ライフサイエンスコーパス: IkappaBalpha

1 IkappaBalpha is an inhibitor of NF-kappaB, a family of t

2 IkappaBalpha mutant --> Rag2(-/-), but not WT-->IkappaBa

3 IkappaBalpha or the combination of IkappaBalpha and RelA

4 IkappaBalpha resides in the cytosol where it retains the

5 rylation of translation initiation factor 2, IkappaBalpha, and JNK, indicating induction of endoplasm

6 3T3 IkappaBalpha(-/-) cells also become protected from apopt

7 ear import and DNA binding without affecting IkappaBalpha degradation.

8 ced IkappaBalpha synthesis without affecting IkappaBalpha degradation.

9 paB inhibitor IkappaBalpha without affecting IkappaBalpha phosphorylation.

10 inhibited the phosphorylation involving AKT, IkappaBalpha, NFkappaB.

11 at MSA inhibited the phosphorylation of AKT, IkappaBalpha, and NFkappaB.

12 tations in the inhibitor of NF-kappaB alpha (IkappaBalpha) are susceptible to severe recurrent infect

13 f the mutant form of inhibitor kappaB-alpha (IkappaBalpha) in BM-MSCs markedly reduced the stromal-me

14 nges of the major molecules of the PKC-alpha/IkappaBalpha- and calcineurin/IkappaB-beta-dependent NF-

15 ibly by reducing NF-kappaB activation via an IkappaBalpha/Akt pathway and by downmodulating pathways

16 in-protein interactions (e.g. with Raf-1 and IkappaBalpha) are altered by CO2 exposure, although othe

17 binding to the promoters of IL-6, IL-8, and IkappaBalpha in response to TNF-alpha with TGF-beta1 pre

18 g inhibitory molecules SOCS1, SHIP1, A20 and IkappaBalpha), exerting an overall inhibitory effect on

19 Hypercapnic acidosis and IkappaBalpha-SuperRepressor transgene overexpression red

20 induced phosphorylation of IKKalpha/beta and IkappaBalpha and degradation of IkappaBalpha and nuclear

21 c levels of phosphorylated IKKalpha/beta and IkappaBalpha, nuclear translocation of p65, and iNOS exp

22 served, and structures show that the DNA and IkappaBalpha binding sites on NF-kappaB are overlapping.

23 ncrease in the Foxp3(+), CD4(+)Foxp3(+), and IkappaBalpha(+) populations in whole blood and pleural f

24 ENP1 promotes the deSUMOylation of GATA2 and IkappaBalpha in endothelial cells, resulting in increase

25 g induced increased IkappaB kinase (IKK) and IkappaBalpha phosphorylation upon TCR stimulation.

26 sphorylation of IkappaB kinase (IKKbeta) and IkappaBalpha in the presence of tumor necrosis factor al

27 he transcriptional activity of NF-kappaB and IkappaBalpha phosphorylation.

28 lation of Bcl-2, MMP-2 and -9, NF-kappaB and IkappaBalpha.

29 treatment acted via PP2A to prevent p38 and IkappaBalpha phosphorylation and matrix metalloproteinas

30 the interface between NFkappaB(RelA/p50) and IkappaBalpha encompasses only the dimerization domains.

31 duces stable nuclear localization of p65 and IkappaBalpha proteins in the absence of additional pro-i

32 blocked Dox-induced p38 phosphorylation and IkappaBalpha degradation and enhanced Dox-induced cytoto

33 on and phosphorylation of canonical RELA and IkappaBalpha and alternative p52 and RELB subunits.

34 r levels of BCL3 and phosphorylated RelA and IkappaBalpha in inflamed vs noninflamed regions.

35 r defects in activation of the ERK1/2-S6 and IkappaBalpha modules.

36 een NF-kappaB, its cognate DNA sequence, and IkappaBalpha was observed.

37 ces the phosphorylation of c-Jun, STAT3, and IkappaBalpha.

