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1 al events lead to the activation of the IKK (IkappaB kinase).
2 manner, and is abolished upon inhibition of IkappaB kinase.
3 ogen synthase kinase 3 and two inhibitors of IkappaB kinase.
4 ine residues within the catalytic domains of IkappaB kinase.
5 heir spatial separation from the cytoplasmic IkappaB kinase.
6 effect of p53 on ubiquitin-related genes or IkappaB kinases.
7 factors RelA and IFN regulatory factor 3 and IkappaB kinases.
11 AK1) phosphorylation of NF-kappaB-activating IkappaB kinase 2 (IKK2), leading to increased NF-kappaB
12 ted NF-kappaB essential modulator (NEMO) and IkappaB kinase 2 (IKK2), two essential mediators of the
13 .1292dupG in exon 13 of IKBKB, which encodes IkappaB kinase 2 (IKK2, also known as IKKbeta)--leading
16 e both inhibited by the NF-kappaB inhibitors IkappaB kinase 2 inhibitor and NF-kappaB essential modul
18 o express either cyclooxygenase-2 (COX-2) or IkappaB kinase-2 (IKK2), and TP53(+/+) or TP53(f/f) spec
19 TNF-induced NF-kappaB signaling upstream of IkappaB kinase activation absolutely requires the influx
20 rom the nucleus to the cytosol, resulting in IkappaB kinase activation by mechanisms not yet fully un
21 , and 42, leading to attenuation of MAPK and IkappaB kinase activation in B cells during BCR signalin
23 lammatory gene expression, increased JNK and IkappaB kinase activation, and increased polyubiquitinat
24 ng IkappaBalpha and IkappaBbeta cleavage and IkappaB kinase activation, DENV protease activates NF-ka
28 concomitant increase in inhibitor of kappaB (IkappaB) kinase activity in cell lysates were observed.
29 these tumors and leads to activation of the IkappaB kinase, Akt, and extracellular signal-regulated
36 as independent of NIK's known function as an IkappaB kinase alpha (IKKalpha) kinase, because mice car
38 by producing lymphotoxin, which activates an IkappaB kinase alpha (IKKalpha)-BMI1 module in prostate
39 Coexpression of dominant-negative mutants of IkappaB kinase alpha (IKKalpha)/IKK1 or IKKbeta/IKK2 als
40 Breast milk appeared to suppress intestinal IkappaB kinase alpha and beta, resulting in inactivation
41 ced the complete degradation of both BTK and IkappaB kinase alpha in MCL lines and CD40-dependent B c
42 tivity was required for maintaining a stable IkappaB kinase alpha subunit (IKKalpha) level because tr
44 ished downstream mediators of NIK signaling, IkappaB kinase alpha/beta (IKKalpha/beta) and NF-kappaB,
45 nhibition of TGFbeta-associated kinase-1 and IkappaB kinase alpha/beta activities and reduced express
46 s associated with reductions in sMLA-induced IkappaB kinase alpha/beta and IFN regulatory factor 3 ac
47 1 significantly increased phosphorylation of IkappaB kinase alpha/beta and IkappaBalpha resulting in
48 d by increased abundance of RelB and phospho-IkappaB kinase alpha/beta, an indirect activator of NF-k
49 (phospho-nuclear factor-kappaB p65, phospho-IkappaB kinase alpha/beta, interleukin 1beta, and tumor
50 glycerophosphoinositol-dependent decrease in IkappaB kinase alpha/beta, p38, JNK, and Erk1/2 kinase p
53 t genome-wide siRNA screen demonstrated that IkappaB kinase-alpha (IKK-alpha) is a crucial host facto
55 nes encoding IFN regulatory factor 6 (IRF6), IkappaB kinase-alpha (IKKalpha), and stratifin (SFN) exh
56 complex, NF-kappaB-inducing kinase-dependent IkappaB kinase-alpha activation, and p52/RelB nuclear tr
57 through inhibitor of nuclear factor-kappaB (IkappaB) kinase-alpha (IKK-alpha), a protein kinase that
58 gnaling pathways in mice with disruptions in IkappaB-kinase-alpha and IkappaB kinase-beta in the inte
59 uced activation of TAK-1 and ERK1/2, whereas IkappaB kinase and IkappaB were phosphorylated, even in
60 lyubiquitination of RIP1, phosphorylation of IkappaB kinase and IkappaBalpha, and IkappaBalpha degrad
61 hyper-proliferation and hyper-activation of IkappaB kinase and MAPKs (ERK, p38, and JNK) upon the li
63 ignaling pathway that involves activation of IkappaB kinase and nuclear factor kappaB (NF-kappaB).
