ライフサイエンスコーパス: NF-kappaB

1 NF-kappaB essential modulator (NEMO) is a key regulatory

2 NF-kappaB is a pro-inflammatory transcription factor tha

3 NF-kappaB upregulated tissue inhibitor metalloproteinase

4 NF-kappaB-regulating signaling cascades, in concert with

5 and upstream regulators (INFgamma, IL-1beta, NF-kappaB, MYD88) associated with inflammation.

6 , extracellular signal-regulated kinase 1/2, NF-kappaB, and p53, responsible for a wide range of cell

7 y the NF-kappaB transcription factor, and 4) NF-kappaB likely regulates MyD88 alternative pre-mRNA sp

8 a-inducible factor-1alpha (HIF1alpha)- and a NF-kappaB-dependent manner to recruit macrophages to IRI

9 cells expressed elevated levels of WNT16, a NF-kappaB target gene.

10 sident cells blunts kidney fibrosis, ablates NF-kappaB signaling, and lessens matrix deposition.

11 scriptionally in S-phase cells that activate NF-kappaB signaling upon innate immune recognition of th

12 ILK-enriched exosomes activated NF-kappaB (nuclear factor kappaB) pathway and NF-kappaB-

13 cally, Shp deletion in hepatocytes activated NF-kappaB and impaired Pparg activation, leading to the

14 d in cystic fibrosis epithelia and activates NF-kappaB signaling, generating inflammation.

15 In addition, NF-kappaB activation following LD-STZ treatment was vali

16 ivation of the IRF pathway without affecting NF-kappaB and MAPK signalling, which indicates that liga

17 STAT6, PI3K-Akt-NF-kappaB, and Src signaling mediated the cellular and m

18 ulated to trigger the activation of PI3K/Akt/NF-kappaB pathway and elevated expression of proliferati

19 Although NF-kappaB is known to play a pivotal role in lung cancer

20 activate the transcription factors AP-1 and NF-kappaB, leading to the down-regulation of LINE-1 prom

21 n versus inhibition of both CDC42:ERK1/2 and NF-kappaB:AP-1 pro-oncogenic signaling pathways in nonma

22 ate increased K310 NF-kappaB acetylation and NF-kappaB transcriptional activity.

23 eta-activated kinase-1 (TAK1) activation and NF-kappaB/p38 MAPK signaling.

24 u RNAs are potent activators of both IFN and NF-kappaB responses via the dsRNA sensors, RIG-I, and TL

25 er, our results link bacterial infection and NF-kappaB-driven innate immune responses to R-loop-depen

26 opherins to disturb their import of IRF3 and NF-kappaB to promote replication in macrophages.

27 vation of the transcription factors IRF3 and NF-kappaB, driven by the kinases TBK1 and TAK1-IKKbeta,

28 LBCL-IRF4 had frequent mutations in IRF4 and NF-kappaB pathway genes (CARD11, CD79B, and MYD88), loss

29 The levels of phosphorylated IRF7 and NF-kappaB inversely correlated with plasma IFNalpha2 lev

30 ation of IFN regulatory factory 7 (IRF7) and NF-kappaB.

31 he c-Jun N-terminal protein kinase (JNK) and NF-kappaB pathways; however, the precise mechanisms gove

32 y and independent of alterations in MAPK and NF-kappaB signaling.

33 n primary tumor growth, lung metastasis, and NF-kappaB signaling modulatory functions.

34 Addressing the interaction between MTA2 and NF-kappaB would provide potential targets for interventi

35 anslocation of the NF-kappaB subunit p65 and NF-kappaB-dependent transcription were decreased in PACR

36 F-kappaB (nuclear factor kappaB) pathway and NF-kappaB-dependent gene transcription in recipient endo

37 rms a ternary protein complex with PPM1G and NF-kappaB at target gene promoters in a stimuli-dependen

38 in lung homeostasis, immune regulation, and NF-kappaB signaling may provide additional insight into

39 B expression by activation of DNA repair and NF-kappaB pathways could promote cancer mutations and ex

40 ALAL-1 is a TNFalpha- and NF-kappaB-induced cytoplasmic lncRNA that specifically i

41 l family of transcription factors TonEBP and NF-kappaB p65 play critical roles in the switch from osm

42 mplex (complex I), RIPK1 ubiquitination, and NF-kappaB activation.