38 non-canonical IkappaB kinase varepsilon and IkappaBalpha, and consequently protects from excessive i

39 nslated into reduced induction of Bcl-xL and IkappaBalpha, 2 bona fide target genes of the canonical

40 wnward arrow, NF-kappaB1/p50 downward arrow, IkappaBalpha upward arrow, IkappaBbeta upward arrow).

41 DXMS) experiments on IkappaBalpha as well as IkappaBalpha bound to dimerization-domain-only construct

42 BMP9/10 increased basal IkappaBalpha protein expression, but did not alter p65/R

43 eincubated with the high dose, reduced basal IkappaBalpha levels were found, accompanied by increased

44 strate binding to IKKbeta and thereby blocks IkappaBalpha phosphorylation and NF-kappaB nuclear trans

45 paB pathway signaling analysis revealed both IkappaBalpha and p65 phosphorylation in ZO-1-overexpress

46 the FRET efficiency was lower for the bound IkappaBalpha molecules (0.67) than for the free IkappaBa

47 f inhibition of nuclear factor (NF)kappaB by IkappaBalpha.

48 Is activates NF-kappaB, which is mediated by IkappaBalpha degradation via the lysosome in an IKK-depe

49 Fetal DNA activates NF-kappaB, shown by IkappaBalpha degradation in human PBMCs resulting in pro

50 al NF-kappaB signaling and was suppressed by IkappaBalpha and a dominant negative form of TRAF6.

51 ession (interleukin-1beta [Il-1beta], CD11b, IkappaBalpha, indolamine 2,3-deoxygenase [Ido]) was quan

52 y that DENV protease interacts with cellular IkappaBalpha and IkappaBbeta and cleaves them.

53 Akt and eNOS phosphorylation and to decrease IkappaBalpha (inhibitor of the transcription factor NF-k

54 n and intrinsic activity, thereby decreasing IkappaBalpha degradation, and subsequent nuclear factor-

55 nock-down by siRNAs for IKKbeta only delayed IkappaBalpha degradation up to 8 h after treatment with

56 ation-resistant form of IkappaBalpha, DeltaN-IkappaBalpha, Tax-induced senescence is averted.

57 inhibition through the expression of DeltaN-IkappaBalpha allows cells of a human osteosarcoma (HOS)

58 te p38alpha activation and IKKbeta-dependent IkappaBalpha degradation in response to UV.

59 The PMA-dependent IkappaBalpha phosphorylation was significantly inhibited

60 thogenesis of dengue hemorrhage and discover IkappaBalpha and IkappaBbeta to be the new cellular targ

61 Activation of NF-kappaB by knocking down IkappaBalpha using siRNA could mimic the suppressive eff

62 nts in the promoter of NFKBIA, which encodes IkappaBalpha, the major negative regulator of NF-kappaB.

63 aB nuclear localization and IL-6 expression, IkappaBalpha and transforming growth factor beta-activat

64 of NFKBIA influenced NFKBIA gene expression, IkappaBalpha protein expression, and TLR-mediated inflam

65 e-specific and total NFKBIA mRNA expression, IkappaBalpha protein expression, and TLR responsiveness;

66 to increased TRAF6 ubiquitination and faster IkappaBalpha degradation.

67 ion of the degron's activity is critical for IkappaBalpha's signaling functions.

68 is not only sufficient but also required for IkappaBalpha's short half-life.

69 ppaBalpha molecules (0.67) than for the free IkappaBalpha molecules (0.74), apparently indicating tha

70 and 0.9 FRET efficiency, whereas in the free IkappaBalpha, the fluctuations extend to <0.5 FRET effic

71 ediate ternary complex than that formed from IkappaBalpha(WT) because DNA dissociated more slowly.

