ライフサイエンスコーパス: IKK

1 IKK activity was reduced by small molecules targeting BE

2 IKK epsilon (IKKepsilon) is induced by the activation of

3 IKK forms a complex with and phosphorylates ASK1 at a se

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

5 IKK-complex subunits transmit a previously unrecognized

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

7 These structures are enriched in activated IKK kinases and ubiquitinated NEMO molecules, which sugg

8 ceptor signaling, one pathway that activates IKK in ABC DLBCL.

9 IL-1, TNF, and TGFbeta and in turn activates IKK-NF-kappaB and JNK, which regulate cell survival, gro

10 ase (IKK) gamma subunits, thereby activating IKK.

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

12 constitutively overexpressing kinase-active IKK-beta, an essential kinase for NF-kappaB activation,

13 prevents RelA-P-Ser536, but does not affect IKK activation of IkappaBalpha.

14 Because the Akt-IKK-JNK-MEK-MK2 pathways regulate many important cellula

15 ed NEMO protein interactions with IKK-alpha, IKK-beta, TNF receptor-associated factor 6, TNF receptor

16 omotes NF-kappaB activation by serving as an IKK scaffold as well as an isomerase.

17 , we demonstrate that TBK1, identified as an IKK-related kinase, may predominantly control the activa

18 ppaBalpha degradation via the lysosome in an IKK-dependent and IKK-independent manner.

19 appaB) kinase gamma (IKKgamma) subunit of an IKK complex and uses this pathway to modulate the expres

20 ction of PTX3 by melanoma cells triggered an IKK/NFkappaB signaling pathway that promotes migration,

21 Treatment of CKD mice with an IKK inhibitor (IKK 16; 1 mg/kg) 1 hour after CLP or LPS

22 tment of WAP-Int3 tumor bearing mice with an IKK inhibitor resulted in tumor regression.

23 Thus, ACHP and IKK 16 hit their NF-kappaB target in mouse and human ker

24 the phosphorylation state of both Aurora and IKK kinases and their physical interactions, and the blo

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 ion via the lysosome in an IKK-dependent and IKK-independent manner.

28 ermore, we found that both IKK-dependent and IKK-independent pathways were required for PI-induced Ik

29 retreatment prevented TLR4-dependent ERK and IKK phosphorylation.

30 h a gene-specific recruitment of IKKbeta and IKK-dependent recruitment of p65 NFkappaB to the IL-8/CX

31 cantly decreased the expression of NF-kB and IKK-beta in THP-1 cells.

32 TAK1 are limited to kinases of the MAPK and IKK families and include no direct effectors of biochemi

33 -inducible nuclear translocation of NEMO and IKK/NF-kappaB activation in stably reconstituted NEMO-de

34 gh a cross-talk between calcineurin-NFAT and IKK-NFkappaB pathways.

35 -(4-piperidinyl)-3-pyridinecarbonitrile) and IKK 16 prevented both nuclear translocation of NF-kappaB

36 th vesicular trafficking involving RAB11 and IKK-related kinase, IKKepsilon, are required for PAR3 tr

37 2915863 and rs2569192, TRAF-6-rs5030411, and IKK-1-rs2230804).

38 ator of atherosclerotic plaque stability and IKK activation thus providing a mechanistic explanation

39 where the LUBAC-A20 axis regulates TAK1 and IKK complex formation.

40 EGLN3 to inhibit IKKgamma ubiquitination and IKK-NF-kappaB signaling.

41 tion of cJUN, cFOS, STAT3, p38-MAPK, AKT and IKKs, and the nuclear translocation of NF-kappaB p-65 su

42 nduced by BCR-ABL1, validating NF-kappaB and IKKs as targets for therapy of Ph(+) leukemias.

43 a-induced activation of ERK1/2, JNK, p38 and IKKs in HUVECs.

44 val signaling by effectively reducing Aurora-IKK kinase interactions and NF-kappaB activation.

45 g times, suggesting that currently available IKK inhibitors may affect hemostasis.