43 Given the fact that PRMT5, YBX1 and NF-kappaB are all among top crucial factors in cancer pr

44 inflammation-independent functions, such as NF-kappaB-mediated cell survival.

45 between TNF-alpha-induced super enhancers at NF-kappaB-relevant loci, coinciding with KDM7A and UTX r

46 t FSTL-1 treatment of macrophages attenuated NF-kappaB p65 phosphorylation in an Nr4a1-dependent mann

47 Nuclear factor kappa B (NF-kappaB) activation in the liver of SCD mice inhibited

48 es demonstrated that nuclear factor kappa B (NF-kappaB) and cholesterol biosynthesis pathways were ac

49 The nuclear factor kappa B (NF-kappaB) signaling system, a key regulator of immunolo

50 model to investigate nuclear factor kappa B (NF-kappaB) signaling, a critical regulator of inflammati

51 nases (JNK), EKR1/2, nuclear factor-kappa B (NF-kappaB)) in the gastrocnemius (G).

52 ase in inhibitors of nuclear factor kappa-B (NF-kappaB) signaling, possibly inappropriately throttlin

53 of KDM7A and UTX at nuclear factor kappa-B (NF-kappaB)-associated elements in human ECs.

54 ructures and DNA-binding activities of basal NF-kappaB proteins resemble those of mammalian NF-kappaB

55 Herein, we review what is known about basal NF-kappaBs and how that knowledge informs on the evoluti

56 performed a specifically designed CD83-based NF-kappaB CRISPR screen which led us to identify TAK1 ki

57 Because NF-kappaB target genes include the STAT3-activating IL-6

58 activation inhibits the interaction between NF-kappaB c-Rel and TonEBP essential for the increased e

59 Blocking NF-kappaB activation rescued FXR signaling and partially

60 s that reovirus infection selectively blocks NF-kappaB, likely to counteract its antiviral effects an

61 n transcriptional interactions hindered both NF-kappaB DNA recruitment and induced primary MCL cells

62 In mBMDCs, NP-R848-PUUC induced both NF-kappaB and interferon signaling.

63 n adjuvant induced robust activation of both NF-kappaB and IFN regulatory factor signaling pathways a

64 dergo a metabolic shift that is regulated by NF-kappaB activation, leading to reprogramming of cell m

65 Defective canonical NF-kappaB activation in the absence of PACRG was accompa

66 3 engages the canonical and/or non-canonical NF-kappaB pathways, and thus stimulates naive and co-sti

67 proteins of the canonical and non-canonical NF-kappaB pathways, such as Nfkb2, and its downstream ef

68 Non-canonical NF-kappaB signaling is implicated in inflammatory synerg

69 we show that activation of the non-canonical NF-kappaB signalling pathway by AZD5582 results in the i

70 Deleting the canonical NF-kappaB kinase, IKKbeta, in Scx-lineage cells in mice

71 ffold to recruit components of the canonical NF-kappaB machinery and (b) a protease to cleave and ina

72 pivotal role as a mediator of the canonical NF-kappaB pathway, which has important functions in infl

73 tained activation of endothelial MAPK causes NF-kappaB-dependent inflammatory stress response within

74 a-light-chain-enhancer of activated B cells (NF-kappaB) activation and interleukin-8 (IL-8) secretion

75 a-light-chain-enhancer of activated B cells (NF-kappaB) as key signaling pathways in NFKBIZ/IkappaBze

76 a-light-chain-enhancer of activated B cells (NF-kappaB) signaling, cell proliferation, programmed cel

77 ppaB and MAPK signaling, whereas in B cells, NF-kappaB and MAPK pathways were regulated by both BTK a

78 This posttranslationally stabilized cellular NF-kappaB depot potentially confers a survival advantage

79 Chronic NF-kappaB activation in inflammation and cancer has long

80 e inhibitor of kappa B kinase (IKK) complex, NF-kappaB essential modifier (NEMO), and IKKbeta.

81 aintain higher expression of the cytoplasmic NF-kappaB inhibitor IkappaBalpha.

