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1 NF-kappa B binding activity in ventricular tissues was e
2 NF-kappa B is a family of transcription factors involved
3 NF-kappa B is a heterodimeric transcription activator co
4 NF-kappa B prevents cell death caused by tumor necrosis
5 NF-kappa B seems to play an important role in the develo
6 NF-kappa B was discovered because of its binding to the
7 th domain, TNF receptor-associated factor 2, NF-kappa B-inducing kinase, and IKK, but not that activa
8 e measured Ca(2+) responses by using Fura-2, NF-kappa B-binding activity by electromobility shift ass
9 proach was used to insert a single copy of a NF-kappa B-dependent EGFP reporter gene 5' of the X-link
10 The interleukin (IL)-8 promoter possesses a NF-kappa B-binding site with affinity to p50p65 and p65p
11 ession, SOCS-3 cDNA was cotransfected with a NF-kappa B (NF-kappaB) luciferase construct into culture
12 ed for induction of apoptosis could activate NF-kappa B but not IFN regulatory factor-3, yet the acti
13 that signals emanating from the TCR activate NF-kappa B during iNKT cell development and function.
15 d the ability of HDAC inhibitors to activate NF-kappa B and dramatically sensitized NSCLC cells to ap
16 wild-type cells in their ability to activate NF-kappa B signaling in response to the following: human
20 avoid apoptosis, thus implicating activated NF-kappa B as a therapeutic target for distinctive subcl
21 ative tumors, suggesting a role of activated NF-kappa B in intercellular signaling between epithelial
22 results demonstrate association of activated NF-kappa B with a subgroup of human breast tumors and ar
24 aling pathways and PVQEET(559-564) activates NF-kappa B and p38 pathways in osteoclasts, whereas PVQE
25 from Ucp2-/- cells constitutively activates NF-kappa B, resulting in a "primed" state to both potent
28 eased nuclear p65, a component of the active NF-kappa B complex, in cytokeratin 19 (CK19)-positive ep
29 B subunits to the nucleus without affecting NF kappa B release from its cytosolic inhibitory sub-uni
33 l lines have constitutive active alternative NF-kappa B pathway and demonstrate high-level expression
34 d proliferation of PEL cells and alternative NF-kappa B pathway plays a key role in this process.
35 e mechanism of activation of the alternative NF-kappa B pathway in PEL cells, we have investigated th
36 Therapeutic agents targeting the alternative NF-kappa B pathway may have a role in the treatment of K
38 BAY11 effects were similar to those of an NF-kappa B inhibitor, Delta N-I kappa B alpha, in effect
39 onucleotide microarrays and parthenolide, an NF-kappa B-specific inhibitor, to identify the NF-kappa
40 form of mitogen-activated protein kinase and NF kappa B and also increased reactive oxygen species le
42 its the transcriptional activity of AP-1 and NF-kappa B transcription factors, respectively, both of
45 ated RIP3 in the regulation of apoptosis and NF-kappa B signaling, but whether RIP3 promotes or atten
46 d cytokine-induced I kappa B degradation and NF-kappa B transcriptional activity in RPE cells and T-9
47 he regulatory cross-talk between the JNK and NF-kappa B pathways appears to be broadly conserved.
49 induced increase in NAG-1 protein levels and NF-kappa B binding/transcriptional activity, whereas an
51 n scurfy-derived T cells lowers the NFAT and NF-kappa B transcriptional activity to the physiological
52 y of two key transcription factors, NFAT and NF-kappa B, which are essential for cytokine gene expres
53 clear factor of activated T cells (NFAT) and NF-kappa B transcriptional activity compared with the T
56 beta/IKK2, receptor-interacting protein, and NF-kappa B-inducing kinase are dispensable for this proc
58 t I kappa B-alpha homeostatic regulation and NF-kappa B activity at later time points is perturbed.