64 nitiated) cells (e.g. through suppression of IkappaB kinase and nuclear factor kappaB as well as othe
65 signal via the adaptor protein connection to IkappaB kinase and stress-activated protein kinases (CIK
69 hibitor of NF-kappaB (IkappaB) proteins, and IkappaB kinases are present in a variety of invertebrate
70 an inducible, constitutively active form of IkappaB kinase beta (CA-IKKbeta), a key kinase in the ca
71 capable of expressing constitutively active IkappaB kinase beta (CAIKKbeta) in airway epithelium wer
72 , IL-1 receptor-associated kinase 4 (IRAK4), IkappaB kinase beta (IKKB), IkappaB kinase iota (IKKI),
73 nvolves an increased nuclear accumulation of IkappaB kinase beta (IKKbeta) and an increased recruitme
74 anonical and noncanonical NF-kappaB pathways IkappaB kinase beta (IKKbeta) and IKKalpha to activate N
75 kinases IkappaB kinase alpha (IKKalpha) and IkappaB kinase beta (IKKbeta) as RelB interacting partne
76 sgenic mice expressing constitutively active IkappaB kinase beta (IKKbeta) in intestinal epithelial c
80 pression enhances LPA-induced MEKK3-mediated IkappaB kinase beta (IKKbeta) phosphorylation and NF-kap
81 d that knockdown or blocking the activity of IkappaB kinase beta (IKKbeta) prevented the aggregation
84 teracts with and promotes the degradation of IkappaB kinase beta (IKKbeta), a component of the Ikappa
85 ownstream of the T-cell receptor (TCR) or of IkappaB kinase beta (IKKbeta), we demonstrate that NF-ka
86 We also demonstrate that IFN-gamma activates IkappaB kinase beta (IKKbeta)-dependent NF-kappaB to reg
87 hysiological basis of canonical or classical IkappaB kinase beta (IKKbeta)-nuclear factor kappaB (NF-
90 ced interleulin-8 production, and diminished IkappaB kinase beta (IKKbeta)/IKKgamma coimmunoprecipita
93 ritive and genetic inhibition of the central IkappaB kinase beta (IKKbeta)/nuclear factor-kappaB (NF-
94 ed LPS-dependent activation of NF-kappaB and IkappaB kinase beta activity, protected against LPS acti
95 sgenic mice expressing constitutively active IkappaB kinase beta in airway epithelium (IKTA (IKKbeta
102 r-associated factor 6 (TRAF6) and attenuates IkappaB kinase beta-dependent (IKKbeta-dependent) phosph
104 [inhibitor of transcription factor NFkappaB (IkappaB) kinase beta; an upstream kinase responsible for
106 s involves hypothalamic immunity mediated by IkappaB kinase-beta (IKK-beta), nuclear factor kappaB (N
107 appaB (NF-kappaB) and its upstream activator IkappaB kinase-beta (IKK-beta, encoded by Ikbkb) in the
111 reduced phosphorylative activation, reducing IkappaB kinase-beta activation and intrinsic activity, t
113 uclear factor-kappaB-alpha level and reduced IkappaB kinase-beta phosphorylation, suggesting a suppre
115 was inhibited by dominant-negative AP-1 and IkappaB kinase-beta, but stimulated by WT AP-1 and Ikapp
116 B kinase-beta, but stimulated by WT AP-1 and IkappaB kinase-beta, suggesting that PKC-theta stimulate
119 ARD11)-TAK1 (MAP3K7)-inhibitor of NF-kappaB (IkappaB) kinase-beta (IKKbeta) module is a switch mechan
120 of ERK, but not Jun NH2-terminal kinase and IkappaB kinase, blocked the downregulation of Baf60c and
121 osphorylation and degradation, inhibition of IkappaB kinase complex (IKK) activation, suppression of
126 g NF-kappaB signaling via its effects on the IkappaB kinase complex and resulting in reduced IL2 gene
127 of exon 20 and a corresponding reduction in ikappaB kinase complex associated protein (IKAP) levels.