82 force the central role of My-T-BCR-dependent NF-kappaB signaling in MCD DLBCL and suggest that the ge

83 n resulted in caspase-8/FADD/RIPK1-dependent NF-kappaB activation and inflammatory cytokine productio

84 hts into the divergent functions of distinct NF-kappaB factors in pro-inflammatory macrophages, revea

85 Diverse NF-kappaB-activating ligands produced different patterns

86 hat dElys depletion re-activates the Dorsal (NF-kappaB) pathway during late larval stages.

87 we investigate the robustness of the Dorsal/NF-kappaB signaling module with respect to perturbations

88 ained receptor responsiveness and downstream NF-kappaB activation, characteristic of clinical manifes

89 Accordingly, Drosophila NF-kappaB Relish expression was increased by osa silenci

90 ted immune response by regulating Drosophila NF-kappaB factor Relish expression.

91 key regulatory protein that functions during NF-kappaB- and interferon-mediated signaling in response

92 ed in suppression of miR-31-associated EGLN3/NF-kappaB-controlled inflammatory pathways.

93 plaque inflammation by enhancing endothelial NF-kappaB signaling.

94 are resolved upon inhibition of endothelial NF-kappaB signaling.

95 l microvesicles increase miR-155 and enhance NF-kappaB at disease-prone sites of disturbed flow in vi

96 in oligodendrocytes and found that enhanced NF-kappaB activation in oligodendrocytes had a minimal e

97 uorescence and transgenic animals expressing NF-kappaB inducible imaging reporter.

98 duced activation of the transcription factor NF-kappaB and the MAPK p38.

99 er transcriptional regulator nuclear factor (NF)-kappaB utilizes the PPM1G/PP2Cgamma phosphatase as a

100 (IFN)-gamma production in a nuclear factor (NF)-kappaB-T-bet-dependent manner.

101 Ca(2+) signaling, increased nuclear factor (NF)-kappaB/cyclin D1 activation and cell proliferation,

102 identify TAK1 kinase as a major mediator for NF-kappaB activation in cells dependent on LUBAC, where

103 rmediaries (called IKKs) that are needed for NF-kappaB function.

104 , which catalyzes K63 polyubiquitination for NF-kappaB activation.

105 MALT1 is also required for NF-kappaB-dependent induction of proinflammatory cytokin

106 lating HE4 and activating the HIF-1alpha/HE4/NF-kappaB signaling pathway.

107 y HL cases, and this is correlated with high NF-kappaB activity and low A20 expression.

108 provided by reactive microglia influence how NF-kappaB impacts Muller glia reprogramming.

109 derstanding has led to a refined view of how NF-kappaB and cell death signaling are interlinked and h

110 However, NF-kappaB factors also massively bind to gene bodies.

111 alpha (TNF-alpha), and CXCL8, and identified NF-kappaB and ATF-4 as key drivers of this proinflammato

112 Finally, we identified NF-kappaB activator 1 (Act1), p38 mitogen-activated prot

113 y unrecognized biphasic role of MTA2 in IKK2/NF-kappaB-driven primary-to-metastatic lung tumor progre

114 Here we report that the IKK2/NF-kappaB signaling pathway modulates metastasis-associa

115 on stimulates NO66 expression and changes in NF-kappaB mediate the response.

116 of ligand-independent TNFR1 dimerization in NF-kappaB signaling.

117 conservation of key sequences and domains in NF-kappaB, as well as the regulation of NF-kappaB activi

118 PS treatment induced a sustained increase in NF-kappaB activation and expression of NF-kappaB-depende

119 nhibits the proteolytic activity of MALT1 in NF-kappaB-dependent assays.

120 D1 similarly interacted with key proteins in NF-kappaB and IFN-I pathways in cells.

121 ecognition, and that gene pathways including NF-kappaB and MAPK downstream of TLR2/6 are upregulated

122 redox changes were associated with increased NF-kappaB (nuclear factor kappa B) binding activity and

123 r results were obtained upon Tax-independent NF-kappaB activation, indicating that Tax likely exacerb

124 alpha (TNF-alpha) and vgRNA failed to induce NF-kappaB-dependent gene expression in infected cells.

125 es that control the amplitude of CLR-induced NF-kappaB could profoundly influence host defense agains

126 CLR-induced NF-kappaB is central to CLR functions in immunity, and t

127 hanisms that negatively regulate CLR-induced NF-kappaB, and molecules which act on the CLR family bro

128 und that miR-145a could suppress LPS-induced NF-kappaB activation.