72 NF-kappaB RelA subunit after liberation from IkappaBalpha inhibitor leading to its ubiquitination and

73 phosphorylation of the NF-kappaB gatekeeper IkappaBalpha and survival occurred in MYD88 L265P-expres

74 r-Grm1, Arg-Atp2b2, Glu-Bak, Arg-Igfbp2, Glu-IkappaBalpha, and Arg-c-Fos), are short-lived substrates

75 ppaBalpha mutant --> Rag2(-/-), but not WT-->IkappaBalpha mutant, bone marrow chimeras formed proper

76 ze the naturally occuring AR domain of human IkappaBalpha to denaturation; however, only the YLTA mut

77 appaB inhibitors: the prototypical IkappaBs (IkappaBalpha, IkappaBbeta, and IkappaBepsilon), which fo

78 Three canonical IkappaBs, IkappaBalpha, IkappaBbeta, and IkappaBepsilon, exist, bu

79 results in increased phosphorylation of IKK, IkappaBalpha, and NF-kappaB p65 in LPS-stimulated cells.

80 ced sequential phosphorylation of TAK1, IKK, IkappaBalpha and RELA in human HNSCC lines.

81 lates CXCL5 expression by activating IKKbeta-IkappaBalpha and p38 MAPK pathways via NF-kappaB nuclear

82 ortalized patient B cells displayed impaired IkappaBalpha phosphorylation and NFkappaB nuclear transl

83 one of the patients showed severely impaired IkappaBalpha degradation and IL-2 production after activ

84 duced "translational interference," impeding IkappaBalpha resynthesis.

85 elial cells resulted in a marked increase in IkappaBalpha phosphorylation, corresponding with elevate

86 be the roles of these consensus mutations in IkappaBalpha.

87 ibitor 2A (Spi2a) was highly up-regulated in IkappaBalpha-deficient mice.

88 ivation that plays a key scaffolding role in IkappaBalpha degradation and RelA Ser 276 phosphorylatio

89 activity of p97 is essential for its role in IkappaBalpha proteolysis.

90 rene-labeled DNA or the native tryptophan in IkappaBalpha were monitored.

91 quently, inhibition of miR-891a-5p increased IkappaBalpha level, prevented nuclear translocation of N

92 aBalpha degradation, suggesting an increased IkappaBalpha turnover.

93 levels were found, accompanied by increased IkappaBalpha degradation, suggesting an increased Ikappa

94 al to the ability of DENV protease to induce IkappaBalpha and IkappaBbeta cleavage and trigger hemorr

95 E2 enhanced TNF-alpha induced IkappaBalpha synthesis without affecting IkappaBalpha de

96 overexpression attenuated TNF-alpha-induced IkappaBalpha phosphorylation and degradation, and nuclea

97 pretreatment inhibited the TNF-alpha-induced IkappaBalpha phosphorylation that targets the IkappaBalp

98 Indeed, knockdown of DDB2-induced IkappaBalpha gene expression restored NF-kappaB activity

99 38 phosphorylation and inhibited Dox-induced IkappaBalpha degradation.

100 urthermore, PRRSV/PCV2 co- infection induced IkappaBalpha degradation and phosphorylation as well as

101 PO also prevented PA-induced IkappaBalpha degradation, RelA nuclear translocation, NO

102 endent pathways were required for PI-induced IkappaBalpha degradation.

103 r knock-down of GSK-3beta delayed PI-induced IkappaBalpha degradation.

104 B expression by siRNAs suppressed PI-induced IkappaBalpha degradation.

105 Inactive GSK-3beta accelerated PI-induced IkappaBalpha degradation.

106 By inducing IkappaBalpha and IkappaBbeta cleavage and IkappaB kinase

107 Instead, it requires p53 to inhibit IkappaBalpha phosphorylation and degradation.

108 rough degradation of its dedicated inhibitor IkappaBalpha, but the mechanism by which NF-kappaB-media

109 DCs also down-regulated NF-kappaB inhibitor IkappaBalpha and increased Bcl-2 expression.

110 olecules: degradation of NF-kappaB inhibitor IkappaBalpha and phosphorylation of MAPK Erk and p38 upo

