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1  in part by the C-terminal activation helix (AF-2).
2 pendent transcriptional activation function (AF-2).
3 ond located in the carboxyl-terminal region (AF-2).
4  and the second in the COOH-terminal region (AF-2).
5 f coactivators for AR activation function 2 (AF-2).
6 f E2-mediated coactivator recruitment to the AF-2.
7 s not suppressed by the physically separated AF-2.
8 this activity requires a functional receptor AF-2.
9 ependent transcriptional activation function AF-2.
10 uterus of mice with mutations in the ERalpha AF-2.
11 strengths with and coactivator effects on AR AF-2.
12 a ligand-dependent transactivation function, AF-2.
13 d both contain activation functions AF-1 and AF-2.
14 activating functional domains (AF), AF-1 and AF-2.
15 Cs (pDC), using mouse lacking either AF-1 or AF-2.
16 ugh two activation functions (AFs): AF-1 and AF-2.
17 through intact AF-1, but not through mutated AF-2.
18 A mutation in the hAR activation function-2 (AF-2) abrogates N-to-C interaction, DNA binding, and tra
19                                  A conserved AF-2 activation domain located in the hormone-binding do
20          Bon binds via an LxxLL motif to the AF-2 activation domain present in the ligand binding dom
21 ly (p160 coactivators) bind to the conserved AF-2 activation function found in the hormone binding do
22  and -dependent gene transcription (AF-1 and AF-2 (activation functions 1 and 2)).
23 t is still not fully understood how AF-1 and AF-2 activities are regulated cooperatively by ligands.
24 identified as an allosteric modulator of the AF-2 activity and is termed binding function-3 (BF-3).
25 51Y mutation allows weak tamoxifen-dependent AF-2 activity but that this activity is only detectable
26             Furthermore, tamoxifen-dependent AF-2 activity can be detected in the presence of ERalpha
27 h IC(50) approximately 50 microM and inhibit AF-2 activity in cells were detected: three nonsteroidal
28 e inhibitory effect of region F on the HNF-4 AF-2 activity is a unique feature among members of the n
29  the N terminus of the receptor protein, and AF-2 activity is dependent on helix 12 of the C-terminal
30 n the N terminus of the receptor protein and AF-2 activity is dependent on helix 12 of the C-terminal
31                                              AF-2 activity is mediated by a hormone-dependent interac
32                                       Whilst AF-2 activity is regulated by estrogen (E2) binding, the
33 lex with estrogen receptor (ER) and enhances AF-2 activity of the receptor.
34 e nuclear receptors, and it is essential for AF-2 activity, but it is not necessary for dimerization
35 es the AF-1 activity of ERalpha, but not the AF-2 activity, suggesting that hMMS19 may be an AF-1-spe
36 s that form BF-3 inhibits AR function and AR AF-2 activity.
37 c nerve glia, axogenesis factor-1 (AF-1) and AF-2, along with ciliary neurotrophic factor.
38 ligand binding domain of ERalpha C terminus (AF-2) and a ligand-independent activation function in th
39  estrogen receptor transactivation function (AF-2) and agonize another (AF-1).
40 50 and DRIP205 functionally link GR AF-1 and AF-2, and represent important mediators of GR transcript
41 ix 12 (H12) in the LBD is a component of the AF-2, and the configuration of H12 is ligand-inducible t
42 RAM-1 binding site in rat TRbeta1 outside of AF-2, as TRAM-1 shows weak ligand-dependent interaction
43 on, since HNF-4 deletion derivatives lacking AF-2 bound TFIIB.
44  p21(Cip1) is agonist dependent and requires AF-2 but not AF-1 or GR dimerization.
45  and enhanced the activity of the C-terminal AF-2 but not the N-terminal AF-1 transactivation domain
46 lpha (ERalpha) activation functions AF-1 and AF-2 classically mediate gene transcription in response
47 tors bind irreversibly to Cys-298 within the AF-2 cleft of TRbeta to disrupt SRC2 association.
48 in ER transactivation is dependent on the ER AF-2 coactivator binding site, prompting us to examine r
49 r E2 or TOT, between the AF-1-containing and AF-2-containing regions of the ER.