129 and CagE were required for H. pylori-induced NF-kappaB activation, IL-8 secretion, and TLR9 activatio

130 ere we reveal that DA inhibited TLR2-induced NF-kappaB activation and inflammation via the DRD5 recep

131 s the dominant gene targeted by TLR9-induced NF-kappaB signaling in CAF.

132 nant-negative mutant IkappaBalphaM inhibited NF-kappaB activity and increased P-p53, p53, and p21(Waf

133 murine macrophages (RAW 264.7) by inhibiting NF-kappaB activation and its nuclear translocation (the

134 ivity, we show that PG specifically inhibits NF-kappaB and Akt signaling pathways and promotes accele

135 cient osteoclasts demonstrate increased K310 NF-kappaB acetylation and NF-kappaB transcriptional acti

136 .N2fl/fl), or loss of nuclear factor kappaB (NF-kappaB) (pL2.Lgr5.p65fl/fl), in Lgr5(+) (progenitor)

137 arkin, PACRG promoted nuclear factor kappaB (NF-kappaB) activation in response to TNF.

138 ption factors such as nuclear factor kappaB (NF-kappaB) and TCF3, as well as widespread changes in th

139 iption factors of the nuclear factor kappaB (NF-kappaB) family, we profiled the single-cell dynamics

140 n requires Drosophila nuclear factor kappaB (NF-kappaB) immune pathways, Toll and Imd, revealing that

141 IGNIFICANCE STATEMENT Nuclear factor kappaB (NF-kappaB) is activated in oligodendrocytes in multiple

142 negative regulator of nuclear factor kappaB (NF-kappaB), as a direct target of miR-31 establishes a f

143 NOD2 and ATG16L1 by a nuclear factor kappaB (NF-kappaB)-independent pathway.

144 nied by activation of nuclear factor kappaB (NF-kappaB).

145 of AQP3 expression in nuclear factor-kappaB (NF-kappaB) cell signaling, hepatic oxidative stress and

146 ons, translocation of nuclear factor-kappaB (NF-kappaB) to the nucleus, signalling via the Janus kina

147 transcription factor, nuclear factor-kappaB (NF-kappaB), contribute to cancer cell survival and thera

148 ing mitogen-activated protein (MAP) kinases, NF-kappaB signaling, or cell migration.

149 14 inactivation allows MCD cells to maintain NF-kappaB signaling in the presence of ibrutinib.

150 ofiled the single-cell dynamics of two major NF-kappaB subunits, RelA and c-Rel, induced by a panel o

151 -kappaB proteins resemble those of mammalian NF-kappaB p100 proteins, and their posttranslational act

152 However, many NF-kappaB-mediated pathways for cell survival and apopto

153 g pathways, including the SMAD2/3, p38 MAPK, NF-kappaB, and AKT cascades.

154 an event that is critical for YBX1-mediated NF-kappaB activation and its downstream target gene expr

155 higher levels of pro-inflammatory mediators, NF-kappaB expression and apoptotic cells when compared w

156 To investigate the role of neuronal NF-kappaB activity in pathogenesis of amyotrophic latera

157 gradation and activation of the noncanonical NF-kappaB pathway.

158 ion of A20 or inhibition of the noncanonical NF-kappaB pathway.

159 SPCs switched from canonical to noncanonical NF-kappaB signaling, a process that was dependent on TLR

160 p38 mitogen-activated protein kinase but not NF-kappaB.

161 Trx1 pathway instrumentally enables nuclear NF-kappaB DNA-binding and thereby pro-inflammatory respo

162 reby preventing NOD2-dependent activation of NF-kappaB and consequent secretion of pro-inflammatory c

163 Notch signaling contributes to activation of NF-kappaB and regulates differentiation of gastric cardi

164 f reactive oxygen species, the activation of NF-kappaB and the upregulation of Ascl1.

165 significant inhibition of the activation of NF-kappaB in lung tissue.

166 1 and TRAF6), thereby blocking activation of NF-kappaB in target cells.

167 LSV endothelium revealed that activation of NF-kappaB occurred within 30 min after exposure to arter

168 ve regulation of MTA2 leads to activation of NF-kappaB signaling, epithelial-mesenchymal transition,

169 d a mouse model that allow for activation of NF-kappaB specifically in oligodendrocytes and found tha

170 he endocrine pancreas involves activation of NF-kappaB, which is believed to be important for determi

171 ely, and are both required for activation of NF-kappaB-dependent inflammatory genes.

