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1 5145, directly alters the binding site for a nuclear factor.
2 the expression of regulatory cytoplasmic and nuclear factors.
4 egulated pathways associated with hepatocyte nuclear factor 1 homeobox A (Hnf1a) and hepatocyte nucle
5 ased on inactivating mutations in hepatocyte nuclear factor 1A, activating mutations in beta-catenin,
6 ased on inactivating mutations in hepatocyte nuclear factor 1A, activating mutations in beta-catenin,
8 nteraction of Akt2 signaling with hepatocyte nuclear factor 1alpha (HNF1alpha) and PPARgamma, transcr
11 e evaluated the potential role of hepatocyte nuclear factor-1beta (HNF-1beta) in regulating PPARGC1A
13 ding the shelterin proteins TRF1-interacting nuclear factor 2 (TIN2) and adrenocortical dysplasia hom
17 ned functional gene regulation by hepatocyte nuclear factor 4 alpha (HNF4alpha), whereas fibrotic mat
19 r factor 1 homeobox A (Hnf1a) and hepatocyte nuclear factor 4A (Hnf4a), known modifiers of bile acid
20 which was down-regulated in mouse hepatocyte nuclear factor 4A knockout mice; were early-stage tumors
21 nted 29% of all HCCs; expressed a hepatocyte nuclear factor 4A-driven gene network, which was down-re
23 al triglyceride transfer protein via hepatic nuclear factor 4alpha and chicken ovalbumin upstream pro
24 e hepatocyte transcription factor hepatocyte nuclear factor 4alpha by modulating its activation and r
28 ranscriptional factors, including hepatocyte nuclear factor-4alpha, that is early down-regulated and
29 ranscriptional activators (STAT5, hepatocyte nuclear factor 6 [HNF6], FOXA1, and FOXA2) and transcrip
30 ression; however, the complete repertoire of nuclear factors affecting these genomic changes is not k
31 enes and their functional replacement by new nuclear factors are important in models for the origin o
32 Levels of neutrophil elastase (NE) and the nuclear factors CCAAT/enhancer-binding protein alpha (C/
33 small blood capillary, chromatin density and nuclear factors could in principle be physically perturb
36 ere, we identified ARF as a key regulator of nuclear factor E2-related factor 2 (NRF2) through comple
37 ctivity is associated with the activation of nuclear factor-E2-related factor 2 (Nrf2), a key anti-in
39 ives also stimulated the expression of NRF2 (nuclear factor erythroid 2 [NF-E2]-related factor 2) and
40 e identify the ER-bound transcription factor nuclear factor erythroid 2 related factor-1, Nrf1/Nfe2L1
43 ICAM) (P < 0.001, respectively) and improved nuclear factor erythroid 2-related factor 2 (Nrf2) and h
44 tified an increased nuclear translocation of nuclear factor erythroid 2-related factor 2 (NRF2) in th
45 ivating the aryl hydrocarbon receptor (AhR), nuclear factor erythroid 2-related factor 2 (Nrf2), and
46 cancer cells attenuated GSH/GSSG, total GSH, nuclear factor erythroid 2-related factor 2 (Nrf2), and
48 vels of estrogen receptor-alpha activity and nuclear factor erythroid 2-related factor 2 activity, an
49 ctivator of p62 through competition of Nrf2 (nuclear factor erythroid 2-related factor 2) for Keap1 b
52 KEAP1), which targets transcriptional factor nuclear factor erythroid-2-related factor 2 (NRF2) for d
54 ancer cell lines via focal amplification and nuclear factor erythroid-2-related factor 2 (NRF2)-media
55 r advanced glycation end products (RAGE) via nuclear factor erythroid-2-related-factor-2 (Nrf2)-depen
56 ated with impaired glutathione synthesis and nuclear factor erythroid-derived 2 related factor 2 (NRF
57 ung fibroblasts is inhibited by silencing of nuclear factor erythroid-derived 2-like 2 (Nrf2), suppor