60 obilization, Ca(2+) influx, trypsinogen, and NF-kappa B activation were all diminished in pancreatic
61 at typical outcomes of BCR signaling such as NF-kappa B activation and cell cycle progression occurre
62 nd concentration-dependent manner as well as NF-kappa B binding/transcriptional activity in LNCaP cel
63 rs197273 near TRAF family member-associated NF-kappa-B activator (TANK) (2p24.2), and rs10163409 in
65 r IL-8 secretion or nuclear factor- kappa B (NF-kappa B) activation on IL-8 induction by dengue 2 vir
66 ta function involves nuclear factor kappa B (NF-kappa B) activation, these data suggest that this inc
69 transcription factor nuclear factor-kappa B (NF-kappa B) has a crucial role in osteoclast differentia
71 eceptor activator of nuclear factor-kappa B (NF-kappa B) ligand (RANKL) as shown by the use of TWEAK-
72 oligonucleotide for nuclear factor kappa B (NF-kappa B) p65 was given prophylactically or therapeuti
73 yD88 to activate the nuclear factor kappa B (NF-kappa B) pathway, a critical regulator of many proinf
74 Phosphorylation of nuclear factor-kappa B (NF-kappa B) subunits emerges as a mechanism by which tra
75 (RelA) component of nuclear factor-kappa B (NF-kappa B) to the endogenous E-selectin promoter after
76 examine the links of nuclear factor-kappa B (NF-kappa B) to treatment-induced signaling in breast can
77 transcription factor nuclear factor kappa B (NF-kappa B), abnormal Ca(2+) responses, and trypsinogen
81 (mI kappa B alpha M), which is able to block NF-kappa B in zebra fish cells, interferes with the noto
83 in osteoclast differentiation, and blocking NF-kappa B is a potential strategy for preventing inflam
84 nstitutive activation of AKT as well as both NF kappa B- and beta-catenin-dependent transcription.
85 actor alpha (TNFalpha), which activates both NF-kappa B and AP-1, increased MAT2A expression in a dos
86 - and time-dependent manner, binding of both NF-kappa B and AP-1 to the MAT2A promoter and MAT2A prom
88 underlying suppression of PTEN expression by NF-kappa B was independent of p65 DNA binding or transcr
89 vival Bcl-2 homologue Bfl-1/A1 is induced by NF-kappa B-activating stimuli, while B and T cells from
90 s activation of protective genes mediated by NF-kappa B transcription factors; however, its basis rem
91 A and are, presumably, directly regulated by NF-kappa B, except, curiously, the cornification markers
92 The COX-2 promoter, which is regulated by NF-kappa B, was also inhibited by celecoxib, and this in
95 light polypeptide gene enhancer in B-cells (NF-kappa B) leading to transcriptional reactivation of v
97 cytes, and dendritic cells isolated from cis-NF-kappa B(EGFP) mice demonstrated a strong induction of
101 PTEN strongly inhibits both the constitutive NF kappa B- and beta-catenin-dependent promoter and endo
106 e proposal is that mutations cause deficient NF-kappa B-dependent T helper type 1 (T(H)1) responses a
110 cornification proteins belong to the "early" NF-kappa B-dependent group, and antigen presentation pro
112 tly increased the number of cells expressing NF-kappa B-dependent beta-galactosidase in the magnocell
113 t of the growth-related transcription factor NF-kappa B and cyclin D1 activities that are partly depe
115 ctive activation of the transcription factor NF-kappa B, one proposal is that mutations cause deficie
117 Biochemical assays indicate that zebra fish NF-kappa B proteins are able to bind consensus DNA-bindi
121 V substitution resulted in 5.5 times greater NF kappa B transcriptional activity and approximately 2
126 ly involved in innate and adaptive immunity, NF-kappa B plays an important role in vertebrate develop
127 transgenic CD4(+) T cells parallels impaired NF-kappa B activity and increased levels of GATA-3, whic
129 mphoma cells leads sequentially to a drop in NF-kappa B and c-Myc, and induction of the p27(Kip1) cyc
131 itutively active PKCs induced an increase in NF-kappa B transcriptional activity and NAG-1 protein le
139 ubstance P to enhance B. burgdorferi-induced NF-kappa B activation, as demonstrated by increased nucl
140 Levels of basal and stimulation-induced NF-kappa B activity were significantly decreased in mice
142 ctivation, which is required for TNF-induced NF-kappa B activation, was also suppressed by this drug.