46 ase C- (PKC-), inhibitor kappaB kinase beta (IKK-beta), c-Jun N-terminal kinase (JNK), or phospho-JNK

47 ic immunity mediated by IkappaB kinase-beta (IKK-beta), nuclear factor kappaB (NF-kappaB) and related

48 Tax engaged a crosstalk between IKK complex and autophagic molecule complex by directly

49 IKK-beta knockout mice showed that blocking IKK-beta activity significantly prolonged tail bleeding

50 Furthermore, we found that both IKK-dependent and IKK-independent pathways were required

51 erent cell lines, but overexpression of both IKKs induced the strongest NF-kappaB activation.

52 Knock down of both IKKs more effectively inhibited NF-kappaB activation, br

53 Conversely, siRNA knock down of both IKKs significantly decreased nuclear localization and ph

54 Direct phosphorylation of ASK1 by IKK also defines a novel IKK phosphorylation motif.

55 inactivation of the BH3-only protein BAD by IKK independently of NF-kappaB activation suppresses TNF

56 sm by which E3 ubiquitination is impaired by IKK-driven phosphorylation remains unclear.

57 endent, Rbpj-independent, and is mediated by IKK activation and P50 phosphorylation causing mammary t

58 e show that TPL-2 Ser-400 phosphorylation by IKK and TPL-2 Ser-443 autophosphorylation cooperated to

59 F-kappaB activity, which could be rescued by IKK and ROCK inhibitors.

60 g the top pathways and networks regulated by IKKs.

61 dentify phosphorylation of RIPK1 on Ser25 by IKKs as a key mechanism directly inhibiting RIPK1 kinase

62 ed levels of upstream intermediaries (called IKKs) that are needed for NF-kappaB function.

63 nd M1-pUb chains in activating the canonical IKK complex.

64 NF-kappaB is activated through the canonical IKK pathway and plays distinct roles in the pathogenesis

65 ith specific genetic inhibition of catalytic IKK activity in liver parenchymal cells (LPCs; IKKalpha/

66 required for the activation of the catalytic IKK subunits, IKKalpha and IKKbeta, during the canonical

67 ght be unrecognized targets of the catalytic IKK-complex subunits, thereby regulating hepatocarcinoge

68 cise activation mechanism by which catalytic IKK subunits gain the ability to induce NF-kappaB transc

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

70 Inhibition of the IkappaB kinase complex (IKK) has been implicated in the therapy of several chron

71 f a key NF-kappaB activating kinase complex, IKK.

72 xyquinomicin twice a week and 500 mug/kg/day IKK-NBD peptide) for 4 weeks.

73 and AP1-binding sites abolished or decreased IKK-induced interleukin-8 (IL-8) promoter activity.

74 to arbitrate subsequent DNA damage-dependent IKK/NF-kappaB signaling.

75 ate current dynamic models of NEMO-dependent IKK complex activation, and further clarify how the huma

76 Compounds such as wedelactone with dual IKK inhibitory activity and geldanomycins that block IKK

77 anistically, the downstream nuclear effector IKK-related kinase (IKKi) facilitates translocation of A

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

79 uced in DCM from PELP1-cyto HMECs expressing IKK shRNA.

80 interacts with IKK subunits, and facilitates IKK complex assembly.

81 n chain ligase LUBAC, which is essential for IKK activation.

82 fies critical B cell-intrinsic functions for IKK-induced NF-kappaB1 p105 proteolysis in the antigen-i

83 -limiting multiprotein complex necessary for IKK activation.

84 Our results establish a new paradigm for IKK-independent NIK signaling and significantly expand t

85 posttranslational modification required for IKK and downstream NF-kappaB activation.

86 platelets and implying a nongenomic role for IKK.

87 rovide evidence that NEMO is disengaged from IKK complex following genotoxic stress induction.

88 or activation in response to TNF, while high IKK-independent degradation prevents spurious activation

89 We previously identified IKK-epsilon and TBK1 as promising therapeutic targets fo

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

91 In line with their roles in IKK activation, TNF-induced Ser25 phosphorylation of RIP

92 ted the activation of IKK complex, including IKK-beta.

93 ghly efficient while avoiding indiscriminate IKK/NF-kappaB inhibition in normal cells.