58 iron levels by binding to and deacetylating nuclear factor erythroid-derived 2-related factor 2 (NRF
59 d with a decreased GSH/GSSG ratio, augmented nuclear factor erythroid-related factor 2, and increased
62 rt therapeutic effects via activation of the nuclear factor (erythroid-derived 2)-like 2 (NRF2) pathw
63 he basic leucine zipper transcription factor nuclear factor (erythroid-derived 2)-like 2 (NRF2) plays
64 t significantly affected genes belong to the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) trans
65 ulator of the cellular antioxidant response, nuclear factor (erythroid-derived 2)-like 2 (NRF2), shut
69 n gene transcription by activating the NRF2 (nuclear factor [erythroid-derived 2]-like 2) transcripti
70 validated a difference in the regulation of nuclear factor, erythroid 2 (Nfe2) and core-binding fact
71 sk tumors were characterized by up-regulated nuclear factor, erythroid 2-like 2 activity; high lin-28
72 The activity of the transcription factor nuclear factor-erythroid 2 p45-derived factor 2 (NRF2) i
75 e mediated by heat shock factor 1 (HSF1) and nuclear factor-erythroid 2 p45-related factor 2 (NRF2),
76 response, we examined here the expression of nuclear factor-erythroid 2-related factor (Nrf-2), a mas
79 so induced expression of the redox regulator nuclear factor-erythroid-derived 2-like 2 (NFE2L2 alias
80 In this study, silencing the expression of a nuclear factor gene, CmNF-YB8, from the short day plant
82 assified into 14 inflammatory, 20 hepatocyte nuclear factor (HNF)-1alpha-mutated, one beta-catenin-ac
85 The discovery of the unique role of Nfic (nuclear factor I C; a transcriptional factor) in control
86 differentiation-related transcription factor nuclear factor I-A (NFI-A) controls MDSC expansion durin
87 /Notch-like EGF repeat containing (Dner) and nuclear factor I/A (Nfia), that are each heavily express
91 ctor IA (NFIA), nuclear factor IB (NFIB), or nuclear factor IX (NFIX) results in abnormal development
92 ecific lipin-1 deficiency diminished hepatic nuclear factor kappa B (NF-kappaB) activity, limited liv
95 MRV miRNAs, we screened for their effects on nuclear factor kappa B (NF-kappaB) signaling in the pres
96 biquitinated chains from key proteins in the nuclear factor kappa B (NF-kappaB) signaling pathway.
97 Here we demonstrate that the dynamics of Nuclear Factor kappa B (NF-kappaB) signalling and the ce
98 decrease in PKC activity, and inhibition of nuclear factor kappa B (NF-kB) translocation, were attri
99 in terms of interleukin (IL)-8 promoter and nuclear factor kappa B (NFkappaB) activity, were observe
100 IkappaBalpha enhances the rate of release of nuclear factor kappa B (NFkappaB) from DNA target sites
102 nate attenuated the HS-induced activation of nuclear factor kappa B and reduced the expression of pro
103 nate attenuated the HS-induced activation of nuclear factor kappa B and reduced the expression of pro
104 ylated and thereby inhibited by inhibitor of nuclear factor kappa B kinase subunit beta (IKKbeta) to
107 vo that depends on Ser536 phosphorylation of nuclear factor kappa B p65; this pathway may hold valuab
108 of the mitogen-activated protein kinase and nuclear factor kappa B pathways in MDSCs was MyD88 depen
109 in the presence of antagonists of NFkappaB (nuclear factor kappa B) or iNOS activity, NO synthesis a
110 location of transcription factors, including nuclear factor kappa B, although its role in PCa was lar
111 in inflammatory and cancer pathways, such as nuclear factor kappa B, EGF, Wnt, and B-cell lymphoma 2.