111 complex, recognizes the NF-kappaB inhibitor IkappaBalpha and precursor p100 for proteasomal degradat

112 maintained levels of the NF-kappaB inhibitor IkappaBalpha in the intestinal epithelium, and systemica

113 endent regulation of the NF-kappaB inhibitor IkappaBalpha leads to enhanced NF-kappaB activity and cy

114 d the degradation of the NF-kappaB inhibitor IkappaBalpha without affecting IkappaBalpha phosphorylat

115 nt ubiquitination of the NF-kappaB inhibitor IkappaBalpha, whereas SVV additionally prevents IkappaBa

116 of Nfkbia mRNA (which encodes the inhibitor IkappaBalpha), largely explained this phenotype.

117 via deletion of one allele of its inhibitor, IkappaBalpha, did not induce prostatic tumorigenesis in

118 expressing genetic NF- kappaBeta inhibitors (IkappaBalpha and p100 super-repressor constructs) to fun

119 f transcript levels of NF-kappaB inhibitors, IkappaBalpha and A20.

120 r activity as a result of lowered inhibitory IkappaBalpha (nuclear factor of kappa light polypeptide

121 owever, although the TGF-beta1 expression is IkappaBalpha dependent and is regulated by the canonical

122 e canonical pathway, the IL-10 expression is IkappaBalpha independent, and its inhibition by BZ is as

123 t degradation of the inhibitor of NF-kappaB (IkappaBalpha), despite efficient bortezomib-mediated inh

124 c degradation of the inhibitor of NF-kappaB, IkappaBalpha, and nuclear NF-kappaB translocation in lun

125 lation of ERK1/2 and inhibitory kappaBalpha (IkappaBalpha), as well as the levels of Bcl-xL and Mcl-1

126 Degradation of inhibitor of kappaBalpha (IkappaBalpha) and p65 phosphorylation, nuclear transloca

127 This compelling and provocative model links IkappaBalpha to the activity of the Polycomb repressors

128 Mechanistically, IkappaBalpha blocks the association of ACTN4 and p65 in

129 At mitochondria, IkappaBalpha stabilises the complex of VDAC1 and hexokin

130 hat accumulate high amounts of mitochondrial IkappaBalpha as a NF-kappaB target gene.

131 ctivation from latency by directly modifying IkappaBalpha, leading to a novel mechanism of NF-kappaB

132 -kappaB inhibition genetically with a mutant IkappaBalpha or pharmacologically with pyrrolidine dithi

133 es) sequence in NFkappaB stripping, a mutant IkappaBalpha was generated in which five acidic PEST res

134 the individual steps of a more folded mutant IkappaBalpha were also measured.

135 ng an endothelial-specific dominant negative IkappaBalpha cassette under the Tie2 promoter display a

136 ectopic overexpression of dominant-negative IkappaBalpha efficiently repressed rHSP90alpha-induced T

137 ectopic overexpression of dominant-negative IkappaBalpha perturbed ET-1-induced integrin alphaV and

138 ive STAT3 and inhibited by dominant-negative IkappaBalpha.

139 the negative feedback regulator of NFkappaB, IkappaBalpha.

140 iology approach, we demonstrated that NFKBIA/IkappaBalpha is a central hub in transcriptional respons

141 TNFalpha-treated PML(-/-) cells show normal IkappaBalpha degradation and NF-kappaB nuclear transloca

142 s intolerance to the accumulation of nuclear IkappaBalpha (also known as NFKBIA), with consequent inh

143 sphorylation, acetylation, and activation of IkappaBalpha kinase.

144 sphorylation, acetylation, and activation of IkappaBalpha kinase.

145 FGF receptors and involves the activation of IkappaBalpha-mediated NFkappaB signaling pathway.

146 er536, but does not affect IKK activation of IkappaBalpha.

