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1 beta-TrCP and SKP2 are two well-studied F-box proteins,
2 beta-TrCP binds to IkappaBalpha only when the latter is
3 beta-TrCP F-box protein mediates ubiquitination of phosp
4 beta-TrCP function is essential for the induction of nuc
5 beta-TrCP thus plays a critical role in both canonical a
6 beta-TrCP ubiquitinates EZH2 and Jak2-mediated phosphory
7 beta-TrCP ubiquitinates LPCAT1 at an acceptor site (Lys(
8 beta-TrCP, the substrate recognition subunit of SCF-type
9 SCF complex, a heterotetramer (Skp1, Cul-1, beta-TrCP [F-box protein], and ROC1) involved with ubiqu
13 entified PHLPP1 as a proteolytic target of a beta-TrCP-containing Skp-Cullin 1-F-box protein (SCF) co
15 f beta-TrCP reduced the expression of Sp1, a beta-TrCP substrate, which, in turn, reduced Skp2 gene e
16 CG12 to mimic glucose starvation to activate beta-TrCP-mediated Sp1 degradation has translational pot
18 howed increased cytosolic levels of Axin and beta-TrCP and decreased phosphorylation of glycogen synt
19 wn to act as a scaffold for beta-catenin and beta-TrCP and thereby to potentiate beta-TrCP-mediated b
21 odulating the expression of beta-catenin and beta-TrCP, suggesting the translation potential of using
23 correlated during cell cycle with FBXW2 and beta-TrCP/SKP2 being high or low, respectively, in arres
24 components, including Ck1alpha, GSK3beta and beta-TrCP, suppress beta-catenin levels in the larval ep
28 IkappaB kinase-dependent phosphorylation and beta-TrCP-dependent ubiquitylation of the N-terminal sig
29 first time that interaction between PRLr and beta-TrCP is less efficient in human breast cancer cells
32 n between expression levels of beta-TrCP and beta-TrCP activity, indicating post-transcriptional regu
33 n of Mcl-1 with the E3 ligase beta-TrCP, and beta-TrCP then facilitates the ubiquitination and degrad
37 but viruses expressing A49 that cannot bind beta-TrCP or bind beta-TrCP constitutively had intermedi
39 ssing A49 that cannot bind beta-TrCP or bind beta-TrCP constitutively had intermediate virulence.
40 stable REST mutant, which is unable to bind beta-TrCP, inhibited Mad2 expression and resulted in a p
47 sults indicate that the turnover of Mcl-1 by beta-TrCP is an essential mechanism for GSK-3beta-induce
48 Binding of IkappaBalpha and beta-catenin by beta-TrCP causes their ubiquitylation and thereafter pro
49 the ubiquitylation of mutant beta-Catenin by beta-TrCP in vitro and induce the degradation of an engi
54 yses indicate that cyclin D1 was targeted by beta-TrCP through an unconventional recognition site, (2
57 SK-3beta and then cannot be ubiquitinated by beta-TrCP, is much more stable than wild-type Mcl-1 and
58 ppaB to the nucleus by sequestering cellular beta-TrCP, a protein required for the degradation of the
62 t the ubiquitination of beta-catenin by CRL1(beta-TrCP) and Nedd8-CRL1(beta-TrCP) almost equally.
68 Stabilized ATF4 mutants exhibit decreased beta-TrCP degron phosphorylation, beta-TrCP interaction,
69 ion of either binding site in Nrf2 decreased beta-TrCP-mediated ubiquitylation of the transcription f
72 e Sp1 degradation, suppression of endogenous beta-TrCP function by a dominant-negative mutant or smal
75 ition of either mTORC1 or p70S6K facilitated beta-TrCP degradation accompanied with enhanced PD-L1 pr
79 her, our findings demonstrate a key role for beta-TrCP in controlling the level of PHLPP1, and activa
80 LPCAT1 is the first lipogenic substrate for beta-TrCP, and the results suggest that modulation of th
83 ased monoubiquitination of Gsk3beta/Gsk3beta-beta-TrCP association suppressed beta-catenin recruitmen
84 n accumulation requires Wnt-induced GSK3beta/beta-TrCP interaction; the current study revealed that p
85 ng axis composed of p38 MAP kinase-MK2-Hsp27-beta-TrCP may promote AUF1 degradation by proteasomes an
87 a specific recognition site for E3RS(IkappaB/beta-TrCP), an SCF-type E3 ubiquitin ligase, thereby exp
89 novel SCF(beta-TrCP) substrate and implicate beta-TrCP as an important negative regulator of PRL sign
90 ation of cells, and deletion of the F-box in beta-TrCP abolishes its ability to ubiquitinate IkappaBb
92 s showed intracellular accumulation of FN in beta-TrCP siRNA-treated cells without showing much alter
96 dependent upon the WD40 repeat sequences in beta-TrCP and on phosphorylation of the GSK3beta sites i
99 and the concurrent down-regulation of known beta-TrCP substrates examined, including Wee1, Ikappabet
100 appears to inhibit binding of the E3 ligase beta-TrCP and prevents beta-catenin ubiquitination and d
101 the association of Mcl-1 with the E3 ligase beta-TrCP, and beta-TrCP then facilitates the ubiquitina
103 o the WD40 domain of the E3 ubiquitin ligase beta-TrCP and blocks its interaction with phosphorylated
105 ctive recruitment of the E3-ubiquitin ligase beta-TrCP to phospho-IkappaBalpha proteosomal degradatio
106 a Delta F-box mutant of the ubiquitin ligase beta-TrCP, which serves as a specific substrate trap for
109 orescent biosensor to quantitatively measure beta-TrCP activity in live, single cells in real-time.