130 re, digitization occurs well upstream of the IkappaB kinase complex, as protein kinase C translocatio
131 s process occurred through activation of the IkappaB kinase complex, which also led to activation of
132 cytoplasm through the kinase activity of the IkappaB kinase complex, which leads to translocation of
139 reduces the survival of pericytes through an IkappaB kinase-dependent pathway, mediates the low peric
140 These results suggest that the control of IkappaB kinase dephosphorylation by gamma(1)34.5 represe
141 tivation of TANK-binding kinase 1 (TBK1) and IkappaB kinase epsilon (IKKepsilon) and the subsequent a
142 manner that requires the kinase activity of IkappaB kinase epsilon (IKKepsilon) and the transactivat
143 we show that the phosphorylation of STAT1 by IkappaB kinase epsilon (IKKepsilon) inhibits STAT1 homod
144 to functionally and physically interact with IkappaB kinase epsilon (IKKepsilon), a known IRF3 kinase
148 1, which interacts with and acts upstream of IkappaB kinase epsilon to contribute to LPS-mediated ind
150 support for a rationale to target IKBKE, an IkappaB kinase family member that activates the AKT and
151 ies have demonstrated that ubiquitination of IkappaB kinase gamma (IKKgamma), a regulatory subunit of
152 B essential modifier (NEMO), also designated IkappaB kinase gamma (IKKgamma), from the nucleus to the
154 binding to the NEMO/inhibitor of NF-kappaB (IkappaB) kinase gamma (IKKgamma) subunit of an IKK compl
155 presses NF-kappaB upstream of the regulatory IkappaB kinase-gamma protein subunit in the NF-kappaB si
156 Here we demonstrate that sumoylation of the IkappaB kinase homolog immune response-deficient 5 plays
157 (PP1), and Akt (SH-5) through inhibition of IkappaB kinase, IkappaBalpha phosphorylation, and inhibi
159 , by assessing the kinetics and amplitude of IkappaB kinase (IKK) activation, we report that TNF-alph
161 d by vorinostat in EOC cells is dependent on IkappaB kinase (IKK) activity and associated with a gene
162 art of a multicomponent complex that induces IkappaB kinase (IKK) activity and NF-kappaB activation.
163 ines with this deletion, exhibited increased IkappaB kinase (IKK) activity and production of proinfla
165 lecule that is an upstream regulator of both IkappaB kinase (IKK) and c-Jun N-terminal kinase (JNK),
166 was preceded by increased phosphorylation of IkappaB kinase (IKK) and IkappaBalpha as well as the nuc
167 on, and B56gamma silencing induced increased IkappaB kinase (IKK) and IkappaBalpha phosphorylation up
170 attern-independent agonist for activation of IkappaB kinase (IKK) and NF-kappaB in HM via activation
171 ibitor of kappaB (IkappaB)alpha degradation, IkappaB kinase (IKK) and p38 activation, RelA nuclear tr
172 In these cells, S1P, but not TNF, promotes IkappaB kinase (IKK) and p65 phosphorylation, IkappaBalp
173 ALT1-BCL10 (CBM) adapter complex to activate IkappaB kinase (IKK) and the classical NF-kappaB pathway
174 es with a novel ubiquitin-like domain in the IkappaB kinase (IKK) beta subunit of the IKK complex.