112 rough regulating the activation of canonical nuclear factor kappa B, phosphatidylinositol-4,5-bisphos
115 ulting in de novo lipogenesis, and increased nuclear factor kappa B-mediated inflammation act in conc
118 0 kDa) binds to macrophage-TLR4 and triggers nuclear factor kappa beta activation that upregulates se
119 aining, and C-X-C chemokine receptor type 4, nuclear factor kappa beta, and tartrate-resistant acid p
120 ified as a critical brake on proinflammatory nuclear factor kappa light chain enhancer of activated B
122 that stimulation with receptor activator of nuclear factor kappa-B ligand (RANKL) resulted in a robu
123 oxidase (MPO), and the cytokine receptor for nuclear factor kappa-B ligand (RANKL) were significantly
124 ted T cells to produce receptor activator of nuclear factor kappa-B ligand (RANKL), which, in turn, p
125 tal tissue and induces receptor activator of nuclear factor kappa-B ligand (RANKL)-RANK-osteoproteger
126 Change in circulating receptor activator of nuclear factor kappa-B ligand was higher in the interven
128 croRNA (miR)-181a is a negative regulator of nuclear factor kappa-light-chain enhancer of activated B
129 th a defect in the capacity to phosphorylate nuclear factor kappa-light-chain-enhancer of activated B
130 o associated with reduced phosphorylation of nuclear factor kappa-light-chain-enhancer of activated B
131 and interleukin (IL)-1alpha, that activated nuclear factor kappa-light-chain-enhancer of activated B
132 of p38 mitogen activated protein kinase and nuclear factor kappa-light-chain-enhancer of activated B
134 tumorigenesis and metastasis-through a TLR4/nuclear factor kappa-light-chain-enhancer of activated B
135 Znrf4 knockdown monocytes have sustained nuclear factor kappa-light-chain-enhancer of activated B
136 atients were less capable in phosphorylating nuclear factor kappa-light-chain-enhancer of activated B
137 of p38 mitogen activated protein kinase and nuclear factor kappa-light-chain-enhancer of activated B
140 GF), inducible nitric oxide synthase (iNOS), nuclear factor-kappa B (NF-kappaB) and intercellular adh
142 affects expression of receptor activator of nuclear factor-kappa B (NF-kappaB) ligand (RANKL), a pot
143 ne of these main signaling mechanisms is the nuclear factor-kappa B (NF-kappaB) pathway, which integr
145 like receptor 4 (TLR4)-dependent pathway via nuclear factor-kappa B (NF-kappaB), while simultaneously
147 ranscription factor-2, receptor activator of nuclear factor-kappa B ligand (RANKL), sclerostin, and D
148 interleukin-1beta and receptor activator of nuclear factor-kappa B ligand than group EP-HN019 (P <0.
149 d that overexpression of LINC00305 activated nuclear factor-kappa beta (NF-kappaB) and that inhibitio
151 and activation of the transcription factors nuclear factor kappaB (NF-kappaB) and interferon regulat
152 additional transcription factors, including nuclear factor kappaB (NF-kappaB) and signal transducer
153 aining adapter-inducing IFN-alpha (TRIF) and nuclear factor kappaB (NF-kappaB) causes the apoptosis o
155 unction mutations in the IKBKG gene encoding nuclear factor kappaB (NF-kappaB) essential modulator (N
156 30 years ago and is due to mutations in the nuclear factor kappaB (NF-kappaB) essential modulator, a
157 in these mice was prevented by inactivating nuclear factor kappaB (NF-kappaB) in microglia/myeloid c
160 turn, PKR stimulates nuclear accumulation of nuclear factor kappaB (NF-kappaB) p65 species phosphoryl
161 in cancer cells, and subsequently activates nuclear factor kappaB (NF-kappaB) pathway which has a st
162 ferential enhancer utilization, and identify nuclear factor kappaB (NF-kappaB) signaling as a key pat
163 constitutive activation of pro-inflammatory nuclear factor kappaB (NF-kappaB) signaling in TNBC.
164 ly demonstrated a key role for the canonical nuclear factor kappaB (NF-kappaB) subunits, p65 and c-Re
165 way which regulates the transcription factor Nuclear Factor kappaB (NF-kappaB) using this method iden
166 nuclear factor of activated T cells (NFAT), nuclear factor kappaB (NF-kappaB), and activator protein
167 ed the pro-inflammatory transcription factor nuclear factor kappaB (NF-kappaB), whereas stable, non-o
168 g to caspase-8-mediated apoptosis as well as nuclear factor kappaB (NF-kappaB)-dependent cell surviva
174 A2AR signaling reduces receptor activator of nuclear factor kappaB (RANK)-mediated osteoclastogenesis
175 ), one of the crucial negative regulators of nuclear factor kappaB activation in myeloid cells and DC
180 actor kappaB receptor, receptor activator of nuclear factor kappaB ligand/macrophage colony-stimulati
182 AhR and some components of the noncanonical nuclear factor kappaB pathway were shown to be downregul
183 The CARD11 defect altered the classical nuclear factor kappaB pathway, resulting in poor in vitr
184 gher expression of the receptor activator of nuclear factor kappaB receptor, receptor activator of nu
185 ive oxygen species that, on one hand, induce nuclear factor kappaB signaling and expression of inflam
186 muscle cells by various mechanisms activates nuclear factor kappaB signaling and increases expression
187 tion of endothelial autophagy and attenuated nuclear factor kappaB signaling in vitro and in vivo.