172 long been linked to persistent activation of NF-kappaB-responsive gene promoters.

173 d IL-1beta mRNA expression and activation of NF-kappaB.

174 sions points to a high receptor activator of NF-kappaB ligand/osteoprotegerin (RANKL/OPG) ratio as th

175 Potent agonists of NF-kappaB such as tumor necrosis factor alpha (TNF-alpha

176 Thus, early non-invasive detection of NF-kappaB in pancreatic islets may serve as a potential

177 nformation through the signaling dynamics of NF-kappaB.

178 Following microglia ablation, the effects of NF-kappaB-agonists on MGPC-formation are reversed, sugge

179 tration of C-miR146a inhibited expression of NF-kappaB target genes and thereby thwarted progression

180 se in NF-kappaB activation and expression of NF-kappaB-dependent inflammatory mediators in mCAT BMDMs

181 igated the feasibility of optical imaging of NF-kappaB transcription factor activation induced by low

182 periodontal health through the inhibition of NF-kappaB activity and the amelioration of SETD1-induced

183 Inhibition of NF-kappaB enhances, whereas activation suppresses, the f

184 Inhibition of NF-kappaB signaling pathway significantly reduces the re

185 Chemical inhibition of NF-kappaB with BAY11-7082 reduced Wnt5a expression in th

186 ndrial-targeted antioxidant and inhibitor of NF-kappaB signaling can abrogate GEM-induced hyperexpres

187 nstrate a physical and direct involvement of NF-kappaB in alternative splicing regulation, which sign

188 In this model, we showed that the levels of NF-kappaB may be visualized and measured by fluorescence

189 guish between the islets with high levels of NF-kappaB transcription factor and control islet cells.

190 further understand the complete mechanism of NF-kappaB activation in A20 mutant HL, we performed a sp

191 lly by means of Fli-1-mediated modulation of NF-kappaB signaling.

192 nuclear translocation and phosphorylation of NF-kappaB, thereby preventing gene expression.

193 on of MTA2/NuRD complex from the promoter of NF-kappaB target genes and IKK2-dependent positive regul

194 paB activity, with consequent recruitment of NF-kappaB to the A3B gene promoter to drive A3B expressi

195 s in NF-kappaB, as well as the regulation of NF-kappaB activity.

196 aling complex stability in the regulation of NF-kappaB by a viral oncoprotein.

197 on on the ubiquitin system and regulation of NF-kappaB by ubiquitination using A20 as a representativ

198 and metastasis, the epigenetic regulation of NF-kappaB in tumor context is largely unknown.

199 art of the NF-kappaB proteome, regulation of NF-kappaB signaling by CARP-1 and the molecular mechanis

200 nin rather participated to the regulation of NF-kappaB transcriptional targets, such as IL6, IL8, and

201 e top hit was Traf3, a negative regulator of NF-kappaB signaling that has never previously been linke

202 substrates, including negative regulators of NF-kappaB.

203 equently maintains a proportional reserve of NF-kappaB in peripheral T cells poised for responding to

204 ncephalomyelitis (EAE); however, the role of NF-kappaB activation in oligodendrocytes in MS and EAE r

205 Ample evidence points to central role of NF-kappaB in such pathologic responses, yet the precise

206 interacted less well with the p65 subunit of NF-kappaB and attenuated the DNA binding ability of p65.

207 lls, we demonstrated that the p65 subunit of NF-kappaB is rerouted to perinuclear puncta in the cytop

208 Neuronal suppression of NF-kappaB activity in SOD1(G93A) mice also resulted in n

209 nuclear translocation and transactivation of NF-kappaB to promote the extracellular release of pro-in

210 ype associated with nuclear translocation of NF-kappaB and production of IL-1beta(+) We conclude that

211 in dexamethasone-induced transrepression of NF-kappaB.

212 This effect was dependent on NF-kappaB activation and associated with altered signali

213 agar colony formation; this was dependent on NF-kappaB activation.

214 Further research on NF-kappaB in invertebrates will reveal information about

215 r knowledge of HTLV-1 pathogenesis and other NF-kappaB-related diseases.