144 NF kappa B inhibitor PTD-p65 peptide inhibit NF kappa B activation and TNF alpha potentiation of glut
146 horylation inhibitor, Bay 11-7082, inhibited NF-kappa B activation, as well as PGE(2) production, COX
147 Restoration of PTEN expression inhibited NF-kappa B transcriptional activity and augmented TNF-in
148 BAY11 rapidly and irreversibly inhibited NF-kappa B, decreased mitochondrial membrane potential,
151 our results indicate that celecoxib inhibits NF-kappa B activation through inhibition of IKK and Akt
153 iption factors, such as Cubitus interruptus, NF-kappa B and sterol regulatory element binding protein
154 iation with Raf-1 and nuclear factor kappaB (NF-kappa B)-inducing kinase (NIK), RKIP negatively regul
158 MAS2 encodes the putative ortholog of NKAP (NF-kappa B activating protein), a conserved eukaryotic p
162 by which transcriptional activity of nuclear NF-kappa B complexes is regulated in an inhibitor kappa
166 mpartment-associated Bcl-2 prevents entry of NF kappa B subunits to the nucleus without affecting NF
167 oduction reflected differential induction of NF kappa B and STAT6 by the two stimuli (both are in the
170 Although the transactivation ability of NF-kappa B has been extensively studied in vitro, limite
172 K), blocked heregulin-mediated activation of NF-kappa B and cell proliferation, and simultaneously in
174 N regulatory factor-3, yet the activation of NF-kappa B could be blocked by superrepressor I kappa B
178 ed Toll-like receptor 2-driven activation of NF-kappa B, particularly of the NF-kappa B subunit c-Rel
179 Toll-like receptor 2-mediated activation of NF-kappa B-c-Rel, and T(H)1 responses were enhanced.
181 ligand (RANKL) and its receptor activator of NF-kappa B (RANK) play pivotal roles in osteoclast diffe
184 kine family member, on receptor activator of NF-kappa B ligand (RANKL)-stimulated osteoclast differen
185 depends to a large extent on the activity of NF-kappa B transcription factors, play important roles i
189 itation assay was used to confirm binding of NF-kappa B subunits to IL-8 and MCP-1 promoters in vivo.
192 trates the conservation and compatibility of NF-kappa B/I kappa B proteins among vertebrates and the
199 eins among vertebrates and the importance of NF-kappa B pathway in mesoderm formation during early em
204 her, these studies reveal that inhibition of NF-kappa B activity in T and NK cells results in defecti
205 udies have shown that targeted inhibition of NF-kappa B can sensitize tumor cells to chemotherapy and
207 these results suggest that the inhibition of NF-kappa B signaling can suppress tumorigenesis of pancr
208 ogeny has been rescued despite inhibition of NF-kappa B signaling, we demonstrate that iNKT cell func
211 rine-induced phosphorylation of inhibitor of NF-kappa B alpha (I kappa B alpha) and NF-kappaB nuclear
212 ling leads to activation of the inhibitor of NF-kappa B kinase (IKK) complex via Carma1, Bcl10 and MA
213 f PI3K/Akt signaling decreased the levels of NF-kappa B and c-Myc, which has been shown to repress p2
214 te the kinetics and cellular localization of NF-kappa B-induced transcription, we created a transgeni
215 e differences indicate that the mechanism of NF-kappa B regulation by PI3K gamma differs from those f
216 an exclude RIP3 as an essential modulator of NF-kappa B signaling downstream of several receptor syst
217 ficant correlation between overexpression of NF-kappa B-p65 and the development of vascular factors.