94 Individually, IKK activity varied among different cell lines, but over

95 ilencing of Bcl10 also inhibited S1P-induced IKK phosphorylation.

96 Treatment of CKD mice with an IKK inhibitor (IKK 16; 1 mg/kg) 1 hour after CLP or LPS administration

97 As a tumor suppressor, A20 directly inhibits IKK activation and HL cell survival via its C-terminal l

98 in EOC cells and that the mechanism involves IKK, suggesting that using IKK inhibitors may increase t

99 aB kinase/nuclear [corrected] factor kappaB (IKK/NF-kappaB) signaling exhibits important yet opposing

100 hibitor-kappaB kinase-nuclear factor-kappaB (IKK-NF-kappaB) and epidermal growth factor receptor-acti

101 cells with inhibitors of PI3K-AKT-NF-kappaB, IKK-NF-kappaB or JAK2-STAT3 pathways killed surviving GB

102 ng activity, activity of the upstream kinase IKK, and amount of IkappaBalpha inhibitor phosphorylated

103 members of the inhibitor of kappa B kinase (IKK) complex, NF-kappaB essential modifier (NEMO), and I

104 egulated by the inhibitor of kappa B kinase (IKK) regulatory complex.

105 inhibitor of nuclear factor kappa-B kinase (IKK) together with cochaperone Cdc37, which is critical

106 , as well as PI3K, MAPK, and IkappaB kinase (IKK) activation.

107 in EOC cells is dependent on IkappaB kinase (IKK) activity and associated with a gene-specific recrui

108 mponent complex that induces IkappaB kinase (IKK) activity and NF-kappaB activation.

109 eletion, exhibited increased IkappaB kinase (IKK) activity and production of proinflammatory cytokine

110 TNFalpha-induced increase in IkappaB kinase (IKK) activity, as well as the expression of NF-kappaB ta

111 n upstream regulator of both IkappaB kinase (IKK) and c-Jun N-terminal kinase (JNK), and an important

112 silencing induced increased IkappaB kinase (IKK) and IkappaBalpha phosphorylation upon TCR stimulati

113 Activation of IkappaB kinase (IKK) and NF-kappaB by genotoxic stresses modulates apopt

114 , S1P, but not TNF, promotes IkappaB kinase (IKK) and p65 phosphorylation, IkappaBalpha degradation,

115 adapter complex to activate IkappaB kinase (IKK) and the classical NF-kappaB pathway.

116 ed through subversion of the IkappaB kinase (IKK) complex (or signalosome), which involves a physical

117 IkappaB kinase (IKK) complex phosphorylation of the TPL-2 C terminus reg

118 IKKbeta), a component of the IkappaB kinase (IKK) complex that regulates nuclear factor-kappaB (NF-ka

119 eracted with subunits of the IkappaB kinase (IKK) complex to inhibit their interaction with each othe

120 ed NF-kappaB proximal to the IkappaB kinase (IKK) complex, and unbiased affinity purification reveale

121 regulatory component of the IkappaB kinase (IKK) complex, controls NF-kappaB activation through its

122 ulator (NEMO) subunit of the IkappaB kinase (IKK) complex.

123 by constitutive activity of IkappaB kinase (IKK) in the cytoplasm.

124 FkappaB-bound IkappaB by the IkappaB kinase (IKK) is required for activation in response to TNF, whil

125 he modulatory subunit of the IkappaB kinase (IKK) kinase, IKKgamma (or NEMO), resulting in the overpr

126 ry mediators such as JNK and IkappaB kinase (IKK) occurs rapidly upon consumption of a high-fat diet,

127 receptor complex, impairing IkappaB kinase (IKK) recruitment and NF-kappaB activation.

128 is and whether inhibition of IkappaB kinase (IKK) reduces the cardiac dysfunction in CKD sepsis.