50 nal (AF-1-containing) and carboxyl-terminal (AF-2-containing) regions of ER as separate polypeptides
51        Furthermore, we demonstrated that the AF-2 contains an AF-1 suppression function using C-termi
52 ranscriptional activation functions AF-1 and AF-2, controls the transcription of target genes presuma
53 wo FXR transactivation-deficient mutants (an AF-2 deletion and a W469A point mutant) failed to transa
54  to the promoter complex; the second step is AF-2 dependent and entails entry of preinitiation comple
55 nvolves primary HNF-4 activation function 2 (AF-2)-dependent interactions with the TRAP220 subunit of
56                   The activation function 2 (AF-2)-dependent recruitment of coactivator is essential
57  increase in receptor activation function-2 (AF-2)-dependent transcriptional activity.
58 h NBD-1 and NBD-2 showed similar ligand- and AF-2-dependent interactions with TR in solution, these t
59  suggesting that the AF-1 is regulated in an AF-2-dependent manner in the male reproductive tract.
60        Estrogen- and antiestrogen-regulated, AF-2-dependent transcriptional activation by purified fu
61 pha protein half-life and markedly inhibited AF-2-dependent transcriptional activity.
62  and ERalpha in the activation helix and the AF-2 dimerization helix indicates that TERP-1 acts predo
63 indings we hypothesized that the mutation of AF-2 disrupted its ability to suppress AF-1, causing the
64 type ER and a mutant ER that had a defective AF-2 domain (ER TAF-1).
65 sual degree of structural flexibility in the AF-2 domain (helix alpha12).
66 o-terminal FXXLF motif and carboxyl-terminal AF-2 domain (N/C interaction) prevented toxicity and AR
67                                     The ERR3 AF-2 domain bound GRIP1 in a ligand-independent manner b
68 matin structure was largely dependent on the AF-2 domain for activation.
69 idues 405-419 on delta419 with the conserved AF-2 domain from the vitamin D3 receptor or the estrogen
70 ndings suggest that an important role of the AF-2 domain in the native ER is to mask the activation p
71  demonstrate that p120 interacts with the TR AF-2 domain in the presence of ligand through a 111-amin
72 nesis studies demonstrated that a functional AF-2 domain is essential for toxicity, a finding corrobo
73  receptor (RXR) heterodimer, whereas the VDR AF-2 domain is required for this interaction.
74 DR translocation, demonstrate that an intact AF-2 domain is required for this translocation, and indi
75                 This activation required the AF-2 domain of both RXR and RAR.
76 A1, and this interaction was mediated by the AF-2 domain of ER-alpha and two domains of BRCA1, the am
77                                          The AF-2 domain of ER-alpha was also shown to induce VEGF ge
78                                          The AF-2 domain of HNF4 is required for this interaction and
79 ormone responsiveness resided near or within AF-2 domain of mCAR.
80 PPARalpha, indicating that the COOH-terminal AF-2 domain of PPAR is not the target of STAT5b inhibiti
81 activator-1 (PGC-1) requires both the intact AF-2 domain of PPARgamma and the LXXLL domain of PGC-1 f
82                                 Although the AF-2 domain of PPARgamma is absolutely required for PGC-
83 lls that harbor a truncated ligand-dependent AF-2 domain of RARalpha do not demonstrate any changes i
84 tivation (AF)-2 domains, but not the AF-1 or AF-2 domain of RXRalpha, nor CAR's DBD.
85  heterodimer binds directly to DNA, with the AF-2 domain of tethered CAR mediating transcriptional ac
86                               Therefore, the AF-2 domain of TR-beta is required for positive and, par
87 n potential of PGC-1alpha requires an intact AF-2 domain of VDR and the LXXLL motif in PGC-1alpha.
88 eins are coactivators that interact with the AF-2 domain of VDR to augment 1,25-dihydroxyvitamin D3-d
89 t chromatin remodeling, but mutations in the AF-2 domain that abolish activity in the native ER also
90  that helix H3 functions in concert with the AF-2 domain to form a transactivation surface for bindin
91             Restoration of ligand-dependent (AF-2 domain) reporter gene activation was achieved by ex
92  RAR in response to ligand displaces the RXR AF-2 domain, allowing RXR ligands to bind and promote th
93                        We also show that the AF-2 domain, although inactive at simple promoters on it
94        Mutation of a specific residue in the AF-2 domain, which renders the VDR trancriptionally inac
95  interact on the outer surface of PXR at the AF-2 domain.
96 beta locus within its activation function-2 (AF-2) domain (E457A).
