ライフサイエンスコーパス: NF-kappaB

1 NF-kappaB activation positively correlated with crescent

2 NF-kappaB and survivin are coordinately up-regulated in

3 NF-kappaB family members p100 and RelB translocate to th

4 NF-kappaB has recently gained attention as a mediator of

5 NF-kappaB is one of the critical transcription factors c

6 NF-kappaB was discovered 30 years ago as a rapidly induc

7 NF-kappaB-inducing kinase (NIK) is a key trigger in the

8 NF-kappaB-p65 activation was induced by all antigens.

9 2q32.3 (STAT1/STAT4), 3q25.33 (IL12A), 4q24 (NF-kappaB) and 22q13.1 (RPL3/SYNGR1).

10 unohistological staining of occludin, Ki-67, NF-kappaB-p65, and terminal deoxynucleotidyl transferase

11 and down-regulation of Bcl-2, MMP-2 and -9, NF-kappaB and IkappaBalpha.

12 mutated promoter constructs, we identified a NF-kappaB site as critical in this activation.

13 (-/-) mice and following pretreatment with a NF-kappaB inhibitor.

14 though Ebola virus VP40 and GP both activate NF-kappaB independently of BST2, VP40 is the more potent

15 (LMP1) functions to constitutively activate NF-kappaB signalling, and we observed mutual exclusivity

16 within the Int3 protein required to activate NF-kappaB consists of the CDC10/Ankyrin (ANK) repeats do

17 onstrated CXCR4 and CXCR2 can both activated NF-kappaB and STAT3 signaling, while NF-kappaBp65 can th

18 Moreover, LINC00305 activated NF-kappaB exclusively in the presence of LIMR and AHRR.

19 -kappaB, and the colocalization of activated NF-kappaB and GDF-15 in epithelial ducts of human pancre

20 e mechanism of how O-GlcNAcylation activates NF-kappaB signaling through phosphorylation and acetylat

21 Here, we show that Int3 activates NF-kappaB in HC11 cells in absence of Rbpj through an as

22 : SMYD2/IL-6/STAT3/SMYD2 and SMYD2/TNF-alpha/NF-kappaB/SMYD2.

23 uction of the pRB-->E2F pathway, and (ii) an NF-kappaB p65 driven enhancer in exon 1.

24 RelB is an NF-kappaB family transcription factor activated in the n

25 xpress the LacZ gene under the control of an NF-kappaB-regulated promoter.

26 d with pyrrolidine dithiocarbamate (PDTC, an NF-kappaB inhibitor) or SB203580 (a MAPK inhibitor) show

27 of the E3 ubiquitin ligase RNF146 through an NF-kappaB-related inhibitory element in the RNF146 promo

28 At mid-anagen, NF-kappaB activity was observed in the inner root sheath

29 Although IL-33 induces AP-1 and NF-kappaB, NFAT signaling has not been described in ILC2

30 ls independently of its effects on COX-2 and NF-kappaB.

31 nsducer and activator of transcription 4 and NF-kappaB signaling pathways.

32 PI3K/Akt and NF-kappaB pathways account for the anti-inflammatory rol

33 lls show normal IkappaBalpha degradation and NF-kappaB nuclear translocation but significantly reduce

34 on of integrin linked kinase (ILK), EGFR and NF-kappaB, as well as transfection of a dominant-negativ

35 avage fluid, decreased TLR2/4 expression and NF-kappaB activation in the lung.

36 blocked proinflammatory gene expression and NF-kappaB activation while enhancing HIF-1alpha levels a

37 nvolving down-regulation of TLR4, IRAK1, and NF-kappaB.

38 vation of IFN regulatory factor 3 (IRF3) and NF-kappaB was observed in EBOV-infected, but not in REST

39 and suppression of cytokine-induced JNK and NF-kappaB activation.

40 D1, and identify c-Jun N-terminal kinase and NF-kappaB as potential therapeutic targets for preventio

41 al feedback control for both MAP kinases and NF-kappaB pathway in response to S. aureus.

42 mediated through the inhibition of MAPKs and NF-kappaB activation but was mediated through the suppre

43 ble for GBS-mediated activation of MAPKs and NF-kappaB and subsequent expression of proinflammatory m

44 f IRAK-1, diminished activation of MAPKs and NF-kappaB, and deficient induction of cytokines in macro

45 reby blocks IkappaBalpha phosphorylation and NF-kappaB nuclear translocation.