176 This is achieved through subversion of the IkappaB kinase (IKK) complex (or signalosome), which inv
177 Because CsA has the capability to impair IkappaB kinase (IKK) complex activation, the IKKalpha/be
179 aB kinase beta (IKKbeta), a component of the IkappaB kinase (IKK) complex that regulates nuclear fact
180 thesized that the MC159 protein targeted the IkappaB kinase (IKK) complex to inhibit these diverse si
181 MC005 inhibited NF-kappaB proximal to the IkappaB kinase (IKK) complex, and unbiased affinity puri
182 ulator (NEMO), a regulatory component of the IkappaB kinase (IKK) complex, controls NF-kappaB activat
183 ignaling pathway is under the control of the IkappaB kinase (IKK) complex, which consists of IKK-1, I
188 cifically inhibit NF-kappaB by targeting the IkappaB kinase (IKK) complex: Compound A and NEMO bindin
193 hanges, we observed significant increases in IkappaB kinase (IKK) in the NAc after social defeat, a m
195 degradation of NFkappaB-bound IkappaB by the IkappaB kinase (IKK) is required for activation in respo
196 a complex with the modulatory subunit of the IkappaB kinase (IKK) kinase, IKKgamma (or NEMO), resulti
197 f key inflammatory mediators such as JNK and IkappaB kinase (IKK) occurs rapidly upon consumption of
201 t of RIP1 to the receptor complex, impairing IkappaB kinase (IKK) recruitment and NF-kappaB activatio
202 n mice with sepsis and whether inhibition of IkappaB kinase (IKK) reduces the cardiac dysfunction in
203 crotic RIP1-RIP3 kinase complex, whereas the IkappaB Kinase (IKK) subunit NEMO appears to function do
204 tion of IkappaBalpha, and phosphorylation of IkappaB kinase (IKK) subunits IKKalpha and IKKbeta, indi
205 ear transcription factor kappaB (IkappaB) by IkappaB kinase (IKK) triggers the degradation of IkappaB
206 tors of c-Jun N-terminal kinase (JNK) and of IkappaB kinase (IKK) were used to investigate the involv
207 lex program is in operation, which activates IkappaB kinase (IKK), a key regulator of inflammatory cy
208 We found that DeltaNp63alpha interacts with IkappaB kinase (IKK), a multisubunit protein kinase that
210 phosphatidylinositol 3-kinase (PI 3-kinase), IkappaB kinase (IKK), IkappaB, NF-kappaB, and FGF-2 were
211 Nuclear factor (NF)-kappaB, activated by IkappaB kinase (IKK), is a key regulator of inflammation
213 , transforming growth factor beta (TGFbeta), IkappaB kinase (IKK), Ras/mitogen-activated protein kina
214 ophagy factor ATG1/ULK1 and the noncanonical IkappaB kinase (IKK), TANK-binding kinase 1 (TBK1), whic
215 mans to yeast, was recently shown to require IkappaB kinase (IKK), the upstream regulator of the nucl
216 ion by nimbolide was caused by inhibition of IkappaB kinase (IKK), which led to suppression of Ikappa
217 nd activation of the pathway is dependent on IkappaB kinase (IKK), which phosphorylates IkappaB, targ
221 acilitates ubiquitination and degradation of IkappaB kinase (IKK)-beta thus terminating IKK activity.
225 lammatory cytokines TNF and IL-17 stimulated IkappaB kinase (IKK)-NF-kappaB and impaired osteogenic d
232 ligase TRAF6 is a key regulator of canonical IkappaB kinase (IKK)/NF-kappaB signaling in response to
234 ptic contacts may depend at least in part on IkappaB kinase (IKK)/NF-kappaB-related synapse-to-nucleu
235 ntial role in inflammation by activating the IkappaB kinase (IKK)/nuclear factor kappaB (NF-kappaB) a
236 inhibition induces a nuclear accumulation of IkappaB kinase (IKK)alpha, and inhibition of IKKalpha en
238 the TCR that activates the protein kinase C-IkappaB kinase (IKK)alpha/beta-NF-kappaB pathway, known
240 activation of IRF5 was dependent on TAK1 and IkappaB kinase (IKK)beta, which thus reveals a physiolog
242 The inhibitor of nuclear factor-kappaB (IkappaB) kinase (IKK) complex is the master regulator of
243 c process by activating inhibitor of kappaB (IkappaB) kinase (IKK) complex, which subsequently recrui
246 Mice lacking the inhibitor of NF-kappaB (IkappaB) kinase (IKK) kinase TAK1 underwent normal posit