129 opic signaling kinases: Akt, IkappaB kinase (IKK), c-jun N-terminal kinase (JNK), mitogen-activated p

130 Chemical inhibition of IkappaB kinase (IKK), mitogen-activated protein extracellular signal-reg

131 G1/ULK1 and the noncanonical IkappaB kinase (IKK), TANK-binding kinase 1 (TBK1), which have not been

132 l to NF-kappaB activation is IkappaB kinase (IKK), which phosphorylates IkappaBalpha, releasing NF-ka

133 nd led to phosphorylation of IkappaB kinase (IKK)-alpha.

134 itination and degradation of IkappaB kinase (IKK)-beta thus terminating IKK activity.

135 otein kinase C) and requires IkappaB kinase (IKK)-beta.

136 The importance of IkappaB kinase (IKK)-induced proteolysis of NF-kappaB1 p105 in B cells w

137 nes TNF and IL-17 stimulated IkappaB kinase (IKK)-NF-kappaB and impaired osteogenic differentiation o

138 ciated factor 6 (TRAF6), and IkappaB kinase (IKK)-related kinases, but not for TRIF-related adaptor m

139 a key regulator of canonical IkappaB kinase (IKK)/NF-kappaB signaling in response to interleukin-1 (I

140 uction of TRAF3IP2 activates IkappaB kinase (IKK)/NF-kappaB, JNK/AP-1, and c/EBPbeta and stimulates t

141 flammation by activating the IkappaB kinase (IKK)/nuclear factor kappaB (NF-kappaB) and stress kinase

142 F5 was dependent on TAK1 and IkappaB kinase (IKK)beta, which thus reveals a physiological role of the

143 ed the inhibitor of kappaB (IkappaB) kinase (IKK) complex regulatory subunit NEMO [nuclear factor kap

144 vating inhibitor of kappaB (IkappaB) kinase (IKK) complex, which subsequently recruited an autophagy

145 the inhibitor of NF-kappaB (IkappaB) kinase (IKK) kinase TAK1 underwent normal positive selection but

146 r of nuclear factor-kappaB (IkappaB) kinase (IKK)/nuclear factor-kappaB (NFkappaB) signaling cascades

147 The IkappaB-Kinase (IKK) complex-consisting of the catalytic subunits, IKKal

148 )26 blocks TNF-alpha-induced IkappaB-kinase (IKK) phosphorylation, a key step in NF-kappaB activation

149 -dependent TLR signals drive IkappaB-kinase (IKK)2-mediated phosphorylation of phagosome-associated S

150 eraction between inhibitor of kappaB kinase (IKK) and apoptosis signal-regulating kinase 1 (ASK1), un

151 up-regulation of inhibitor of kappaB kinase (IKK) and increased phosphorylation of the NF-kappaB subu

152 subunits of the inhibitor of kappaB kinase (IKK) complex, IKK1 and IKK2, to investigate this questio

153 0-272) of the inhibitor of NF-kappaB kinase (IKK) gamma subunits, thereby activating IKK.

154 g subunit of the inhibitor of kappaB kinase (IKK) holocomplex and is required for the activation of t

155 The I-kappaB kinase (IKK) subunit NEMO/IKKgamma (NEMO) is an adapter molecule

156 e activity of inhibitor of NF-kappaB kinase (IKK), a key regulator of NF-kappaB activation, by oxidiz

157 lpha activation of inhibitory kappaB kinase (IKK)-alpha, and MEKK1 mediated the activation of IKK com

158 lammatory genes and inhibitor kappaB kinase (IKK)/nuclear factor-kappaB (NF-kappaB) pathway activatio

159 Inhibitor of kappaB kinase (IKK)/nuclear factor-kappaB (NF-kappaB) signaling is a ma

160 etions in either inhibitor of kappaB kinase (IKK)alpha or IKKbeta, two critical regulators of NFkappa

161 he regulatory subunit of the IkappaB kinase [IKK] complex).

162 suggests that the NFkappaB inducing kinase, IKK, a signaling hub onto which many signaling pathways

163 tein STING, which then activates the kinases IKK and TBK1 to induce interferons and other cytokines(2

164 sters that are phosphorylated by the kinases IKK and/or TBK1 in response to stimulation.

165 function by recruiting the IkappaB kinases (IKK) to the IKK complex.