216 le unchallenged PBMCs, total NF-kappaB and p-NF-kappaB were significantly increased in developed gran

217 rived PGE2-mediated induction of nuclear p50 NF-kappaB epigenetically reprograms the response of mono

218 urvival in MS patients by targeting the PERK-NF-kappaB pathway.

219 of tendon repair, suggesting that persistent NF-kappaB signaling may facilitate myofibroblast surviva

220 s and ATM by chemotherapeutic drugs promotes NF-kappaB activity, with consequent recruitment of NF-ka

221 decreased the NADH/NAD(+) ratio and reduced NF-kappaB activation.

222 Anti-CD44 antibody treatment reduced NF-kappaB p65 subunit nuclear levels, IL-1beta expressio

223 ated protein translation, and down-regulated NF-kappaB- and STAT-dependent transcription of prosurviv

224 ll type: In pDCs, IRAK4 positively regulated NF-kappaB and MAPK signaling, whereas in B cells, NF-kap

225 or suppressor target EGLN3, and up-regulated NF-kappaB-controlled inflammation signaling.

226 uRD corepressor complex negatively regulates NF-kappaB signaling and tumor growth, whereas later diss

227 nt role in granulopoiesis through regulating NF-kappaB signaling pathway in BM-MSC.

228 t in cells infected with mammalian reovirus, NF-kappaB is inactive.

229 Here, we describe a myeloid cell-selective NF-kappaB inhibitor using an miR-146a mimic oligonucleot

230 tor of NEMO-CARP-1 binding, termed selective NF-kappaB inhibitor 1 (SNI)-1).

231 Several studies suggest that the single NF-kappaB proteins found in some basal organisms have du

232 and (iii) downregulation of the JAK1, STAT1, NF-kappaB, and ERK1/2 pathways.

233 ls of IL-12, IFN-gamma, and the JAK1, STAT1, NF-kappaB, and extracellular signal-regulated kinase 1/2

234 1 expression by M2 TAMs by activating STAT5, NF-kappaB, and/or ERK signaling.

235 s sirtuin1 (SIRT1) repression and stimulates NF-kappaB p65 nuclear translocation and transactivation

236 ort that during T. gondii infection a strong NF-kappaB and inflammatory cytokine transcriptional sign

237 ivity of SAMHD1 is important for suppressing NF-kappaB activation.

238 Further, we demonstrate that NF-kappaB is rendered inactive because virus infection r

239 We demonstrate that NF-kappaB signaling is blocked due to loss of critical m

240 We further demonstrated that NF-kappaB activation contributed to the protective effec

241 These findings suggest that NF-kappaB activation accounts for the cytoprotective eff

242 Together, these data suggest that NF-kappaB may contribute to fibrotic tendon healing thro

243 The NF-kappaB family of proteins is important for the cell t

244 The NF-kappaB pathway integrates signals from many receptors

245 herosclerosis by its ability to activate the NF-kappaB pathway and promote inflammatory cytokine rele

246 HE4 overexpression activated the NF-kappaB pathway through the NF-kappaB transcription-ac

247 in MoDM and possibly in AM by activating the NF-kappaB and JAK/STAT pathways, respectively.

248 ivity to cytokines possibly by affecting the NF-kappaB-inducible nitric oxide synthase-endoplasmic re

249 downstream of IBIN Moreover, Osa affects the NF-kappaB-mediated immune response by regulating Drosoph

250 is part of a protein complex that binds the NF-kappaB DNA consensus sequence, strengthening the idea

251 thway, 3) MyD88 splicing is regulated by the NF-kappaB transcription factor, and 4) NF-kappaB likely

252 However, the NF-kappaB-dependent production of pro-inflammatory media

253 anges the phosphorylation of proteins in the NF-kappaB and MAPK pathways, both known to regulate cyto

254 ely regulate its coactivator function in the NF-kappaB circuit thereby promoting insult resolution.

255 liferative signaling pathways, including the NF-kappaB, AKT, and extracellular signal-regulated kinas

256 n and inflammatory stimuli by inhibiting the NF-kappaB and type I interferon (IFN-I) pathways.

257 Here, we demonstrate that recruitment of the NF-kappaB factor RELA to intragenic regions regulates al

258 rn, directly repressed the expression of the NF-kappaB family member RELA/p65.