110 that although small interfering RNA-mediated beta-TrCP knockdown protected cells against STG28-facili
111 ruction box ((727)DSGAGS(732)) that mediates beta-TrCP recognition and encompasses a glycogen synthas
112 Our study introduces a method to monitor beta-TrCP activity in live cells and identifies a key si
114 ssion of wild-type but not DeltaF-box mutant beta-TrCP leads to decreased expression and increased ub
115 CP to a specific site, and dominant negative beta-TrCP blocks phosphorylation-dependent degradation o
116 by forced expression of a dominant-negative beta-TrCP mutant suppresses growth and survival of human
120 e C terminus of REST critical for binding of beta-TrCP and targeting of REST for proteasomal degradat
122 quitin ligase activity as well as binding of beta-TrCP to phosphorylated I kappaB alpha was decreased
123 ggested that the NSP1-induced degradation of beta-TrCP is an uncommon mechanism of subverting IFN-bet
126 small interfering RNA-mediated knock-down of beta-TrCP enhanced and protected against STG28-facilitat
128 itutive processing of p100 is independent of beta-TrCP but rather is regulated by the nuclear shuttli
135 no correlation between expression levels of beta-TrCP and beta-TrCP activity, indicating post-transc
140 ation suppressed beta-catenin recruitment of beta-TrCP, leading to long-term inhibition of beta-caten
142 motif of TRIM9 and the WD40 repeat region of beta-TrCP prevented beta-TrCP from binding its substrate
147 ubstrates, Vpu leads to the stabilization of beta-TrCP substrates such as beta-catenin, IkappaBalpha,
148 (NF-kappa-B inhibitor), a known substrate of beta-TrCP, was rescued by Src, suggesting a wider effect
149 6K signaling is likely due to suppression of beta-TrCP-mediated proteasomal degradation of PD-L1, bec
153 decreased beta-TrCP degron phosphorylation, beta-TrCP interaction, and ubiquitination, as well as el
154 enin and beta-TrCP and thereby to potentiate beta-TrCP-mediated beta-catenin ubiquitination and degra
155 he WD40 repeat region of beta-TrCP prevented beta-TrCP from binding its substrates, stabilizing Ikapp
156 ecruits the ubiquitin ligase adapter protein beta-TrCP to a specific site, and dominant negative beta
157 nd by interacting with F-box-binding protein beta-TrCP, undergoes ubiquitin-dependent proteolysis.
158 nd Ser33 are recognized by the F-box protein beta-TrCP, a component of a ubiquitin ligase complex tha
162 n beta-transducin repeat containing protein (beta-TrCP) acts as a substrate adapter for the SCF E3 ub
163 s beta-transducin repeat-containing protein (beta-TrCP) and mediates proteasomal degradation of CD4.
164 t beta-transducin repeat-containing protein (beta-TrCP) E3 ubiquitin ligase is required for Gli2 degr
165 f beta-transducin repeat-containing protein (beta-TrCP) expression represents a cellular response in
166 e beta-transducin repeat-containing protein (beta-TrCP) is required for FAF1 to suppress Wnt signalin
167 t beta-transducin repeat-containing protein (beta-TrCP) targets Sp1 for proteasomal degradation in re
169 f beta-transducin repeat-containing protein (beta-TrCP), a component of the SCF ubiquitin ligase comp
170 e beta-transducin repeat-containing protein (beta-TrCP), a component of the Skp-Cullin-F-box-containi
171 f beta-transducin repeat-containing protein (beta-TrCP), an F-box component of the Skp1-Cul1-F-box pr
172 , beta-transducin repeat-containing protein (beta-TrCP), and occurs only in the cytoplasm, the consti
173 , beta-transducin repeat-containing protein (beta-TrCP), that polyubiquitinates LPCAT1, thereby targe
174 r beta-transducin repeat-containing protein (beta-TrCP), which acts as a substrate receptor for the S
178 ex containing the F-box/WD40-repeat protein, beta-TrCP, a vertebrate homolog of Drosophila Slimb.