166 ubstrate for the inhibitory kappa B kinases (IKKs), IKKalpha and IKKbeta, and, in human hepatic myofi

167 plex formation of CD91 with IkappaB kinases (IKKs) alpha and beta and increased the levels of phospho

168 e aspirin directly inhibits IkappaB kinases (IKKs) to phosphorylate IkappaBalpha for NF-kappaB activa

169 ly target IKKs or other factors that mediate IKK activation.

170 d, inhibition of Akt suppressed S1P-mediated IKK and p65 phosphorylation and degradation of IkappaBal

171 ractions is a new viral strategy to minimize IKK activation and to control NEMO polyubiquitination.

172 ation, highlighting a new pathway modulating IKK-NF-kappaB activity.

173 bicyclic peptidyl inhibitor against the NEMO-IKK interaction.

174 t will greatly facilitate the design of NEMO/IKK inhibitors.

175 Inhibition of the NEMO/IKKs interaction is an attractive therapeutic paradigm f

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

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

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

179 Noncanonical IKKs reduce catecholamine sensitivity by phosphorylating

180 activation of UPR signaling, neither JNK nor IKK appeared to be activated.

181 ACHP, but not IKK 16, was nontoxic to mouse or human keratinocytes at

182 rylation of ASK1 by IKK also defines a novel IKK phosphorylation motif.

183 ubunits individually decreased 8/15 (53%) of IKK-targeted genes sampled and similarly inhibited cell

184 naling complex, leading to the activation of IKK and TBK1.

185 ally, NEMO deficiency hampered activation of IKK complex in osteoclast precursors, causing arrest of

186 -alpha, and MEKK1 mediated the activation of IKK complex, including IKK-beta.

187 pathways but does not prevent activation of IKK- or TBK1-dependent pathways.

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

189 overexpression resulted in the activation of IKK/NF-kappaB, JNK/AP-1, c/EBPbeta, and p38 MAPK and ind

190 the cytotoxic effect of TNF in conditions of IKK inhibition.

191 This conservation of IKK activation among the cFLIP family using different me

192 The prosurvival function of IKK centers on activation of the transcription factor NF

193 coring the NF-kappaB-independent function of IKK during thymic development.

194 stence of NF-kappaB-independent functions of IKK subunits with potential impact on liver physiology a

195 ing pathways and highlight the importance of IKK signaling and the HCMV U(L)26 protein in shaping the

196 This function was independent of IKK kinase, a major downstream target of the CARMA1 comp

197 oposed mechanisms suggest that inhibition of IKK activation is an essential component of its regulato

198 Pharmacological inhibition of IKK-beta during IgE-dependent stimulation strongly reduc

199 Here we show that acute inhibition of IKK-epsilon and TBK1 with amlexanox treatment increases

200 In contrast, the inhibition of IKK-NF-kappaB significantly enhanced MSC-mediated bone f

201 ator resveratrol or BMS-345541 (inhibitor of IKK) inhibited IL-1beta- and NAM-induced suppression of

202 mice with MLN120B, a selective inhibitor of IKK-2, resulted in suppression of neutrophil infiltratio

203 nteracts with TRAF2, an upstream mediator of IKK activation.

204 mplex through the regulatory subunit NEMO of IKK, and specifically inhibited K63-linked ubiquitinatio

205 evidence for the existence of two phases of IKK activation: the immediate phase, induced by TRAF2/cI

206 n reduced S1P-induced the phosphorylation of IKK and p65.

207 arly to LPS, blocking the phosphorylation of IKK and the p65 subunit of NF-kappaB and inducing the sy

208 ency results in increased phosphorylation of IKK, IkappaBalpha, and NF-kappaB p65 in LPS-stimulated c

209 own of USP18 enhanced the phosphorylation of IKK, the degradation of IkappaB, and augmented the expre

210 nd on BCL10, resulting in the recruitment of IKK and the linear ubiquitin chain ligase LUBAC, which i

211 also called NEMO), the regulatory subunit of IKK complex.

212 P3 kinase, TAK1, is known to act upstream of IKK and MAPK cascades in several cell types, and is typi

213 n network downstream of TNFR and upstream of IKK, and depends on the level of the NF-kappaB system ne

214 nd raise potential concerns about the use of IKK inhibitors in colorectal cancer patients.