147 Notably, constitutive activation of IkappaBalpha/NF-kappaB(p65) in this circuit is not depen

148 ur results reveal the unexpected activity of IkappaBalpha in guarding the integrity of the OMM agains

149 ty of the upstream kinase IKK, and amount of IkappaBalpha inhibitor phosphorylated following TNFalpha

150 g of NFkappaB(RelA/p50) stretches the ARD of IkappaBalpha.

151 ed out on the ankyrin repeat domain (ARD) of IkappaBalpha, the temporally regulated inhibitor of cano

152 he second and sixth ankyrin repeats (ARs) of IkappaBalpha were labeled with FRET pairs showed slow fl

153 equal to the rate constant of association of IkappaBalpha with the NF-kappaB-DNA complex, showing tha

154 tatically repels the DNA, and the binding of IkappaBalpha appears to twist the NFkappaB heterodimer s

155 h the high TNF dose, we observed blockade of IkappaBalpha phosphorylation/proteolysis and nuclear p65

156 IkappaBalpha or the combination of IkappaBalpha and RelA selectively were deleted from panc

157 ed feedforward signaling circuit composed of IkappaBalpha/NF-kappaB(p65), miR-196b-3p, Meis2, and PPP

158 tirely separate from its upstream control of IkappaBalpha degradation, thereby identifying a novel Ca

159 onse, resulting in accelerated mRNA decay of IkappaBalpha, an inhibitor of proinflammatory nuclear fa

160 machinery, which promoted the degradation of IkappaBalpha and further supported NF-kappaB activity.

161 pha/beta and IkappaBalpha and degradation of IkappaBalpha and nuclear translocation of p65, and suppr

162 -derived cells show increased degradation of IkappaBalpha and nuclear translocation of the NF-kappaB

163 otein (VCP), resulting in the degradation of IkappaBalpha and subsequent activation of NF-kappaB in t

164 PI3K-Akt activation mediated degradation of IkappaBalpha protein and impaired NF-kappaB self-negativ

165 duction of NF-kappaB, reduced degradation of IkappaBalpha, and increased expression of the NF-kappaB

166 timulated phosphorylation and degradation of IkappaBalpha, or on TNFalpha induction of a NFkappabeta

167 ion of IKK, IkappaB and RELA, degradation of IkappaBalpha, RELA nuclear translocation and DNA binding

168 from phosphorylation-induced degradation of IkappaBalpha, whereas HIF-1alpha up-regulation is NF-kap

169 K and p65 phosphorylation and degradation of IkappaBalpha.

170 ase complex that mediates the degradation of IkappaBalpha.

171 ay that is independent of the degradation of IkappaBalpha.

172 ation was not associated with degradation of IkappaBalpha; instead, enhanced phosphorylation of the N

173 d in mice with pancreas-specific deletion of IkappaBalpha and RelA.

174 Mice with pancreas-specific deletion of IkappaBalpha had constitutive activation of RelA and a g

175 Selective deletion of IkappaBalpha in vivo resulted in enhanced expression of

176 Pancreas-specific deletion of IkappaBalpha results in nuclear translocation of RelA an

177 own about the postubiquitinational events of IkappaBalpha proteolysis.

178 ion of miR-942-5p relieved the expression of IkappaBalpha and reduced Vpr inhibition of KSHV lytic re

179 appaB activity by upregulating expression of IkappaBalpha by binding the proximal promoter of this ge

180 our study is that the induced expression of IkappaBalpha is altered significantly in Hsp72 expressin

181 s blocked by a degradation-resistant form of IkappaBalpha, DeltaN-IkappaBalpha, Tax-induced senescenc

182 ng NF-kappaB signaling through impairment of IkappaBalpha ubiquitination and a general reduction of T

183 ene promoter, this effect was independent of IkappaBalpha degradation/phosphorylation.

184 translocation and activity independently of IkappaBalpha status, prevents intestinal inflammation th

185 The kinetics of interaction of IkappaBalpha with NF-kappaB and its complex with DNA wer

186 signaling pathway is blocked due to lack of IkappaBalpha ubiquitination and, hence, degradation.