46 onses by negatively regulating PPARgamma and NF-kappaB transcriptional activities.

47 cytosolic pattern recognition receptors and NF-kappaB.

48 way and a positive feedback between SOX9 and NF-kappaB are involved in this inducing process.

49 okines such as CXCL5 by activating Stat3 and NF-kappaB(p65) signaling.

50 tion of lincRNA-Cox2 and lincRNA-AK170409 as NF-kappaB regulators, and this tool will be useful for i

51 iated Akt and ERK phosphorylation as well as NF-kappaB- and AP-1-mediated transcription.

52 iated endocytosis and resulted in astroglial NF-kappaB activation and secretion of chemokines.

53 ition of BET bromodomain proteins attenuated NF-kappaB signaling and reduced cytokine production in v

54 phages and confers anti-apoptotic attributes.NF-kappaB p65 silencing identified that these proteins i

55 eceptor activator of nuclear factor-kappa B (NF-kappaB) ligand (RANKL), a potent osteoclast-stimulati

56 ng mechanisms is the nuclear factor-kappa B (NF-kappaB) pathway, which integrates multiple extracellu

57 key proteins in the nuclear factor kappa B (NF-kappaB) signaling pathway.

58 ependent pathway via nuclear factor-kappa B (NF-kappaB), while simultaneously inhibiting expression o

59 K) and the NF-kappaB pathway (IKKalpha/beta, NF-kappaB p65) in bone marrow-derived macrophages (BMDMs

60 fic expression of IkappaBalphaDeltaN blocked NF-kappaB activation in oligodendrocytes and resulted in

61 s a new p53-dependent mechanism for blocking NF-kappaB survival pathways in cancer cells.

62 me was enriched in genes commonly altered by NF-kappaB in response to TNF, by IL-6 via STAT3, and in

63 by assisted loading of STAT3 on chromatin by NF-kappaB.

64 Expression of AMPs is regulated mainly by NF-kappaB factors Dorsal, Dif and Relish.

65 roduction of GDF-15 is directly regulated by NF-kappaB, and the colocalization of activated NF-kappaB

66 rter activity and intracellular signaling by NF-kappaB and MAPK pathways were comparable in oxLDL-loa

67 BCR-mediated canonical NF-kappaB signaling was impaired in all mature naive CVI

68 the preferential activation of non-canonical NF-kappaB pathway in LPS-conditioned DCs.

69 These dual roles of canonical NF-kappaB in Tconv and Treg cells highlight the function

70 ified that conditional deletion of canonical NF-kappaB signaling (p65) in myeloid cells inhibited syn

71 signaling pathways implicated the canonical NF-kappaB pathway and the proinflammatory cytokine IL-6

72 It operates via subversion of the canonical NF-kappaB pathway, which requires a physical interaction

73 eared to require activation of the canonical NF-kappaB pathway.

74 a, 2 bona fide target genes of the canonical NF-kappaB pathway.

75 Ghosh and colleagues show that the canonical NF-kappaB subunits p65 and c-Rel have non-redundant, cri

76 a-light-chain-enhancer of activated B cells (NF-kappaB) activation, and Znrf4 knockdown mice have red

77 a-light-chain-enhancer of activated B cells (NF-kappaB)/signal transducer and activator of transcript

78 serum AST level as well as hepatic cellular NF-kappaB activation.

79 nonical WNT5A signaling mechanism comprising NF-kappaB and MMP7 that is essential for TNBC cell invas

80 pment of various cancers, where constitutive NF-kappaB activation is often found to promote the expre

81 zed, and the extent to which lncRNAs control NF-kappaB expression is unknown.

82 cRNA-Cox2 and lincRNA-AK170409, that control NF-kappaB signaling.

83 se 1 (RIPK1), a key regulator of cell death, NF-kappaB, and MAPK signaling.

84 However, estradiol significantly decreased NF-kappaB transcriptional activity while increasing TLR5

85 uced recruitment of MyD88 to TLR2, decreased NF-kappaB activation, and impaired IL-8 expression upon

86 appaB nuclear localization and downregulates NF-kappaB targets.