220 ose further studies to elucidate the role of NF-kappa B in breast cancer response to chemotherapy and
223 of stimulation with TNFalpha and the role of NF-kappa B in regulating this response, a 23k human cDNA
225 the main transactivator, the p65 subunit of NF-kappa B has an outstanding position in the hierarchy
227 eurons immunoreactive for the p65 subunit of NF-kappa B was previously localized within the caudal do
228 r(536) phosphorylation of the p65 subunit of NF-kappa B, an event required for maximal transcriptiona
230 a B proteins allows nuclear translocation of NF-kappa B and hence plays a critical role in NF-kappa B
231 bacteria induced the rapid translocation of NF-kappa B and the production of a variety of proinflamm
232 indicated that the nuclear translocation of NF-kappa B is not sufficient to activate NF-kappa B-depe
233 kappa B kinase and nuclear translocation of NF-kappa B subunits, are all remarkably enhanced in Ucp2
234 ade did not inhibit nuclear translocation of NF-kappa B, but did prevent Ser(536) phosphorylation of
236 of BLT1 deficiency in receptor activator of NF-kappa-B ligand-induced activation of intracellular ca
240 of all TNF alpha-regulated genes depends on NF-kappa B; 17% are regulated early (1-4 h post-treatmen
242 sis that certain breast cancer cells rely on NF-kappa B for aberrant cell proliferation and simultane
243 o activate either IFN regulatory factor-3 or NF-kappa B but was dependent on the presence of an intac
244 he phosphoinositide 3-kinase/Akt pathway, or NF-kappa B itself blocked the ability of HDAC inhibitors
248 B kinase (IKK) pathway positively regulates NF kappa B and beta-catenin, both important transcriptio
252 e chemoattractant protein (MCP)-1 promoter's NF-kappa B-binding site has exclusive affinity to p50p65
254 inding activity by treatment with a specific NF-kappa B inhibitor, MG-132, inhibited cell migration d
255 was conducted to determine whether specific NF-kappa B blockade by mutant inhibitory (I)-kappa B (I
259 on experiments, the CARD6 protein suppressed NF-kappa B induction by Nod1 or Cardiak but did not inte
263 mmunoprecipitation assay for p65 showed that NF-kappa B binds the NAG-1 promoter in LNCaP cells.
265 al. in this issue of Immunity suggests that NF-kappa B regulates Ig kappa rearrangement after all, b
266 idant butylated hydroxytoluene (BHT) and the NF kappa B inhibitor PTD-p65 peptide inhibit NF kappa B
270 , TWEAK binding to Fn14/TweakR activated the NF-kappa B and c-Jun N-terminal kinase pathways but indu
272 ti-CD3, or TNF-alpha that was blocked by the NF-kappa B inhibitors BAY 11-7082 and NEMO-binding pepti
274 lytic event could be actively induced by the NF-kappa B-inducing kinase and the human T-cell leukemia
275 -kappa B-specific inhibitor, to identify the NF-kappa B-dependent set of the TNF alpha-regulated gene
277 clusive affinity to p50p65 and to mutate the NF-kappa B binding motif in the wild-type MCP-1 reporter
278 f wild-type promoters was used to mutate the NF-kappa B-binding motif in the wild-type IL-8 reporter
280 IP3 promotes or attenuates activation of the NF-kappa B family of transcription factors has been cont
282 uld be rescued by specific inhibition of the NF-kappa B pathway with I kappa B overexpression as well
283 is a required step in the activation of the NF-kappa B signaling pathway and the subsequent expressi
284 domethacin by blocking the activation of the NF-kappa B significantly reduces the amyloid pathology i
287 n, apoptosis, and differentiation are on the NF-kappa B pathway, and cell cycle, metabolism, and RNA
289 esis of pancreatic cancer cells and that the NF-kappa B signaling pathway is a potential target for a
291 ri, HEK293 cells were cotransfected with the NF-kappa B-Luc reporter, CD14 and MD2 expression plasmid
292 ously expressed among the embryonic tissues, NF-kappa B/I kappa B members present distinct patterns o
293 tion from proinflammatory stimuli leading to NF-kappa B-dependent gene expression is mediated by the
295 ice deficient in MyD88 failed to translocate NF-kappa B and produced virtually no cytokines in respon
296 this study was to determine whether the two NF-kappa B sites play a role in the capacity of tumor ne
298 n factors; (b) Bcl-2 does not interfere with NF kappa B activation but prevents entrance of its activ
299 y Nod1 or Cardiak but did not interfere with NF-kappa B activation by the CARD-containing adapter pro
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