187 iRNA was found to enhance cytosolic level of IkappaBalpha and block p65 nuclear translocation and DNA

188 expression of a dominant negative mutant of IkappaBalpha that leads to NF-kappaB degradation or the

189 Moreover, overexpression of IkappaBalpha or IkappaBbeta protects endothelial cells f

190 virus serotype 2-mediated overexpression of IkappaBalpha, which inhibits NF-kappaB nuclear transloca

191 activation by suppressing phosphorylation of IkappaBalpha and ERK.

192 er, which was mediated by phosphorylation of IkappaBalpha and its subsequent degradation via the alte

193 n MyD88 and the inducible phosphorylation of IkappaBalpha and NF-kappaB.

194 oate (4alpha-PDD), caused phosphorylation of IkappaBalpha and stimulated the nuclear translocation of

195 d SAHA, yielded increased phosphorylation of IkappaBalpha, ERK, p38, and JNK in HIV-infected cells ac

196 ired for the CD86-induced phosphorylation of IkappaBalpha, which we previously reported leads to NF-k

197 rate: the negatively charged PEST region of IkappaBalpha electrostatically repels the DNA, and the b

198 that the postubiquitinational regulation of IkappaBalpha by the p97-UFD1L-NPL4 complex is important

199 le in the postubiquitinational regulation of IkappaBalpha turnover after tumor necrosis factor alpha

200 ntrol the postubiquitinational regulation of IkappaBalpha.

201 A neutralizes LPS involves rapid reversal of IkappaBalpha phosphorylation.

202 s as an E3 SUMO ligase in the SUMOylation of IkappaBalpha, which in turn enhances the sequestration o

203 edback loop mediated less newly synthesis of IkappaBalpha mRNA in thoracic aortas (gestational day 20

204 ssembly with reconstituted ubiquitination of IkappaBalpha and beta-catenin by the Skp1-cullin 1-betaT

205 en/deuterium exchange (HDXMS) experiments on IkappaBalpha as well as IkappaBalpha bound to dimerizati

206 tory and adaptive immune responses, yet only IkappaBalpha was shown to limit NF-kappaB activation and

207 paB (RelA-p50) heterodimer induced by DNA or IkappaBalpha binding.

208 showed a direct interactions of p38, ERK or IkappaBalpha with MKP-1, and demonstrated that MKP-1 was

209 tabilizing consensus residues than the other IkappaBalpha ARs, probably contributing to the ease with

210 1 inhibition resulted in reduced levels of P-IkappaBalpha and p65 activity.

211 ha although it, to some extent, suppressed p-IkappaBalpha expression, suggesting that TLR3,4/NF-kappa

212 crystal structures of the NFkappaB(RelA/p50)-IkappaBalpha complex.

213 ptional activity and phosphorylation of p65, IkappaBalpha, IkappaB kinase, and Akt.

214 the E3-ubiquitin ligase beta-TrCP to phospho-IkappaBalpha proteosomal degradation.

215 bits IkappaB kinases (IKKs) to phosphorylate IkappaBalpha for NF-kappaB activation, triptolide does n

216 g TNFRII levels and elevating phosphorylated IkappaBalpha by SUMOylation.

217 ases in the cardiac levels of phosphorylated IkappaBalpha, Akt, and extracellular signal-regulated ki

218 vity by binding directly and phosphorylating IkappaBalpha in cells.

219 kappaB kinase (IKK) and p65 phosphorylation, IkappaBalpha degradation, p65 nuclear translocation, and

220 inding domain of UFD1L and polyubiquitinated IkappaBalpha.

221 oduced into cells, the rate of postinduction IkappaBalpha-mediated export of NFkappaB from the nucleu

222 ins of VZV and SVV are sufficient to prevent IkappaBalpha ubiquitination upon ectopic expression.

223 since SVV with ORF61 deleted still prevented IkappaBalpha phosphorylation and degradation.

