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 can be activated by growth factor stimulation or tum

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

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

5 IKK phosphorylates BAD at serine-26 (Ser26) and primes i

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

7 IKK-complex subunits transmit a previously unrecognized

8 IKK/NF-kappaB signaling is required for wild-type and fu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

24 ntify a novel interaction between Aurora and IKK kinases and show that these pathways can cooperate t

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

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

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

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

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

30 retreatment prevented TLR4-dependent ERK and IKK phosphorylation.

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

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

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

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

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

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

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

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

39 ma interaction, IKKgamma ubiquitination, and IKK-NF-kappaB signaling.

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

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

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

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

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

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

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

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

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

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

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

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

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

53 venting ageing-related hypothalamic or brain IKK-beta and NF-kappaB activation.

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 and cRel due to lack of inhibition of BAD by IKK.

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

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

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

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

61 g the top pathways and networks regulated by IKKs.

62 l Modifier (NEMO) component of the canonical IKK complex bind to K63-pUb chains and M1-pUb chains, re

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 ogether, these results suggest that the CD91/IKK/NF-kappaB signaling cascade is involved in secreted

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

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

72 The IkappaB kinase complex (IKK) is a key regulator of immune responses, inflammatio

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

74 n in controlling the ASK1-JNK axis, coupling IKK to ROS and ER stress response.

75 genetic manipulation (platelet factor 4 Cre:IKK-beta(flox/flox)), blocked SNAP-23 phosphorylation, p

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

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

78 TRAF2 and cIAP1 cooperatively induce delayed IKK activation by recruiting LUBAC to TNFR1.

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

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

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

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

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

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

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

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

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

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

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

90 platelets and implying a nongenomic role for IKK.

91 Cell, Kuo et al. show the essential role for IKK/NF-kappaB signaling in epigenetic regulation by MLL

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

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

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

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

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

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

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

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

100 ind that SK1 is not required for TNF-induced IKK phosphorylation, IkappaB degradation, nuclear transl

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

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

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

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

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

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

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

108 he kinetics and amplitude of IkappaB kinase (IKK) activation, we report that TNF-alpha-induced immedi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124 activation of the canonical IkappaB kinase (IKK) complex.

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

126 Activation of the IkappaB kinase (IKK) is central to NF-kappaB signaling.

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

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

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

130 N-terminal kinase (JNK) and IkappaB kinase (IKK) pathway.

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

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

133 n factor kappaB (IkappaB) by IkappaB kinase (IKK) triggers the degradation of IkappaB and migration o

134 terminal kinase (JNK) and of IkappaB kinase (IKK) were used to investigate the involvement of intrace

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

136 rowth factor beta (TGFbeta), IkappaB kinase (IKK), Ras/mitogen-activated protein kinase (MAPK), phosp

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

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

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

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

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

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

143 IKKepsilon, an IkappaB kinase (IKK)-related kinase, is implicated in inflammation-drive

144 ding BCL10, MALT1, and other IkappaB kinase (IKK)-signalosome components.

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

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

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

148 es a nuclear accumulation of IkappaB kinase (IKK)alpha, and inhibition of IKKalpha enzymatic activity

149 However, phosphorylated IkappaB kinase (IKK)alpha/beta expression and NF-kappaB activity were su

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

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

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

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

154 )26 blocks TNF-alpha-induced IkappaB-kinase (IKK) phosphorylation, a key step in NF-kappaB activation

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

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

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

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

159 0-272) of the inhibitor of NF-kappaB kinase (IKK) gamma subunits, thereby activating IKK.

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

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

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

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

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

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

166 5 subunit or the inhibitor of kappaB kinase (IKK)2 in pancreatic acinar cells of mice.

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

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

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

170 polymers that activate the cytosolic kinases IKK and TBK1, which in turn activate NF-kappaB and IRF3,

171 The noncanonical IkappaB kinases IKK-varepsilon and TANK-binding kinase 1 (TBK1) are indu

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

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

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

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

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

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

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

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

180 bicyclic peptidyl inhibitor against the NEMO-IKK interaction.

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

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

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

184 Noncanonical IKKs reduce catecholamine sensitivity by phosphorylating

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

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

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

188 lation, resulting in decreased activation of IKK and NF-kappaB.

189 of IKK, is instrumental in the activation of IKK and NF-kappaB.

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

191 ly impairs the recruitment and activation of IKK but does not affect K63-linked ubiquitination of TRA

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

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

194 Activation of IKK is achieved by phosphorylation of its main subunit,

195 a-induced immediate and robust activation of IKK requires K63-linked and linearly linked ubiquitinati

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

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

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

199 Blockade of IKK activity using insolubilization by heat shock (HS) a

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

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

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

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

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

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

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

207 Inhibition of IKK-beta, either pharmacologically (with BMS-345541, BAY

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

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

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

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

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

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

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

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

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

217 creased TGF-beta1-induced phosphorylation of IKK, IkappaB and RELA, degradation of IkappaBalpha, RELA

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

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

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

221 An inhibitory role of IKK in JNK signaling has been previously reported to dep

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

223 se gamma (IKKgamma), a regulatory subunit of IKK, is instrumental in the activation of IKK and NF-kap

224 Analyzing the signaling events upstream of IKK activation, we found diminished TGF-beta-activated k

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

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

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

228 IPK1 or RIPK3 might be downstream targets of IKKs.

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

230 mbination with other modulators of oncogenic IKK signaling.

231 DAGs), rather than the activation of JNK or IKK, is pivotal for ER stress to cause hepatic insulin r

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

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

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

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

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

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

238 ubiquitin chain is not capable of recruiting IKK in vivo.

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

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

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

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

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

244 cIAP1 interactions to strategically suppress IKK activation.

245 induced sequential phosphorylation of TAK1, IKK, IkappaBalpha and RELA in human HNSCC lines.

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

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

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

249 Mechanistically, we found that IKK-NF-kappaB activation promoted beta-catenin ubiquitin

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

251 Mechanistic studies further revealed that IKK-beta and NF-kappaB inhibit gonadotropin-releasing ho

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

253 Our data suggest that IKK has a dual role: a transcription-dependent and a tra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

277 ed TNF release in mast cells, preventing the IKK-dependent phosphorylation of SNAP-23, which is neces

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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