188 immunodeficiency caused by mutations in the nuclear factor kappaB signaling pathway (IKBKG and NFKBI
189 es reactive oxygen species levels, activates nuclear factor kappaB signaling, and increases AngII rec
190 reactive oxygen species and increased basal nuclear factor kappaB signaling, leading to an increase
191 Treatment with AZD8835 induced inhibition of nuclear factor kappaB signaling, prompting us to combine
192 Tet methylcytosine dioxygenase 2 (TET2) and nuclear factor kappaB to DNA demethylation was tested by
193 activator of transcription 3) and NFkappaB (nuclear factor kappaB), the pro-inflammatory and cancer-
195 mechanism of action correlated with reduced nuclear factor-kappaB (NF-kappaB) activation and decreas
196 We purified nuclear extracts and quantified nuclear factor-kappaB (NF-kappaB) activation and DNA bin
198 horylation and subsequent activation of both nuclear factor-kappaB (NF-kappaB) and mechanistic target
199 OT in human amnion; atosiban alone activates nuclear factor-kappaB (NF-kappaB) and mitogen activated
201 rantly overexpressed in NSCLC, activates the nuclear factor-kappaB (NF-kappaB) p65-->ZEB1 pathway and
202 an early-primary response gene controlled by nuclear factor-kappaB (NF-kappaB) signaling in murine ma
204 ists stems from TLR5-dependent activation of nuclear factor-kappaB (NF-kappaB) that mediates innate a
205 inflammatory responses through activation of nuclear factor-kappaB (NF-kappaB), has been implicated a
206 ty with concomitant nuclear translocation of nuclear factor-kappaB (NF-kappaB), indicating that NF-ka
207 ceptor cooperativity with factors, including nuclear factor-kappaB (NF-kappaB), may enhance regulator
208 utive activation of the transcription factor nuclear factor-kappaB (NF-kappaB), which controls expres
209 hown to direct gene expression by regulating nuclear factor-kappaB (NF-kappaB)-mediated inflammatory
212 and activator of transcription 3 (STAT3) and nuclear factor-kappaB activation in response to the bact
213 ammation and lung injury in vivo and reduced nuclear factor-kappaB activation predominantly by inhibi
214 ia across the apical epithelial barrier, (3) nuclear factor-kappaB activation, (4) accumulation of ma
215 der normocapnia or hypercapnic acidosis, and nuclear factor-kappaB activation, animal survival, lung
216 epithelial morphology, SIgA, bacterial DNA, nuclear factor-kappaB activation, neutrophil and macroph
219 ponse gene 88 (MyD88) pathway that activates nuclear factor-kappaB and increases monocyte chemotaxis.
220 upon antigen receptor-induced activation of nuclear factor-kappaB and mammalian target of rapamycin
221 subtype that showed increased sensitivity to nuclear factor-kappaB and mitogen-activated protein kina
222 matory endotoxin lipopolysaccharide via both nuclear factor-kappaB and signal transducer and activato
223 atory cytokines with or without aldosterone, nuclear factor-kappaB inhibitor BAY 11-7082, or plasma f
226 = 0.003), and soluble receptor activator of nuclear factor-kappaB ligand (sRANKL) concentrations wer
227 c sensitization to the receptor activator of nuclear factor-kappaB ligand and increased osteoblastic
228 -selectin, fibrinogen, receptor activator of nuclear factor-kappaB ligand, high-sensitivity C-reactiv
229 , the repressor of the receptor activator of nuclear factor-kappaB ligand-mediated osteoclastogenesis
230 )IgM(+)) with active B cells (phosphorylated nuclear factor-kappaB p65(+)), proliferation markers (Ki
231 pha in microglia, and the recruitment of the nuclear factor-kappaB pathway while restoring hypothalam
232 Mechanistically, Nrp1 deletion activates the nuclear factor-kappaB pathway, which in turn accentuates
236 one marrow-derived macrophages by activating nuclear factor-kappaB signaling and reactive oxygen spec
237 med that clofibrate abrogates the binding of nuclear factor-kappaB to the PTPRZ1 and Wnt8a promoters,
238 Adelmidrol treatment, moreover, reduced nuclear factor-kappaB translocation, cyclooxygenase-2, a
239 opathy, characterized by elevated NF-kappaB (nuclear factor-kappaB) activation and TNF (tumor necrosi
240 q are common and include genes that modulate nuclear factor-kappaB, BCL2, BTK, apoptosis, differentia
241 ion of SMAD6, which required the activity of nuclear factor-kappaB, but not transforming growth facto
242 extravascular albumin), and immunoblotting (nuclear factor-kappaB, hypoxia-inducible factor-1alpha,
243 at infection with HCV leads to activation of nuclear factor-kappaB, resulting in increased expression
244 UMA, whereas inhibition of mTORC2 results in nuclear factor-kappaB-mediated expression of the Early G
249 dependent of Tpl2 kinase, a key regulator of nuclear factor kappaB1-mediated MAPK activation in macro
250 ere we report that the receptor activator of nuclear factor-kB (RANK), the key regulator of osteoclas
251 IL-1beta production, IL-1beta secretion and nuclear factor-kB activity were reduced by knocking down
252 cells were able to induce Ca(2+) influx and nuclear factor (NF) kappaB signaling, whereas extracellu
253 sion of Toll-like receptor (TLR)2, TLR4, and nuclear factor (NF)-kappa B mRNA levels were analyzed us
254 cell activation was evaluated by quantifying nuclear factor (NF)-kappa B-p65 and cytokine expression
255 ased lymphocytic infiltration, and decreased nuclear factor (NF)-kappaB activation compared with cont
256 , downregulation of Bcl-xL levels, decreased nuclear factor (NF)-kappaB activity, and apoptosis.