97                   The activation function-2 (AF-2) domain of ERalpha and the C-terminal regulatory do
98 re, we found that the activation function-2 (AF-2) domain of the retinoid X receptor interferes with
99 nteraction between the activator function-2 (AF-2) domain of the VDR and C terminus of beta-catenin.
100 terized C-terminal AR activation function-2 (AF-2) domain was critical for strong, ligand-dependent a
101 inding domain, the human ER hormone binding (AF-2) domain, and the VP16 activation domain, functions
102 erved carboxyl-terminal activation function [AF-2] domain of ER-alpha.
103 e results demonstrate directly that AF-1 and AF-2 domains accomplish their transactivation activities
104  two signal input domains (one that binds NR AF-2 domains and one that binds AF-1 domains of some but
105 OPR1 and its longer variant COPR2 target the AF-2 domains of NR but exhibit quantitative differences
106          Truncation of LBD and truncation of AF-2 each abolished hormone-dependent translocation and
107  mice and mice with mutations in the ERalpha AF-2 (ERalphaAF-2(0)) were treated with ICI, estradiol,
108 A ligand-inducible transactivation function (AF-2) exists in the extreme carboxyl terminus of the vit
109                                   We used an AF-2 flexible region mutant and an AF-2 static region mu
110 ; COPR2, 32.4 kDa), and strict dependence on AF-2 for interaction distinguish COPR1 and COPR2 from th
111  evaluate the physiological role of AF-1 and AF-2 for the tissue-selective function of TAM, we genera
112 st conformation termed activator function-2 (AF-2) for coactivator binding.
113 ndent interactions between the ERalpha D351Y AF-2 function and GRIP1, a representative p160, can be d
114 essing L543A,L544A mutations in H12 disrupts AF-2 function and reverses antagonists such as fulvestra
115 se they were completely dependent on the RXR AF-2 function but independent of both the RXR A/B domain
116                             We find that the AF-2 function of ERalpha D351Y lacks detectable tamoxife
117 iated activation by BPA and BPAF was via the AF-2 function of ERalpha, but Zea activated via both the
118 hormone, which was independent of ligand and AF-2 function.
119 vates PPARgamma through the ligand-dependent AF-2 function.
120 nic activity and activated both the AF-1 and AF-2 functions of ERalpha.
121 pha, but Zea activated via both the AF-1 and AF-2 functions.
122 a small compound-binding surface adjacent to AF-2 has been identified as an allosteric modulator of t
123 o post-translational modification on AF-1 or AF-2 has been reported.
124 ty and induces a distinct orientation in the AF-2 helix (H12).
125                              Mutation of the AF-2 helix 12 domain partially inhibits the induction of
126 inforced by the antagonist, which blocks the AF-2 helix from adopting the active position.
127 nding cavity were mapped to helix H3 and the AF-2 helix H12, indicating conformational changes in the
128        The C-terminal helix named alphaAF or AF-2 helix in other nuclear receptors is responsible for
129  Activation of PPARgamma by AJA requires the AF-2 helix of the receptor, suggesting that AJA activate
130 cent to the ligand-dependent transactivation AF-2 helix on the surface of PXR.
131 e most striking of which is a packing of the AF-2 helix onto the LBD adjacent to helices H3 and H4.
132                   In this configuration, the AF-2 helix physically excludes the binding of coactivato
133                         In each monomer, the AF-2 helix protrudes away from the core domain and spans
134  phenylalanine 435 and a displacement of the AF-2 helix relative to the unliganded structures with li
135            Inhibition of SMRT binding by the AF-2 helix requires specific amino acid sequences and th
136 on of RXR results from a rotation of the RXR AF-2 helix that places it in contact with the RAR coacti
137 from the C2 symmetry, allowing the PPARgamma AF-2 helix to interact with helices 7 and 10 of RXRalpha
138 g domain (LBD) of hPXR, interacting with the AF-2 helix to stabilize the LBD for coactivator binding.
139 repression mechanism that is mediated by the AF-2 helix within the tetramer.
140 the cofactor binding site is occupied by the AF-2 helix, thus preventing ligand-independent activatio
141 trinsic repression activity is masked by the AF-2 helix, which antagonizes SMRT binding.
142 nding site and only partially stabilizes the AF-2 helix.
143 tor's ligand-binding pocket and contacts the AF-2 helix.