179 beta-Transducin repeat-containing proteins (beta-TrCP) serve as substrate recognition component of E
180 Beta-transducin repeats-containing proteins (beta-TrCP) serve as the substrate recognition subunits f
181 beta-transducin repeats-containing proteins (beta-TrCP)-mediated degradation due to phosphorylation b
183 liver triglyceride content, through reduced beta-TrCP-mediated degradation of the Akt phosphatase, P
185 inase signaling as a key axis for regulating beta-TrCP activity by inhibiting binding between beta-Tr
186 n this regulatory pathway is to create a SCF(beta-TrCP) E3 ubiquitin ligase binding site for beta-cat
187 etween phosphorylated I kappaB alpha and SCF(beta-TrCP) but no change in the composition of the SCF(b
188 new gene (RING) E3 enzymes SCF(Cdc4) and SCF(beta-TrCP) work with the E2 Cdc34 to build polyubiquitin
190 vidence that the distinct Cullin-1 based SCF(beta-TrCP)complex regulates beta-catenin stability, our
193 kp-Cullin 1-F-box protein (SCF) complex (SCF(beta-TrCP)) E3 ubiquitin ligase in a phosphorylation-dep
197 n and degradation of a target of the E3- SCF(beta-TrCP) ubiquitin ligase, the NF-kappaB inhibitor Ika
200 egraded by means of the ubiquitin ligase SCF(beta-TrCP) during the G2 phase of the cell cycle to allo
201 t are recognized by the ubiquitin ligase SCF(beta-TrCP), since deletion or mutation of either degron
202 cyclin D1 by up-regulating the E3 ligase SCF(beta-TrCP), we hypothesized that beta-transducin repeat-
203 pha is triggered by the ubiquitin ligase SCF(beta-TrCP), which requires the modification of the culli
206 These data indicate that PRLR is a novel SCF(beta-TrCP) substrate and implicate beta-TrCP as an impor
208 imulate the ubiquitin ligase activity of SCF(beta-TrCP) toward its target beta-catenin, resulting in
209 ic because IkappaB, another substrate of SCF(beta-TrCP), is not sensitive to NORE1A-promoted degradat
213 ion of a degron for either Keap1-Cul3 or SCF(beta-TrCP)-mediated degradation decreased the fluorescen
216 ild-type APC protein is recruited to the SCF(beta-TrCP) complex, ubiquitin conjugated, and degraded.
219 nstead, we found that Src attenuates the SCF(beta-TrCP) E3-ligase activity in blunting Taz proteasoma
220 at these residues by PP2A eliminates the SCF(beta-TrCP) recognition site and blocks beta-catenin ubiq
230 reasoned that the human homologs of Slimb - beta-TrCP and its isoform beta-TrCP2 (KIAA0696) - might
234 ducin repeats-containing protein) (SCF(Slimb/beta-TrCP)) as the E3 ubiquitin ligase complex responsib
235 and genetic data strongly suggest that Slimb/beta-TrCP is the specificity determinant for the signal-
238 l cancer as well as prospective of targeting beta-TrCP as a means of anticancer therapy are also disc
239 rovide the proof of principle that targeting beta-TrCP might be beneficial for anticancer therapies.
244 interference technique, we demonstrated that beta-TrCP is essential for NIK-induced p100 ubiquitinati
247 icantly, our pull-down assays indicated that beta-TrCP binds a phosphorylated version of DSGIS more t
248 vide an explanation for the observation that beta-TrCP can act as a tumor suppressor or an oncogene i
252 ssociated with Cdc25A phosphorylation at the beta-TrCP docking site (DS82G motif) and physical associ
253 V3 was post transcriptional, mediated by the beta-TrCP ubiquitin E3 ligase and occurred via an endoly
254 ubsequent processing of p100 mediated by the beta-TrCP ubiquitin ligase and 26 S proteasome, respecti
257 chanism for TRIM9-mediated regulation of the beta-TrCP SCF complex activity but also identifies TRIM9
260 rcPVT1 in the progression of NPC through the beta-TrCP/c-Myc/SRSF1 positive feedback loop, and circPV
261 ins, which promotes CHD1 degradation via the beta-TrCP-mediated ubiquitination-proteasome pathway.
262 nd 2-deoxyglucose, we demonstrated that this beta-TrCP accumulation resulted from decreased Skp2 expr
263 Moreover, we obtained evidence that this beta-TrCP-dependent degradation takes part in controllin
264 catenin-associated E-cadherin levels through beta-TrCP-dependent stabilization of the transcriptional
266 ha and GSK3 promotes beta-catenin binding to beta-TrCP, leading to beta-catenin degradation through t
267 nics, effects that were overcome by siRNA to beta-TrCP and GSK-3beta or LPCAT1 gene transfer, respect
275 rolled at the level of protein stability via beta-TrCP-dependent, ubiquitin-based proteasomal degrada
276 ions were combined with mutations of the Vpu beta-TrCP binding site, resulting in Vpu proteins that i
277 rmore, USP47 deubiquitinates itself, whereas beta-TrCP promotes USP47 ubiquitination through interact
278 A forms a direct, Ras-regulated complex with beta-TrCP, the substrate recognition component of the SC
279 d an increased association of cyclin D1 with beta-TrCP, whereas no specific binding was noted with ot
281 that partly depends on its interaction with beta-TrCP, a substrate adaptor for an SCF (Skp-Cullin 1-
284 er demonstrate that SVV ORF61 interacts with beta-TrCP, a subunit of the SCF ubiquitin ligase complex
285 loss of the known interaction of Rassf1 with beta-TrCP that usually mediates degradation of beta-cate