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 resides in the cytosol where it retains the

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

5 3T3 IkappaBalpha(-/-) cells also become protected from apopt

6 ear import and DNA binding without affecting IkappaBalpha degradation.

7 inhibited the phosphorylation involving AKT, IkappaBalpha, NFkappaB.

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

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

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

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

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

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

14 5 decreased the phosphorylation of IRF-3 and IkappaBalpha mediated by IKKepsilon and IKKbeta, respect

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

16 Hypercapnic acidosis and IkappaBalpha-SuperRepressor transgene overexpression red

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

18 pha degradation, inhibited IKKalpha/beta and IkappaBalpha phosphorylation, and suppressed nuclear tra

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

20 of the transcriptional regulators CEBPD and IkappaBalpha.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

36 rn activates the anti-inflammatory SMAD7 and IkappaBalpha factors in mesangial cells.

37 eased the endogenous expression of SMAD7 and IkappaBalpha, which are key inhibitory factors in renal

38 also resulted in reduced levels of SMAD7 and IkappaBalpha.

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

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

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

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

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

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

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

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

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

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

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

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

51 The mitigation of TDP-43 neuropathology by IkappaBalpha-SR, which is likely due to an induction of

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

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

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

55 B and cRel to enable elevated cytosolic cRel:IkappaBalpha complex formation and subsequent 4-1BB-indu

56 sequence abnormally accumulate inactive cRel:IkappaBalpha complexes in the nucleus following stimulat

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

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

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

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

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

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

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 but loses its deubiquitinating activity for IkappaBalpha deubiquitination, resulting in excessive NF

68 This motif contains two serines, and for IkappaBalpha and beta-catenin, phosphorylation of these

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

70 n of TRAF6 or IKKbeta, the kinase needed for IkappaBalpha phosphorylation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 duced "translational interference," impeding IkappaBalpha resynthesis.

88 tif near the N terminus that is conserved in IkappaBalpha, beta-catenin, HIV Vpu, and some other prot

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

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

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

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

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

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

95 aBalpha degradation, suggesting an increased IkappaBalpha turnover.

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

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

98 mplex formation and subsequent 4-1BB-induced IkappaBalpha degradation, sustained cRel activation, hei

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

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

101 38 phosphorylation and inhibited Dox-induced IkappaBalpha degradation.

102 somes, reduces tumor necrosis factor-induced IkappaBalpha degradation, and decreases expression level

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

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

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

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

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

108 By inducing IkappaBalpha and IkappaBbeta cleavage and IkappaB kinase

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

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

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

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

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

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

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

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

117 ssion of the cytoplasmic NF-kappaB inhibitor IkappaBalpha.

118 r-repressor form of the NF-kappaB inhibitor (IkappaBalpha-SR), which were then crossed with mice of b

119 uclear factor kappa-B (NF-kappaB) inhibitor (IkappaBalpha)-mediated phosphorylation by IKKepsilon and

120 s, 3) several kinases, and 4) one inhibitor (IkappaBalpha) whose transcript level is itself regulated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

138 bia(NES/NES) CD8 T cells harboring a mutated IkappaBalpha nuclear export sequence abnormally accumula

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

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

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

142 ive STAT3 and inhibited by dominant-negative IkappaBalpha.

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

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

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

146 sphorylation, acetylation, and activation of IkappaBalpha kinase.

147 sphorylation, acetylation, and activation of IkappaBalpha kinase.

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

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

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

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

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

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

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

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

156 Binding of IkappaBalpha and beta-catenin by beta-TrCP causes their

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

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

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

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

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

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

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

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

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

166 tivation, as evidenced by the degradation of IkappaBalpha and the phosphorylation and nuclear translo

167 isingly, the thrombin-induced degradation of IkappaBalpha in the cytosol was not affected in ATG7-dep

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

169 cation, although blunting the degradation of IkappaBalpha was due, at least in part, to a decrease in

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

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

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

173 K and p65 phosphorylation and degradation of IkappaBalpha.

174 ase complex that mediates the degradation of IkappaBalpha.

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

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

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

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

179 an NF-kappaB inhibitor acting downstream of IkappaBalpha degradation, preventing gene transcription

180 own about the postubiquitinational events of IkappaBalpha proteolysis.

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

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

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

184 Remarkably, neuronal expression of IkappaBalpha-SR transgene in mice expressing TDP-43(A315

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

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

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

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

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

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

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

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

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

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

195 activation by suppressing phosphorylation of IkappaBalpha and ERK.

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

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

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

199 tion with each other, the phosphorylation of IkappaBalpha, and the activation of NF-kappaB.

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

201 aling pathway by inducing phosphorylation of IkappaBalpha.

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

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

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

205 ntrol the postubiquitinational regulation of IkappaBalpha.

206 A neutralizes LPS involves rapid reversal of IkappaBalpha phosphorylation.

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

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

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

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

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

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

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

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

215 1 inhibition resulted in reduced levels of P-IkappaBalpha and p65 activity.

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

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

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

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

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

221 g TNFRII levels and elevating phosphorylated IkappaBalpha by SUMOylation.

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

223 D to its recruited substrate, phosphorylated IkappaBalpha.

224 s IkappaB kinase (IKK), which phosphorylates IkappaBalpha, releasing NF-kappaB to the nucleus.

225 vity by binding directly and phosphorylating IkappaBalpha in cells.

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

227 inding domain of UFD1L and polyubiquitinated IkappaBalpha.

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

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

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

231 ppaBalpha, whereas SVV additionally prevents IkappaBalpha phosphorylation.

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

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

234 Following pulmonary IkappaBalpha-SuperRepressor transgene overexpression or

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

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

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

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

239 nt downregulation of the NF-kappaB repressor IkappaBalpha.

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

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

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

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

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

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

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

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

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

249 nd induces the accumulation of its substrate IkappaBalpha to block NF-kappaB transcriptional activity

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

251 riptional repression function for SUMOylated IkappaBalpha.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

266 Thus, these results reveal that IkappaBalpha, via its unique nuclear export function, en

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

291 Using various IkappaBalpha mutants, we demonstrate that apoptosis inhi

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

293 When IkappaBalpha is reduced in tumour cells with constitutiv

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

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

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

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

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.