224 ppaBalpha, whereas SVV additionally prevents IkappaBalpha phosphorylation.

225 ial novel role for lincRNA-Cox2 in promoting IkappaBalpha degradation in the cytoplasm.

226 its interaction with the inhibitory protein IkappaBalpha and binds to the promoter of critical migra

227 Following pulmonary IkappaBalpha-SuperRepressor transgene overexpression or

228 f tumor-bearing relative to tumor-free rats, IkappaBalpha was greater in hippocampus, and Ido was gre

229 -->inhibition of protein synthesis-->reduced IkappaBalpha production-->activation of NF-kappaB-->incr

230 Suppression of miR-942-5p relieved IkappaBalpha expression and reduced Vpr inhibition of KS

231 had anti-inflammatory activity and repressed IkappaBalpha activation induced by S. aureus via PKA-MKP

232 nt downregulation of the NF-kappaB repressor IkappaBalpha.

233 ed that the inhibitor of NFkappaB signaling, IkappaBalpha, dramatically accelerates the dissociation

234 In nonendotoxemic muscle-specific IkappaBalpha super-repressor diaphragms, caspase-3 activ

235 In muscle-specific IkappaBalpha super-repressor mice subjected to endotoxem

236 Wild-type and transgenic (muscle-specific IkappaBalpha super-repressor) mice with skeletal muscle-

237 ther pharmacologic (curcumin) or genetic (SR-IkappaBalpha) means significantly enhanced the efficacy

238 Stable expression of the super-repressor, SR-IkappaBalpha, that blocks the classical NF-kappaB pathwa

239 rCP from binding its substrates, stabilizing IkappaBalpha and p100 and thereby blocking NF-kappaB act

240 Upon inflammatory stimuli, IkappaBalpha is rapidly degraded via the ubiquitin-prote

241 Although we expected the stretched IkappaBalpha to have regions with increased exchange, in

242 ic effect of both stimuli resulted in strong IkappaBalpha phosphorylation, its rapid degradation, and

243 of NEMO for IKKbeta and the kinase substrate IkappaBalpha and promoting membrane association.

244 riptional repression function for SUMOylated IkappaBalpha.

245 pression of the IkappaBalpha superrepressor (IkappaBalpha-SR) blocked PI-induced NF-kappaB activation

246 pression of the IkappaBalpha superrepressor (IkappaBalpha-SR) or of p65 mutated at Lys-310 prevented

247 ific inhibitor, SC-514, partially suppressed IkappaBalpha degradation and IL-8 production by PIs.

248 ated protein (RAP), which included sustained IkappaBalpha phosphorylation and activation of all 3 MAP

249 the DNA in the presence of newly synthesized IkappaBalpha (termed stripping) is unknown.

250 TAK1/IkappaBalpha/NF-kappaB pathway contributed to induction

251 f SOX9 in HPNE and HPDE cells, and Kras/TAK1/IkappaBalpha/NF-kappaB pathway and a positive feedback b

252 ough upregulating a cellular miRNA to target IkappaBalpha, internalized HIV-1 Vpr inhibits KSHV lytic

253 ough upregulating a cellular miRNA to target IkappaBalpha, internalized Vpr inhibits KSHV lytic repli

254 sion of miR-891a-5p, which directly targeted IkappaBalpha 3' untranslated region, leading to NF-kappa

255 (miRNA), miR-942-5p, that directly targeted IkappaBalpha.

256 ulated by Vpr, miR-942-5p, directly targeted IkappaBalpha.

257 Our results illustrate that, by targeting IkappaBalpha to activate the NF-kappaB pathway, miR-891a

258 We previously demonstrated that IkappaBalpha markedly increases the dissociation rate of

259 We recently discovered that IkappaBalpha enhances the rate of release of nuclear fac

260 We found that IkappaBalpha knockdown activated HIV in both U1 and J-La

261 We show that IkappaBalpha also localises to the outer mitochondrial m

262 Here we show that IkappaBalpha contains an ubiquitin-independent degron wh

263 Previous kinetic studies showed that IkappaBalpha accelerates NF-kappaB dissociation from DNA

264 with the NF-kappaB-DNA complex, showing that IkappaBalpha is optimized to repress transcription.