87 B cell receptor signaling and downstream NF-kappaB activity are crucial for the maturation and fu

88 n human TNBC cells and suppressed downstream NF-kappaB target gene expression, including the metastas

89 l endotheliopathy, characterized by elevated NF-kappaB (nuclear factor-kappaB) activation and TNF (tu

90 , driving progression via p21 loss, elevated NF-kappaB expression and tenascin C-associated rigidity,

91 -stimulated neutrophils activate endothelial NF-kappaB, which contributes to NCGN and provides a pote

92 deficient mice, and activation of epithelial NF-kappaB and PI3K signaling pathways are restricted by

93 OGG1 initiated BER evoked by ROS facilitates NF-kappaB DNA occupancy and gene expression.

94 The transcription factor NF-kappaB controls key features of hair follicle (HF) de

95 ERK/MAPK and the master transcription factor NF-kappaB in response to FGF and IL-1/TNF, respectively.

96 The transcription factor NF-kappaB plays an important role in the immune system,

97 Transcription factor NF-kappaB regulates expression of numerous genes that co

98 MCT1 activates transcription factor NF-kappaB to promote cancer cell migration independently

99 infiltration, and decreased nuclear factor (NF)-kappaB activation compared with controls.

100 obial stimuli, DCs activated nuclear factor (NF)-kappaB, which induced expression of a proinflammator

101 activate the inducible transcription factors NF-kappaB, NFAT, and AP-1.

102 g LPS, members of the TLR and PPAR families, NF-kappaB, and TNF-related weak inducer of apoptosis (TW

103 ses (IKKs) to phosphorylate IkappaBalpha for NF-kappaB activation, triptolide does not directly targe

104 urthermore, we identified several functional NF-kappaB, activator protein 1 (AP1), STAT, and Smad DBS

105 ted proteinuria, podocyte injury, glomerular NF-kappaB activity, glomerular expression of inflammator

106 cellular proliferation and apoptosis guards (NF-kappaB, Bcl-2 and p53) in these NPs-treated cancer ce

107 Functional validation did not identify NF-kappaB or AMP-activated protein kinase phosphorylatio

108 bly, constitutive activation of IkappaBalpha/NF-kappaB(p65) in this circuit is not dependent on the a

109 E and HPDE cells, and Kras/TAK1/IkappaBalpha/NF-kappaB pathway and a positive feedback between SOX9 a

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

111 ent on the activation of traditional IKKbeta/NF-kappaB pathways that are important in normal immune r

112 Ectopic expression of LRRC25 impaired NF-kappaB activation, whereas knockout of LRRC25 potenti

113 Rela(+/-) mice have similarly impaired NF-kappaB activation, develop cutaneous ulceration from

114 This could be attributed to impaired NF-kappaB activation, as shown by the absence of nuclear

115 ng inhibition of CD40L-induced activation in NF-kappaB sensor cells, THP-1 myeloid cells, and primary

116 further demonstrate a concurrent increase in NF-kappaB signaling that is correlated with aneurysm sev

117 -Bcl10-MALT1 signalosome complex involved in NF-kappaB translocation.

118 ubstrate specificity and the role of PKD2 in NF-kappaB signaling remain unaffected.

119 ein phosphatase 2A mediated the reduction in NF-kappaB translocation by HA.

120 oxidative stress and inflammation including NF-kappaB and Nrf2 signaling pathways in the retina whic

121 opriate activation of macrophages, including NF-kappaB, may hold promise as an adjunct therapeutic av

122 Increased NF-kappaB nuclear translocation and macrophage chemoattr

123 ic ablation or inhibition by cdNs, increased NF-kappaB activation and reduced bacterial survival, sug

124 er)/HK1.ras(1205) wdSCCs exhibited increased NF-kappaB and novel tenascin C, indicative of elevated r

125 it does not inhibit BST2's ability to induce NF-kappaB activity.

126 Further studies found that netrin-1 induced NF-kappaB p65(ser536) phosphorylation and c-Myc expressi

127 ed NEMO polyubiquitination and cIAP1-induced NF-kappaB activation.

128 n LPS, ox-LDL or cholesterol crystal-induced NF-kappaB, c-jun and p38 activation, as well as IL-1beta

129 esterone and amplified by DNA damage-induced NF-kappaB signaling, that likely accounts for the suscep

130 However, the mechanism of EGFR-induced NF-kappaB activation is not fully defined.

131 that PELP1-cyto expression in HMECs induced NF-kappaB signaling pathways.