259 Members of the NF-kappaB family of transcription factors are key driver

260 Transcription factors of the NF-kappaB family play a crucial role for immune response

261 expression of a super-repressor form of the NF-kappaB inhibitor (IkappaBalpha-SR), which were then c

262 lised endothelial-specific inhibition of the NF-kappaB pathway may be beneficial to prevent vein graf

263 Inhibition of the NF-kappaB pathway prevented acute arterial WSS-induced C

264 and JAK-STAT pathways, and activation of the NF-kappaB pathway were also attenuated by chrysin pretre

265 e JNK pathway and the secondary phase of the NF-kappaB pathway.

266 s have reported that CARP-1 is a part of the NF-kappaB proteome, regulation of NF-kappaB signaling by

267 nd that CD5 alters the basal activity of the NF-kappaB signaling in resting peripheral T cells.

268 ccompanied by an increased activation of the NF-kappaB signaling pathway in bone marrow and BM-MSC of

269 TNF-induced nuclear translocation of the NF-kappaB subunit p65 and NF-kappaB-dependent transcript

270 gnaling which relies on sequestration of the NF-kappaB subunit p65 to a biomolecular condensate-a mec

271 domestic pig RELA protein; a subunit of the NF-kappaB transcription factor that plays a key role in

272 ent manner to provide tunable control of the NF-kappaB transcriptional program.

273 These findings identify activation of the NF-kappaB/LIF/STAT3 signaling cascade as involved in ind

274 tients with IPF produces CXCL13 and that the NF-kappaB and JAK/STAT pathways are required to induce t

275 evidence that tentatively suggests that the NF-kappaB transcription factor can multiplex information

276 modulates inflammatory signaling through the NF-kappaB pathway.

277 activated the NF-kappaB pathway through the NF-kappaB transcription-activating group P65 by phosphor

278 r cytokines and CXCR2 ligands, utilizing the NF-kappaB activity.

279 press proinflammatory proteins-often through NF-kappaB-dependent transcription, assemble inflammasome

280 consequence of beta-ADP-heptose/ ALPK1/TIFA/NF-kappaB signaling.

281 DNA hypermethylation of the IL-2/STAT5, TNF/NF-kappaB, and IFN-gamma signaling pathways.

282 Survival functions previously attributed to NF-kappaB are in fact mediated by these upstream kinases

283 ns of NEMO, a scaffolding protein central to NF-kappaB signaling, exemplify this challenge.

284 These results link disturbed blood flow to NF-kappaB-mediated inflammation, which promotes atherosc

285 his resulted in enhanced formation of TonEBP/NF-kappaB p65 complexes and enhanced proinflammatory gen

286 with microparticle unchallenged PBMCs, total NF-kappaB and p-NF-kappaB were significantly increased i

287 ole in immune cell activation by transducing NF-kappaB signaling, and its proteolytic activity repres

288 s suggest that in addition to TMZ treatment, NF-kappaB can be used as a potential target to increase

289 increased several canonical pathways (TREM1, NF-kappaB, complement, IL-6 signaling) and upstream regu

290 tch that controls whether the cell undergoes NF-kappaB (nuclear factor kappa-light-chain-enhancer of

291 regions regulates alternative splicing upon NF-kappaB activation by the viral oncogene Tax of HTLV-1

292 racellular NADH/NAD(+) ratio and upregulated NF-kappaB activation after LPS treatment, whereas treatm

293 ver through mechanisms related to a PKG/VASP/NF-kappaB/NLRP3 inflammasome circuit.

294 es driven by TNF and Toll-like receptors via NF-kappaB, eicosanoid biosynthesis via the lipoxygenase

295 expression occurs via JNK activation, while NF-kappaB and p38/MAPK inhibition did not affect RUNX1 e

296 gulating signaling cascades, in concert with NF-kappaB-mediated transcriptional events, control the m

297 nted a quiescent phenotype, correlating with NF-kappaB nuclear translocation, suggesting a mechanism

298 inverse correlation of miR-146a levels with NF-kappaB-related genes and with patient survival.

299 ight on the regulation of a novel PRMT5/YBX1/NF-kappaB axis through PRMT5-mediated YBX1-R205 methylat

300 ew therapeutics for CRC and other PRMT5/YBX1/NF-kappaB-associated cancers.