215 IPK1 or RIPK3 might be downstream targets of IKKs.

216 teins BRD2 and BRD4 in maintaining oncogenic IKK activity in ABC DLBCL.

217 mbination with other modulators of oncogenic IKK signaling.

218 levels of NF-kappaB, AP1, p-STAT3, p-AKT, p-IKKs and p-p38 MAPK were also determined.

219 naling, demonstrated by reduction of phospho-IKK-beta, -IkappaB-alpha, and p65 nuclear translocation

220 he IKK complex, implying that MC159 prevents IKK activation via an as-yet-unidentified strategy.

221 of p300, IKKalpha, and IKKbeta and promoted IKK-mediated activating phosphorylation of p65 at Ser-53

222 Mechanistically, LUBAC promotes IKK/NF-kappaB activity and NEMO linear ubiquitination in

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

224 F (TNF receptor-associated factor) proteins, IKK, NF-kappaB, ubiquitin ligases, and deubiquitinating

225 found that inducible IkappaB kinase-related (IKK-related) kinase IKBKE expression and JAK/STAT pathwa

226 rs4807000), current wheeze (ST-2-rs17639215, IKK-1-rs2230804, and TRIF-rs4807000), and atopy (CD14-rs

227 ies with IKK inhibitors or platelet-specific IKK-beta knockout mice showed that blocking IKK-beta act

228 attenuates I/R-induced nitroxidative stress, IKK/NF-kappaB and JNK/AP-1 activation, inflammatory cyto

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

230 cIAP1 interactions to strategically suppress IKK activation.

231 downstream signaling proteins, such as TAK1, IKKs, and PP2A, that impairs TRAF6-mediated activation o

232 nia infection, a physiological model of TAK1/IKK inhibition, and rescues the cell death-induced multi

233 ivation, triptolide does not directly target IKKs or other factors that mediate IKK activation.

234 nfection, our results suggest that targeting IKK-NF-kappaB may have dual benefits in enhancing bone r

235 f IkappaB kinase (IKK)-beta thus terminating IKK activity.

236 during development of SP thymocytes and that IKK was required to prevent RIPK1-kinase-dependent death

237 Instead, we found that IKK controlled thymocyte survival by repressing cell-dea

238 Our results reveal that IKK inhibits TNFalpha-induced apoptosis through two dist

239 d mathematical modeling analyses showed that IKK activity is regulated by positive feedback from IKKb

240 Finally, we showed that IKK was required to protect Rel-deficient thymocytes fro

241 The IKK complex, which is composed of two catalytic subunits

242 emonstrate that combining vorinostat and the IKK inhibitor Bay 117085 significantly reduces tumor gro

243 hysical interaction between ks-vFLIP and the IKK kinase modulatory subunit IKKgamma.

244 itor of kappaB kinase beta (IKKbeta) and the IKK-related kinase epsilon (IKKepsilon) to enable host N

245 pstream activators of NF-kappaB, such as the IKK complex, arrests their development.

246 ontrolling NF-kappaB activation, such as the IKK complex, serve dual independent functions because th

247 question the importance of NF-kappaB as the IKK target required for thymocyte survival.

248 its, IKK-alpha and -beta, and attenuates the IKK catalytic activity.

249 involvement of ASK1 in diverse diseases, the IKK/ASK1 interface offers a promising target for therape

250 inding of MC159 to NEMO does not disrupt the IKK complex, implying that MC159 prevents IKK activation

251 expected, NF-kappaB-independent role for the IKK complex in protecting cells from RIPK1-dependent dea

252 V-1 reactivation from latency by keeping the IKK complex functional and thus connects T-cell activati

253 roximal events lead to the activation of the IKK (IkappaB kinase).