144 act directly with the activation function 2 (AF-2) helix.
145 ins, constitutive AF-1 in the N terminus and AF-2 in the C terminus.
146  functions (AFs), AF-1 in the N-terminal and AF-2 in the ligand-binding domain.
147 MFA-1 binds with its D ring-facing helix 12 (AF-2) in a manner reminiscent of hormone binding to clas
148 dependent transcriptional activation domain (AF-2) in the C-terminal region of the human vitamin D re
149  vitro, the F domain was found to obscure an AF-2-independent binding site for GRIP1 that did not map
150 titutive, ligand-independent AR activity was AF-2-independent but instead dependent on N-terminal AR
151  for this interaction, which can occur in an AF-2-independent manner.
152                 Importantly, the ligand- and AF-2-independent mode of AR activation observed in ADI P
153                      The first step involves AF-2-independent recruitment of TFIIB to the promoter co
154 subunit of TRAP/SMCC/Mediator and secondary (AF-2-independent) interactions with TRAP170/RGR1.
155 n A-CDK2 on ER transcriptional activation is AF-2-independent.
156 e-dependent activation domain (named tauc or AF-2) inhibits the ability of RXR-PPARgamma heterodimers
157  two activating functions of HNF-4, AF-1 and AF-2, interact with the N terminus and the N and C termi
158 was selectively impaired in interaction with AF-2-interacting coactivator proteins such as SRC-1 and
159 at interacts simultaneously with the primary AF-2 interaction site.
160 oborated by a genetic screen that identified AF-2 interactors as dominant modifiers of degeneration.
161                                              AF-2 is composed of two domains with flexible and static
162              We propose that ERalpha lacking AF-2 is constitutively active in the absence of ligand i
163 1 is localized in the N-terminal region, and AF-2 is distributed in the C-terminal ligand-binding dom
164 kably, the full transactivation potential of AF-2 is inhibited by the region spanning residues 371-46
165 cating that the conserved charged residue in AF-2 is not essential for this PGC-1 function.
166 ntexts, the synergistic activity of AF-1 and AF-2 is required for full estradiol (E2)-stimulated acti
167 s a predominant ligand response, whereas RXR AF-2 is required for liganded RAR AF-2 to efficiently tr
168 ligand-independent AF-1 and ligand-dependent AF-2, located in the A/B and E domains, respectively.
169                                To assess the AF-2-mediated AF-1 suppression, we analyzed the transcri
170 activation, a conformational change releases AF-2-mediated repression and transcriptional activation
171 for the ligand-independent activity, whereas AF-2 mediates ligand-dependent PR activation.
172 response requires the DNA binding domain and AF-2 motif of CAR3 and is markedly enhanced by retinoid
173  strong ligand-dependent interaction with an AF-2 mutant of TR (E457A), while SRC-1 fails to interact
174                                          The AF-2 mutants were not activated by agonists, but surpris
175 en receptor modulators (SERMs) activated the AF-2 mutants.
176 ly coprecipitated the wild-type hVDR and the AF-2 mutants.
177 ent for 3 wk beginning at age 21 d activated AF-2-mutated ERalpha (AF2ER) and restored expression of
178 e-selective function of TAM, we generated an AF-2-mutated ERalpha knock-in (AF2ERKI) mouse model.
179 ctivation functions using AF-1-truncated and AF-2-mutated ERalpha mutants.
180                        In addition, an E457A AF-2 mutation had no effect on the ligand-induced PGC-1
181      These results indicate that the ERalpha AF-2 mutation results in male infertility, suggesting th
182 d for repression, because anti-estrogens and AF-2 mutations impair repression.
183 n domains, ID1 and ID2, whereas the putative AF-2 of ARP1 was required for interaction with CTIP1.
184 lock the transcriptional activation function AF-2 of ER-alpha.
185 t mouse lacking the transactivation function AF-2 of ERalpha (ERalpha-AF2(0)) provided selective loss
186 ng coactivator protein(s) interacts with the AF-2 of PR or TR and mediates transactivation by the lig
187 e conserved COOH-terminal activation domain (AF-2) of ER-alpha.
188 nd estrogen-dependent activation function 2 (AF-2) of ERalpha, AKT increased the activity of only AF-
189 vents the carboxy-terminal activation helix (AF-2) of the receptor from assuming the active conformat
190 p1) is agonist independent, does not require AF-2 or AF-1, but depends on GR dimerization.