248 in the activation of inhibitor of NF-kappaB (IkappaB) kinase (IKK) through a proteasome-independent m
251 ith MHC-I, MyD88-dependent TLR signals drive IkappaB-kinase (IKK)2-mediated phosphorylation of phagos
253 lacking the p65 subunit of NF-kappaB or the IkappaB kinases IKKalpha or IKKbeta, and in cells treate
254 macological inhibition of both the canonical IkappaB kinases (IKKalpha/beta) and the IKK-related kina
255 er demonstrated decreased phosphorylation of IkappaB kinase (IKKbeta) and IkappaBalpha in the presenc
259 cilitated the complex formation of CD91 with IkappaB kinases (IKKs) alpha and beta and increased the
261 st lethal challenge from wild-type virus via IkappaB kinase in dendritic cells (DCs), which sense vir
263 utive noncanonical NF-kappaB activation, and IkappaB kinase inhibition reduced their proliferation to
264 S422D)SGK1-transfected MEG-01 cells with the IkappaB kinase inhibitor BMS-345541 (10muM) abolished SG
266 nin (a PI3K inhibitor), and parthenolide (an IkappaB kinase inhibitor), inhibited pathogen-induced NF
268 lls increased > 2-fold in the presence of an IkappaB-kinase inhibitor, indicating a protective effect
269 ha receptor-associated factor 6 and NEMO, by IkappaB kinase inhibitors, and by the IkappaBalpha super
270 inase 4 (IRAK4), IkappaB kinase beta (IKKB), IkappaB kinase iota (IKKI), interferon regulatory factor
271 amycin; DAF, decay-accelerating factor; IKK, IkappaB kinase; IRF, interferon regulatory factors; TBK1
272 platform for recruitment and stimulation of IkappaB kinase, leading to activation of the transcripti
273 ivation in tumor cells through inhibition of IkappaB kinase, leading to inhibition of phosphorylation
275 romoted constitutive activation of PI3K/Akt, IkappaB kinase/NF-kappaB, mitogen-activated protein kina
276 ignature included "protein kinase cascade," "IkappaB kinase/NFkappaB cascade," and "regulation of pro
277 in cytosolic Ca(2+) levels or the classical IkappaB kinase/NFkappaB inflammatory response elicited b
280 histone deacetylase activity and blockade of IkappaB kinase/nuclear factor-kappaB signaling during re
281 Gram-negative bacteria, Akt did not enhance IkappaB kinase or NF-kappaB p65 phosphorylation, but rat
282 ts activation of NF-kappaB by inhibiting the IkappaB kinase pathway and by promoting direct inhibitor
283 ies implicate Erb3 binding protein-1 and the IkappaB kinase pathway in the mechanism of action of WS6
284 phoma cells with inhibitors of the NF-kappaB/IkappaB kinase pathway or deletion of c-Rel or RelA resu
285 activated CaMKII in cardiomyocytes leads to IkappaB kinase phosphorylation and concomitant increases
286 NF-alpha activity was mediated by inhibiting IkappaB kinase phosphorylation, which attenuated the LPS
288 cids via mammalian target of rapamycin 2 and IkappaB kinase regulate Akt activity and Akt association
290 Genetic studies in mice have identified the IkappaB kinase-related kinase TANK-binding kinase 1 (TBK
291 demonstrated that kinetic considerations of IkappaB kinase-signaling input and IkappaBepsilon's inte
292 B (NF-kappaB) essential modulator (NEMO) and IkappaB kinase subunit beta (IKKbeta), an interaction th
293 Hippo kinases MST1, MST2, and the oncogenic IkappaB kinase TBK1 as the most enriched RASSF1A-interac
294 tment of TAX1BP1 and A20 to the noncanonical IkappaB kinases TBK1 and IKKi in response to poly(I:C) t
295 K Binding Kinase 1 (TBK1) is a non-canonical IkappaB kinase that contributes to KRAS-driven lung canc
296 Tid1 is an essential mediator that connects IkappaB kinases to the Beclin1-containing autophagy prot
297 a macrophage-specific constitutively active IkappaB Kinase transgenic model (IKFM), we demonstrated
298 y inhibiting the activation of non-canonical IkappaB kinase varepsilon and IkappaBalpha, and conseque
299 its downstream molecules, including JNK and IkappaB kinase, were enhanced in DUSP14-deficient T cell
300 more, the gamma(1)34.5 null mutant activates IkappaB kinase, which facilitates p65/RelA phosphorylati
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