132 LPS-induced NF-kappaB reporter activity and intracellular signaling

133 NO2-OA inhibited TNFalpha-induced NF-kappaB transcriptional activity in human TNBC cells a

134 oll-like receptor 4- or interleukin-induced, NF-kappaB activation.

135 a membrane in infected cells, and it induces NF-kappaB activity, especially in the context of retrovi

136 atory activity due to its ability to inhibit NF-kappaB.

137 suppression of UNC5A significantly inhibited NF-kappaB p65(ser536) phosphorylation, c-Myc up-regulati

138 d glycolysis while simultaneously inhibiting NF-kappaB signaling and apoptosis.

139 (+) T cells upon TCR stimulation, inhibiting NF-kappaB signaling via its effects on the IkappaB kinas

140 PumA is essential for virulence and inhibits NF-kappaB, a property transferable to non-PumA strain PA

141 Furthermore, we found that NO inhibits NF-kappaB activity to prevent hyperinflammatory response

142 he vaccinia virus (VACV) K1 protein inhibits NF-kappaB activation among its other antagonistic functi

143 ssion of Bcl-xL-coding Bcl2l1 transgene into NF-kappaB signalling-deficient IkappaBDeltaN transgenic

144 transcription factors nuclear factor kappaB (NF-kappaB) and interferon regulatory factor 3 (IRF-3), c

145 IFN-alpha (TRIF) and nuclear factor kappaB (NF-kappaB) causes the apoptosis of MDCC-MSB1 cells.

146 e IKBKG gene encoding nuclear factor kappaB (NF-kappaB) essential modulator (NEMO; the regulatory sub

147 n of pro-inflammatory nuclear factor kappaB (NF-kappaB) signaling in TNBC.

148 transcription factor Nuclear Factor kappaB (NF-kappaB) using this method identifies two types of inc

149 transcription factor nuclear factor kappaB (NF-kappaB), whereas stable, non-oxidizable analogs were

150 apoptosis as well as nuclear factor kappaB (NF-kappaB)-dependent cell survival.

151 SP110b modulates nuclear factor-kappaB (NF-kappaB) activity, resulting in downregulation of tumo

152 NSCLC, activates the nuclear factor-kappaB (NF-kappaB) p65-->ZEB1 pathway and confers a poor prognos

153 pendent activation of nuclear factor-kappaB (NF-kappaB) that mediates innate and adaptive antitumor i

154 lear translocation of nuclear factor-kappaB (NF-kappaB), indicating that NF-kappaB is the downstream

155 ression by regulating nuclear factor-kappaB (NF-kappaB)-mediated inflammatory gene transcription.

156 ated antioxidant response genes, and limited NF-kappaB and proinflammatory signaling.

157 Low NF-kappaB activators cause more severe lung infections i

158 These results suggest that low NF-kappaB activation is a virulence property of pneumoco

159 To measure NF-kappaB activity we used a line of transgenic mice tha

160 emic autoimmunity and implicate TLR-mediated NF-kappaB proinflammatory signaling from the late endocy

161 (CD58, RFXAP), MAPK signaling (MAP2K1, NF1), NF-kappaB signaling (PRKCB, CSNK1A1), PI-3-kinase signal

162 f CD63 in limiting LMP1-induced noncanonical NF-kappaB and ERK activation.

163 of increased expression of the noncanonical NF-kappaB transcription factor RelB.

164 illomas in the context of p53 loss and novel NF-kappaB expression, whereas increased tissue rigidity

165 p53 loss, increased proliferation and novel NF-kappaB expression.

166 hese Nv-TLR-expressing cells also express Nv-NF-kappaB.

167 fects the phosphorylation and acetylation of NF-kappaB subunit p65/RelA.

168 Sequential activation of NF-kappaB and an increased Gata3/T-bet mRNA level ratio,

169 ation of TRAF6, which promotes activation of NF-kappaB and MAPK signalling and increases the producti

170 Interestingly, activation of NF-kappaB by netrin-1 was dependent on UNC5A receptor, b

171 This data indicates that the activation of NF-kappaB canonical signaling by Notch-4/Int3 is ANK rep

172 eceptor family members via the activation of NF-kappaB in cultured renal proximal tubular cells.

