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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.
10 unohistological staining of occludin, Ki-67, NF-kappaB-p65, and terminal deoxynucleotidyl transferase
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
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
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
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
36 blocked proinflammatory gene expression and NF-kappaB activation while enhancing HIF-1alpha levels a
38 vation of IFN regulatory factor 3 (IRF3) and NF-kappaB was observed in EBOV-infected, but not in REST
40 D1, and identify c-Jun N-terminal kinase and NF-kappaB as potential therapeutic targets for preventio
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
50 tion of lincRNA-Cox2 and lincRNA-AK170409 as NF-kappaB regulators, and this tool will be useful for i
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
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
62 me was enriched in genes commonly altered by NF-kappaB in response to TNF, by IL-6 via STAT3, and in
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
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
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
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
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
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
95 ERK/MAPK and the master transcription factor NF-kappaB in response to FGF and IL-1/TNF, respectively.
100 obial stimuli, DCs activated nuclear factor (NF)-kappaB, which induced expression of a proinflammator
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
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
111 ent on the activation of traditional IKKbeta/NF-kappaB pathways that are important in normal immune r
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
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
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
126 Further studies found that netrin-1 induced NF-kappaB p65(ser536) phosphorylation and c-Myc expressi
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
135 a membrane in infected cells, and it induces NF-kappaB activity, especially in the context of retrovi
137 suppression of UNC5A significantly inhibited NF-kappaB p65(ser536) phosphorylation, c-Myc up-regulati
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
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
146 e IKBKG gene encoding nuclear factor kappaB (NF-kappaB) essential modulator (NEMO; the regulatory sub
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
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.
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
164 illomas in the context of p53 loss and novel NF-kappaB expression, whereas increased tissue rigidity
169 ation of TRAF6, which promotes activation of NF-kappaB and MAPK signalling and increases the producti
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
176 and the purified PF triggered activation of NF-kappaB through TLR2, as determined using a variety of
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.
181 ng events, including the rapid activation of NF-kappaB, c-Jun N-terminal kinase (JNK), extracellular
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
187 ence of ApN markedly reduced the activity of NF-kappaB, a key player in muscle inflammation and myoge
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
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
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.
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
205 d is sufficient to reduce cellular levels of NF-kappaB and calpain-2 and secreted levels of the proan
210 and was mediated by decreased recruitment of NF-kappaB p65 and RNA polymerase II to COX-2 and IL-8 pr
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
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
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
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
233 lear translocation but significantly reduced NF-kappaB DNA binding and phosphorylation of NF-kappaB p
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
240 sphorylation levels of ERK-1/2 and p65/RelA (NF-kappaB) and inducible NO synthase expression, suggest
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
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
252 ons and LMP1-overexpression, suggesting that NF-kappaB activation is selected for by both somatic and
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
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
273 s highlight the functional plasticity of the NF-kappaB signaling pathway and underscores the need for
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-
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
287 gulatory network where co-activation of Toll/NF-kappaB and EGFR signaling by ROS levels in the PSC/ni
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
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
300 ways associated with uric acid priming, with NF-kappaB and mammalian target of rapamycin (mTOR) signa
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