--IKK alpha/beta complex leading to I kappa B alpha phosph

75 -1-inducible IKK complexes that contain NIK, IKK-alpha, IKK-beta, IkappaB-alpha, NF-kappaB/RelA and a

76 Bifurcation of NTHi-induced NIK-IKK alpha/beta-I kappa B alpha and MKK3/6--p38 MAP kinas

77 ates NF-kappa B via TLR2-TAK1-dependent NIK--IKK alpha/beta-I kappa B alpha and MKK3/6--p38 MAP kinas

78 NIK/IKK-alpha axis regulated the activation of both NF-kappa

79 Moreover, NIK/IKK-alpha/NF-kappaB p50/p65 axis mediated the TNF-alpha-

80 In conclusion, our data show that NIK/IKK-alpha/regulates the activation of NF-kappaB p50/p65

81 alicylate, an inhibitor of IKK beta, but not IKK alpha, activity, inhibited IL-2 promoter activation

82 1 also induced transfected IKK beta, but not IKK alpha, activity.

83 Moreover, IKK beta, but not IKK alpha, overexpression enhanced transcriptional activ

84 IKK genes have shown that IKK-beta, but not IKK-alpha, is critical for cytokine-induced IkappaB degr

85 kappa B alpha turnover and the activities of IKK alpha and IKK beta.

86 In contrast, ectopic expression of IKK alpha assembled into a complex with negligible I kap

87 hibit NF-kappaB activation via inhibition of IKK alpha or IKK beta, whereas proteosome inhibitors ins

88 Cells with a high proportion of IKK alpha (the IKK kinase activated by Akt) to IKK beta

89 -/- or wild-type cells in which the ratio of IKK alpha to IKK beta is low.

90 Expression and the ratios of IKK alpha and IKK beta, which homo- and heterodimerize,

91 Treatment of IKK alpha(-/-) cells with tumor necrosis factor alpha (T

92 Here we demonstrate nuclear accumulation of IKK-alpha after cytokine exposure, suggesting a nuclear

93 d region (UTR), leading to the activation of IKK-alpha and a cascade of lipogenic signaling to facili

94 over IKK-beta, leading to the activation of IKK-alpha kinase activity.

95 inflammatory infiltration and activation of IKK-alpha, which stimulates metastasis by an NF-kappaB-i

96 d that IKK is composed of similar amounts of IKK-alpha, IKK-beta and two other polypeptides, for whic

97 fically elevated in the limb bud ectoderm of IKK-alpha-deficient mice.

98 ugh the basal level of protein expression of IKK-alpha or IKK-beta are the same in both Hs294T and RP

99 A mutant form of IKK-alpha containing alanine at residue 176 cannot be ph

100 Conversely, a mutant form of IKK-alpha containing glutamic acid at residue 176 is con

101 dent and kinase-mediated nuclear function of IKK-alpha in HCV assembly.

102 Chemical inhibitors of IKK-alpha suppress HCV infection and IKK-alpha-induced l

103 gene expression is suppressed by the loss of IKK-alpha and this correlates with a complete loss of ge

104 nce of TNF-alpha solely by overexpression of IKK-alpha/beta or strong activation of NF-kappaB.

105 omplex with MEKK1 induces phosphorylation of IKK-alpha in vitro.

106 This phosphorylation of IKK-alpha occurs specifically on Ser-176 in the activati

107 Thus, the phosphorylation of IKK-alpha on Ser-176 by NIK may be required for cytokine

108 erase promoter assays and phosphorylation of IKK-alpha/beta.

109 These results define a new nuclear role of IKK-alpha in modifying histone function that is critical

110 osteoclast differentiation was dependent on IKK alpha, suggesting that synergy between RANKL and TNF

111 ull mice, which completely lack osteoclasts, IKK alpha(-/-) mice did possess normal numbers of TRAP(+

112 ar activity and significant selectivity over IKK-alpha.

113 show that NIK preferentially phosphorylates IKK-alpha over IKK-beta, leading to the activation of IK

114 amic associations with HCV RNA and proteins, IKK-alpha, SG, and LD surfaces for its crucial role in t

115 We show herein that recombinant IKK-alpha and IKK-beta can, in fact, directly phosphoryl

116 PKK-mediated NF-kappa B activation required IKK alpha and IKK beta but not IKK gamma, the regulatory

117 g of IKKgamma to the IKK catalytic subunits, IKK-alpha and -beta, and attenuates the IKK catalytic ac

118 These subunits, IKK-alpha and IKK-beta, are protein kinases whose functi

119 anced activation of the protein kinases TAK, IKK-alpha/beta, c-Jun N-terminal kinases, and p38alpha m

120 The experiments show that IKK alpha controls mTOR kinase activity in Akt-active, P

121 nd regulation of NF-kappaB activity and that IKK-alpha can only partially compensate for the loss of

122 We conclude that IKK-alpha and IKK-beta can mediate the NF-kappaB-inducin

123 We propose that IKK-alpha is an essential regulator of NF-kappaB-depende

124 mmunoprecipitation (ChIP) assays reveal that IKK-alpha was recruited to the promoter regions of NF-ka

125 Furthermore, we show that IKK-alpha can directly phosphorylate histone H3 in vitro

126 Here we show that IKK-alpha functions in the nucleus to activate the expre

127 Finally, we show that IKK-alpha is present in the MEKK1-inducible, high molecu

128 We showed that IKK-alpha and IKK-beta were coexpressed in most human ad

129 a B kinase (IKK) complex, which includes the IKK alpha (IKK-1) and IKK beta (IKK-2) kinases.

130 gnals in NK cells involves activation of the IKK alpha kinase, inhibitory protein kappa B alpha degra

131 The IKK-alpha and IKK-beta genes are distinct but evolutiona

132 Moreover, the IKK-alpha gene locus was mapped to human chromosome 10q2

133 KK epsilon, two kinases distantly related to IKK alpha/beta, but the underlying mechanisms remained u

134 s identified that is 52 percent identical to IKK-alpha.

135 dapting an oncoprotein-specific signaling to IKK-alpha and IKK-beta.

136 teoclastogenesis was observed in vitro using IKK alpha(-/-) hematopoietic cells treated with colony-s

137 We found that, whereas IKK alpha is a weak kinase for the N-terminal serines of

138 osphorylated IkappaB constitutively, whereas IKK-alpha was not active in the absence of cell stimulat

139 cytokine-induced NF-kappaB function, whereas IKK-alpha is thought to be involved in other regulatory

140 observations raised the question of whether IKK-alpha might regulate a previously undescribed step t

141 One way by which IKK-alpha controls skeletal and craniofacial morphogenes

142 ced p65 phosphorylation on serine 536, while IKK alpha was partially required for the p65 phosphoryla

143 keletal defects that are not associated with IKK alpha-kinase activity, we wished to directly examine

144 294T and RPE cells, immunoprecipitation with IKK-alpha antibody combined with activity assay reveal a

145 the truncated NEMO protein interactions with IKK-alpha, IKK-beta, TNF receptor-associated factor 6, T