173 Conversely, virally mediated activation of NF-kappaB signaling decreased cortical synaptic plastici

174 cted with proteins involved in activation of NF-kappaB signaling.

175 al p62 aggregate formation and activation of NF-kappaB signaling.

176 and the purified PF triggered activation of NF-kappaB through TLR2, as determined using a variety of

177 Activation of NF-kappaB transcription factors is critically required f

178 Salmeterol also attenuated activation of NF-kappaB via inhibition of nuclear translocation of p65

179 of the pathways leading to the activation of NF-kappaB, an essential regulator of innate immunity.

180 LPS induced similar activation of NF-kappaB, and stimulated the expression of cytokines an

181 ng events, including the rapid activation of NF-kappaB, c-Jun N-terminal kinase (JNK), extracellular

182 TNFR1 stimulation causes activation of NF-kappaB, p38alpha, and its downstream effector kinase

183 of 5-8 months, with increased activation of NF-kappaB, stress pathways, and spontaneous inflammation

184 responsiveness of the receptor activator of NF-kappaB (RANK), which is central for mTEC differentiat

185 Binding of receptor activator of NF-kappaB ligand (RANKL) to its receptor RANK on osteocl

186 65-NFkappaB, the transcriptional activity of NF-kappaB and IkappaBalpha phosphorylation.

187 ence of ApN markedly reduced the activity of NF-kappaB, a key player in muscle inflammation and myoge

188 We also observed an attenuation of NF-kappaB pathway, an upstream regulator of the aforemen

189 xhibited an aging-related loss in binding of NF-kappaB and STAT factors.

190 tivation resulted in genome-wide blockade of NF-kappaB interaction with chromatin and directly induce

191 moter regions of specific genes, blockade of NF-kappaB pathway activation, and modulation of the Th17

192 rarin led to SIRT1-mediated deacetylation of NF-kappaB and suppression of NOX4 expression.

193 ed in the noncanonical pathway downstream of NF-kappaB-inducing kinase (NIK) and TNF receptor family

194 findings imply the cytoprotective effects of NF-kappaB activation on oligodendrocytes in MS and EAE.S

195 1) and significantly increased expression of NF-kappaB mRNA in neutrophils (P <0.05).

196 cytoplasm, alongside elevated expression of NF-kappaB pathway genes.

197 ed Ser-165 sites regulate distinct groups of NF-kappaB target genes, suggesting the unique and irrepl

198 rsistence through a synergistic induction of NF-kappaB-dependent MMP1 expression in cancer cells.

199 s proteins affect BST2-mediated induction of NF-kappaB.

200 ur studies therefore establish inhibition of NF-kappaB c-Rel as a viable therapeutic approach for enh

201 er genetic knockdown of p62 or inhibition of NF-kappaB sensitized tumor cells to CQ, resulting in inc

202 p.DelQ134_R256 mutation caused inhibition of NF-kappaB signaling, although the truncated NEMO protein

203 ionality and were mediated via inhibition of NF-kappaB subunit p65 activity.

204 chromatin and directly induced inhibitors of NF-kappaB and AP-1.

205 d is sufficient to reduce cellular levels of NF-kappaB and calpain-2 and secreted levels of the proan

206 Protein expression levels of NF-kappaB, AP1, p-STAT3, p-AKT, p-IKKs and p-p38 MAPK we

207 The pattern of NF-kappaB dynamics in TRIF-deficient cells does not, how

208 NF-kappaB DNA binding and phosphorylation of NF-kappaB p65.

209 duced gene expression and phosphorylation of NF-kappaB.

210 and was mediated by decreased recruitment of NF-kappaB p65 and RNA polymerase II to COX-2 and IL-8 pr

211 econciles seemingly contradictory reports of NF-kappaB-STAT3 crosstalk.

212 to date, attempts to understand the role of NF-kappaB activation in oligodendrocytes in MS have been

213 r follicle (HF) development, but the role of NF-kappaB in adult HF cycle regulation remains obscure.

214 faip3 is required for the transactivation of NF-kappaB-regulated inflammatory genes in response to ba

215 e mechanisms by which the core transducer of NF-kappaB signaling pathway, RelA/p65 is regulated under

216 mechanism, as indicated by the transition of NF-kappaB from its inactive to active state.