254 ), which was essential for activation of the IKK complex and subsequent signaling through the extrace

255 The loss of the IKK complex components prevents nuclear translocation an

256 otein that participates in activation of the IKK complex in response to signals transduced from prote

257 O prevents the conformational priming of the IKK complex that occurs when NEMO binds to ubiquitin cha

258 By promoting recruitment of the IKK complex to complex I, LUBAC also promotes TRAIL-indu

259 otein interacts with the NEMO subunit of the IKK complex to prevent NEMO interactions with the cIAP1

260 iation of Bcl10 with the NEMO subunit of the IKK complex.

261 that activation occurs at or upstream of the IKK complex.

262 this ligase complex in the regulation of the IKK family.

263 uitin binding function for activation of the IKK kinase (or kinase complex), but none form a stable c

264 ex and the kinase TAK1 for activation of the IKK kinase.

265 ss of expression of IKK2, a component of the IKK-nuclear factor kappaB (NF-kappaB) pathway.

266 y is an early and crucial determinant of the IKK/NF-kappaB signaling arm of the mammalian DNA damage

267 This step turns off the IKK/NF-kappaB/SOD2 antioxidant pathway.

268 lation-resistant PKD1 mutant potentiates the IKK/NF-kappaB/SOD2 oxidative stress detoxification pathw

269 Moreover, USP18 targeted the IKK complex through the regulatory subunit NEMO of IKK,

270 We demonstrate here that the IKK complex phosphorylates RIPK1 at TNFR1 complex I and

271 In this issue, Meng et al. reveal that the IKK regulator NLRC5 shapes NF-kappaB activity through a

272 tial clinic applications, we showed that the IKK small molecule inhibitor, IKKVI, enhanced osteogenic

273 FKBP51 isomerase activity, we found that the IKK-regulatory role of FKBP51 involves both its scaffold

274 down inhibits the binding of IKKgamma to the IKK catalytic subunits, IKK-alpha and -beta, and attenua

275 recruiting the IkappaB kinases (IKK) to the IKK complex.

276 Many receptors signal via adaptors to the IKK-NF-kappaB axis, transducing extracellular cues to tr

277 ence of Rbpj through an association with the IKK signalosome.

278 ation revealed that MC005 interacts with the IKK subunit NEMO (NF-kappaB essential modulator).

279 Here, we analyzed the requirements for the IKKs in myeloid cells in vivo in response to Francisella

280 pha (IKKalpha) and IKKbeta, we find that the IKKs are host restriction factors that contribute to cyt

281 Collectively, our data indicate that the IKKs restrict infection but HCMV targets their signaling

282 radiation dermatitis and skin aging through IKK modulation and motivate the exploration of HOCl use

283 , including those of the Notch, Wnt and TNFR/IKK/NF-kappaB pathways, and discuss the potential role o

284 We demonstrate that HDAC9 binds to IKK (inhibitory kappa B kinase)-alpha and beta, resultin

285 old protein by recruiting E3 ligase TRAF6 to IKK complex to activate NF-kappaB in response to EGF sti

286 c stress-induced NEMO nuclear translocation, IKK/NF-kappaB activation, and inflammatory cytokine tran

287 enes (CD14, TLR4, IRF3, TRAF-6, TIRAP, TRIF, IKK-1, ST-2, SOCS1) were found to modulate the effect of

288 Further, IL-1 triggered IKK/NF-kappaB signaling and induction of target genes is

289 zation of PELP1 up-regulates pro-tumorigenic IKK and secreted inflammatory signals, which through par

290 kinase inhibitor library, we identified two IKK inhibitors that were high-affinity substrates for p-

291 bitors suggest that the proteasome-ubiquitin-IKK-TPL2-MNK1 axis was required during activation recept

292 echanism involves IKK, suggesting that using IKK inhibitors may increase the effectiveness of HDAC in

293 known to activate the NF-kappaB pathway via IKK activation.

294 While IKK-deficient thymocytes were acutely sensitive to tumor

295 -23), which was found forming a complex with IKK in LPS-activated BMMCs.

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

297 strate that FKBP51 physically interacts with IKK subunits, and facilitates IKK complex assembly.

298 of NF-kappaB activation by interfering with IKK activity.

299 In vivo studies with IKK inhibitors or platelet-specific IKK-beta knockout mi

300 mponents and their spatial interactions with IKKs in determining the binding targets of NF-kappaB com