257 iRNA that inhibits multiple factors from the nuclear factor (NF)-kappaB pathway in various cell types
259 and upregulated miR-19a can in turn activate nuclear factor (NF)-kappaB signaling and TNF-alpha produ
260 -1180 directly targets key inhibitors of the nuclear factor (NF)-kappaB signaling pathway (i.e., OTUD
261 ts neuroprotection by up-regulating c-REL, a nuclear factor (NF)-kappaB subtype that, in turn, enhanc
262 exposed to microbial stimuli, DCs activated nuclear factor (NF)-kappaB, which induced expression of
264 translocation of transcription factors from Nuclear Factor (NF)-kB and Interferon Regulatory Factor
266 tabolic regulators through the activation of nuclear factor of activated T cells (NFAT) and the PI3K-
267 osphatase required for the activation of the nuclear factor of activated T cells (NFAT) family of tra
269 ut had no effect on G1-mediated signaling to nuclear factor of activated T cells (NFAT) luciferase.
270 ites is strongly involved in CaV1.2-mediated nuclear factor of activated T cells (NFAT) signaling, lo
272 itogenic effect of Ex-4 requires calcineurin/nuclear factor of activated T cells (NFAT) signaling.
273 ignaling activates the transcription factors nuclear factor of activated T cells (NFAT), nuclear fact
274 ulatory factor 4 (IRF4) mRNA expression, and nuclear factor of activated T cells (NFAT1) protein expr
275 ment and its substrate transcription factor, nuclear factor of activated T cells (NFAT4), appear in a
276 have identified an autocrine pathway linking nuclear factor of activated T cells 2 (NFAT1), autotaxin
277 CaMKIV) activation, and interactions between nuclear factor of activated T cells 3 (NFATc3) and FosB
279 that the osmoprotective transcription factor nuclear factor of activated T cells 5 (NFAT5) critically
281 in PPR patients upregulates the calcineurin/nuclear factor of activated T cells signaling triggering
282 cium signaling, cytosolic calcium activating nuclear factor of activated T cells translocation direct
283 phage colony-stimulating factor induction of nuclear factor of activated T cells type c-1 and catheps
284 of the osteoclast transcriptional activator nuclear factor of activated T cells type c-1, associated
285 GF), E-cadherin, SRY-box 7 (SOX7), and NFAT (nuclear factor of activated T cells) kinase dual-specifi
286 hat cooperates with the transcription factor nuclear factor of activated T cells, c1 (NFATc1) to driv
287 t to be mediated by the transcription factor nuclear factor of activated T cells, cytoplasmic 1 (NFAT
288 at suppresses the expression and activity of nuclear factor of activated T cells, cytoplasmic, calcin
289 ent (MAPK, JNK) and non-catalytic-dependent (nuclear factor of activated T cells, NFAT) VAV1 effector
293 a result of lowered inhibitory IkappaBalpha (nuclear factor of kappa light polypeptide gene enhancer
294 eus accumbens-associated protein-1 (NAC1), a nuclear factor of the BTB/POZ gene family, has emerging
295 6) and/or c-fos signaling to induce NFATc1 (nuclear factors of activated T cells, cytoplasmic 1).
297 We have identified a large set of candidate nuclear factors that may underpin immunity to pathogens
298 associated with an astonishing collection of nuclear factors, which serve to not only store the nucle
299 ociated protein Basp1, thereby de-repressing nuclear factors WT1, Esrrb and Lin28a (Lin28) independen
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