217 Nuclear translocation of NF-kappaB was detected by immunofluorescence.

218 ) production and concomitant upregulation of NF-kappaB-induced antiapoptotic gene expression, thereby

219 The actions of this network converge on NF-kappaB, and support the idea that NF-kappaB is respon

220 -486 partially reversed the effects of P4 on NF-kappaB pathway.

221 in vitro, responds to NFATc1, FoxO1, and/or NF-kappaB signaling pathways.

222 inase 1 (IRAK-1), p38, ERK1/2 MAPKs, and p65 NF-kappaB, suggesting that the R753Q TLR2 polymorphism a

223 avonoids were found to be involved in pAkt - NF-kappaB signaling pathway through a reduction in phosp

224 sphotyrosine specific antibody and permitted NF-kappaB binding to a DNA duplex sequence corresponding

225 induce endoplasmic reticulum stress, perturb NF-kappaB, and p53 signaling, and diminish mitochondrial

226 tion, whereas knockout of LRRC25 potentiated NF-kappaB activation and enhanced the production of infl

227 .ras(1205) papilloma context (wound-promoted/NF-kappaB(+)/p53(-)/p21(+)) preceded K14.ROCK(er)-mediat

228 s in the conserved immune regulatory protein NF-kappaB and cnidarian symbiotic status.

229 yet the binding of p65/RelA (the prototypic NF-kappaB family member) was reduced at IL-6 and CCL5 pr

230 availability reduces the NADH:NAD(+) ratio, NF-kappaB transcriptional activity, and pro-inflammatory

231 n molecules in endothelial cells and reduced NF-kappaB activation and monocyte arrest on activated en

232 CD44 knockdown reduced NF-kappaB nuclear translocation and downstream IL-1beta

233 lear translocation but significantly reduced NF-kappaB DNA binding and phosphorylation of NF-kappaB p

234 Anti-CD44 Ab and HA treatments reduced NF-kappaB translocation, IL-1beta and TNF-alpha expressi

235 prohealing phenotype associated with reduced NF-kappaB activation, proinflammatory markers, endoplasm

236 e NF-kappaB pathway and consequently reduces NF-kappaB nuclear localization and downregulates NF-kapp

237 fies a new mechanism by which KLF6 regulates NF-kappaB signaling, and how this mechanism is circumven

238 ulates osteoclastogenesis by down regulating NF-kappaB activation.

239 The RelA NF-kappaB subunit is activated by acetylation of lysine

240 sphorylation levels of ERK-1/2 and p65/RelA (NF-kappaB) and inducible NO synthase expression, suggest

241 Accordingly, mutations in several NF-kappaB pathway genes cause immunodeficiency.

242 ion, and nuclear phospho-p65 staining showed NF-kappaB activation within CD31-expressing endothelial

243 utual exclusivity among tumours with somatic NF-kappaB pathway aberrations and LMP1-overexpression, s

244 n activity, RBF206 O-Vpu potently suppresses NF-kappaB activation and reduces CD4 cell surface expres

245 lective strategies to therapeutically target NF-kappaB.

246 erge on NF-kappaB, and support the idea that NF-kappaB is responsive to mechanical stimuli.

247 Additionally, we identified that NF-kappaB and MAPK signaling pathways are both involved

248 Data indicate that NF-kappaB activation in inflammatory cells facilitates t

249 tered in the HF matrix, which indicates that NF-kappaB activity is also involved in hair fiber morpho

250 r factor-kappaB (NF-kappaB), indicating that NF-kappaB is the downstream pathway for the transcriptio

251 We also showed that NF-kappaB inactivation in oligodendrocytes aggravated IF

252 ons and LMP1-overexpression, suggesting that NF-kappaB activation is selected for by both somatic and

253 The NF-kappaB essential modulator (NEMO) is the scaffolding

254 dual inhibitors of both EGFR kinase and the NF-kappaB activity.