265 Mice heterozygous for the IkappaBalpha S32I mutation found in patients exhibited t

266 RET pairs showed slow fluctuations as if the IkappaBalpha AR domain was unfolding in its native state

267 a plausible mechanism for a twisting of the IkappaBalpha ARD induced by interactions of the IkappaBa

268 called "stripping." To test the role of the IkappaBalpha C-terminal PEST (rich in proline, glutamic

269 Prenatal or postnatal exposure of the IkappaBalpha degradation inhibitor, pyrollidine dithioca

270 Under native conditions, most of the IkappaBalpha molecules showed stable, high FRET signals

271 ppaBalpha ARD induced by interactions of the IkappaBalpha proline-glutamate-serine-threonine-rich seq

272 Overexpression of the IkappaBalpha superrepressor (IkappaBalpha-SR) blocked PI

273 on in mouse muscles by overexpression of the IkappaBalpha superrepressor (IkappaBalpha-SR) or of p65

274 We performed microarray analyses of the IkappaBalpha- and RelA-deficient pancreata.

275 fluorescence complementation reporters, the IkappaBalpha reporter for NF-kappaB pathway and the cell

276 kappaBalpha phosphorylation that targets the IkappaBalpha protein for degradation and inhibited NF-ka

277 m exchange mass spectrometry showed that the IkappaBalpha(5xPEST) appears to be "caught in the act of

278 r high FRET efficiencies were found when the IkappaBalpha molecules were either free or in complex wi

279 This IkappaBalpha(5xPEST) mutant was impaired in stripping NF

280 The rate constant of this IkappaBalpha-mediated dissociation is nearly equal to th

281 verse responses; NF-kappaB signaling through IkappaBalpha degradation resulted in MnSOD upregulation

282 strated that PKA-calpha can directly bind to IkappaBalpha upon S. aureus stimulation, which influence

283 NF-kappaB was elevated and SUMO1 binding to IkappaBalpha was decreased.

284 factor that directs IKKbeta activity toward IkappaBalpha.

285 tPA independently induced transient IkappaBalpha phosphorylation and extracellular signal-re

286 s with NF-kappaB more rapidly than wild-type IkappaBalpha, but it associates with the NF-kappaB-DNA c

287 x specifically associates with ubiquitinated IkappaBalpha via the interactions between p97 and the SC

288 CF(beta-TRCP) ubiquitin ligase ubiquitinates IkappaBalpha upon stimulation, little is known about the

289 Using various IkappaBalpha mutants, we demonstrate that apoptosis inhi

290 When IkappaBalpha is added to the NF-kappaB-DNA complex, we o

291 When IkappaBalpha is reduced in tumour cells with constitutiv

292 ls also become protected from apoptosis when IkappaBalpha is specifically reconstituted at the OMM.

293 Conversely, when IkappaBalpha binds to the dimerization domains, amide ex

294 of inflammatory responses is associated with IkappaBalpha-independent inhibition of NF-kappaBp65 acti

295 Subsequently, p53 competes with IkappaBalpha for substrate binding to IKKbeta and thereb

296 led that SCF(betaTrCP) formed a complex with IkappaBalpha and that the Nedd8 modified E3-substrate pl

297 ded in our crystal structure, interacts with IkappaBalpha in the NF-kappaB pathway.

298 sion, surprisingly inhibiting NF-kappaB with IkappaBalpha-SR or by GCN5 knockdown in these muscles al

299 cy and poor outcome of HSCT in patients with IkappaBalpha deficiency and suggests that correction of

300 the mechanism by which the half-life of YLTA IkappaBalpha is extended in vivo.