255 ved in MAPK pathways (p38, ERK, JNK) and the NF-kappaB pathway (IKKalpha/beta, NF-kappaB p65) in bone

256 st time found that knockdown of Akt1 and the NF-kappaB-activating kinase IKKbeta cooperatively downre

257 NE1, ANGPLT4, CCL20, and SAA1 as well as the NF-kappaB (p65) binding sites on GR-transrepressed promo

258 MT5 expression was regulated upstream by the NF-kappaB pathway, and it promoted IL-2 production and p

259 es multiple genes negatively controlling the NF-kappaB pathway and consequently reduces NF-kappaB nuc

260 heterozygous mutation in RELA, encoding the NF-kappaB subunit RelA, segregated with the disease phen

261 y several novel CO2-dependent changes in the NF-kappaB pathway.

262 otein family, as a negative regulator in the NF-kappaB signaling pathway.

263 wnstream signaling components, including the NF-kappaB pathway.

264 3C(pro) proteins cleave TAK1 to inhibit the NF-kappaB response.

265 rget the NF-kappaB1/p50 gene and inhibit the NF-kappaB signaling pathway (p-P65 downward arrow, NF-ka

266 ic mutations, especially those involving the NF-kappaB pathway, have been characterized in primary cu

267 dies showing that concurrent blockage of the NF-kappaB and Akt signaling pathways sensitizes lung can

268 ed protein 3 [TNFAIP3]), an inhibitor of the NF-kappaB pathway and a negative regulator of TLR signal

269 t, besides its role in the inhibition of the NF-kappaB pathway, NLRC3 interferes with the assembly an

270 constructed to quantify five proteins of the NF-kappaB pathway.

271 independent of the levels of activity of the NF-kappaB pathway.

272 d by rare monogenic variants in genes of the NF-kappaB pathway.

273 s highlight the functional plasticity of the NF-kappaB signaling pathway and underscores the need for

274 e (IKK) and increased phosphorylation of the NF-kappaB subunit RelB.

275 ficantly inhibited IL-1beta induction of the NF-kappaB target genes, COX-2 and IL-8 P4-PRWT transrepr

276 (NLR) family, was found to down-regulate the NF-kappaB pathway and stimulator of interferon genes (ST

277 we found that BCA2 negatively regulates the NF-kappaB pathway-a signaling cascade necessary for HIV-

278 olling embryonic polarity and regulating the NF-kappaB signaling pathway.

279 We found that the NF-kappaB complex signaling component, p65, binds to the

280 Mechanistically, our data indicate that the NF-kappaB signaling cascade is significantly upregulated

281 portant regenerative signals in part through NF-kappaB-mediated signaling that activates neural stem

282 es treatment with drugs that antagonize TLR4-NF-kappaB signaling or the SPAK-NKCC1 co-transporter com

283 etylation of p65 at Lys-310, contributing to NF-kappaB transcriptional activation.

284 CalpTG mice, especially cytokines related to NF-kappaB and NLRP3 inflammasome activation.

285 onizes TRAF6/p62-dependent IL-1 signaling to NF-kappaB.

286 e-1, which is required for IL-1 signaling to NF-kappaB.

287 gulatory network where co-activation of Toll/NF-kappaB and EGFR signaling by ROS levels in the PSC/ni

288 Here, we establish that Toll/NF-kappaB pathway activation in the PSC in response to w

289 o dissect the molecular mechanisms that tune NF-kappaB activity.

290 t protection during infection by fine-tuning NF-kappaB activity, suggesting that SP110b may serve as

291 , concomitant with reduced expression of two NF-kappaB-signaling related genes RELB and NFkappaBIZ, i

292 at miR-19a has a direct role in upregulating NF-kappaB signaling and that miR-19a has roles in inflam

293 ted IL-8 expression by 9-fold (P < 0.01) via NF-kappaB compared to TNF-alpha-treated control.

294 ovo induction of pro-IL-1beta, generally via NF-kappaB-dependent transduction pathways; and the assem

295 ha leads to RIPK1-independent apoptosis when NF-kappaB activation is inhibited by cycloheximide.

296 eveal an enhancer-specific crosstalk whereby NF-kappaB enables STAT3 binding at some enhancers while

297 results establish a novel mechanism by which NF-kappaB and Akt contribute to chemoresistance involvin

298 plex of bromodomain containing 4 (BRD4) with NF-kappaB and cyclin-dependent kinase 9 (CDK9).

299 bserve that RSV induces BRD4 to complex with NF-kappaB/RelA.

300 ways associated with uric acid priming, with NF-kappaB and mammalian target of rapamycin (mTOR) signa