191  functions (activation function 1 [AF-1] and AF-2) or receptor dimerization fail to fully inhibit cel
192 -aa deletion in helix 12 of ERalpha, lacking AF-2, or ERalpha(-/-) mice.
193 rated that the activation function 2 domain (AF-2) plays an essential role in VDR transactivation.
194             Several coactivators bind to the AF-2 pocket through conserved LXXLL or FXXLF sequences t
195 is conclusion, we have identified an ERalpha AF-2 point mutant (L540Q) that selectively binds and rec
196 on the opposite side of the protein from the AF-2 region critical for receptor regulation.
197                                          The AF-2 region in NRs has been thought to play a critical r
198  displaying strong homology to the conserved AF-2 region of nuclear receptors.
199 nteraction also requires the presence of the AF-2 region of RXR to interact with the LXXLL motif of P
200 teraction also requires both helix 1 and the AF-2 region of the TR ligand-binding domain.
201               Coactivator recruitment to the AF-2 region of TR in the presence of T(3) is central to
202 acting with subdomains of NRs other than the AF-2 region, in contrast to SRC-1/TIF2.
203 nd-binding domain/activation function-2 (LBD/AF-2) region (within aa 282-420) of ER-alpha.
204  of which bind to the activation function 2 (AF-2) region of the androgen receptor.
205  sequence, a putative activation function 2 (AF-2) region.
206 ion activities through different mechanisms: AF-2 requires GRIP1 as a coactivator, but AF-1 does not.
207 -terminal transcriptional activation domain, AF-2, retained elevated basal activity, while mutation o
208 c binding pocket on the outer surface at the AF-2 site and fitted comfortably, making interactions wi
209  on the outer surface of the receptor at the AF-2 site and validated by docking studies.
210 e used an AF-2 flexible region mutant and an AF-2 static region mutant.
211 id expressing rat CAR lacking the C-terminal AF-2 subdomain inhibited squalestatin 1-inducible CYP2B1
212 two LXXLL motifs and requires the receptor's AF-2 subdomain.
213  by ERbeta, probably by interacting with the AF-2 surface and blocking the binding of endogenous coac
214 e that E(2)-mediated repression requires the AF-2 surface and the participation of coactivators or ot
215                       The requirement of the AF-2 surface for repression is probably due to its capac
216 protein-1 mutant unable to interact with the AF-2 surface is ineffective.
217 e clamp residues Gln-272, and Phe-264 on the AF-2 surface of PXR.
218 vered a role for coactivators binding to the AF-2 surface of the vitamin D receptor (VDR) in its nega
219                   The activation function-2 (AF-2) surface in the ligand-binding domain is required f
220 othesized to bind the activation function-2 (AF-2) surface on the exterior of PXR when agonists are c
221 detectable when AF-1 is strong, and AF-1 and AF-2 synergize, or when p160s are overexpressed.
222 tains a transcriptional activation function (AF-2) that mediates hormone-dependent binding of coactiv
223 elical region, termed activation function-2 (AF-2), that forms part of the ligand-binding pocket and
224 ds at the AR surface reveals weak binding at AF-2, the most potent inhibitors bind preferentially to
225 n SPA70 compromises its interaction with the AF-2, thus explaining its antagonism.
226 nRXR alpha) lacking transactivation function AF-2 to differentiated suprabasal keratinocytes in the e
227 hereas RXR AF-2 is required for liganded RAR AF-2 to efficiently trans-activate target genes, and (2)
228  BF-3 remodels the adjacent interaction site AF-2 to weaken coactivator binding.
229 -binding domain linked to the ligand binding/AF-2 trans-activation domain of PPARalpha, indicating th
230 ostructure, but an important pocket near the AF-2 transactivation domain becomes accessible only in s
231  SHP proteins specifically interact with the AF-2 transactivation domain of LRH-1 both in vivo and in
232 ocusing on the C-terminal ligand-binding and AF-2 transactivation domains, an assembly of an active t
233 ivators, their interaction also requires the AF-2 transactivation motif of VDR.
234                             In contrast, the AF-2 transactivator is complex, spanning the 128-366 reg
235  on the presence of the conserved C-terminal AF-2 transcriptional activation motif.
236 elix 12 (AF2ER) minimized estrogen-dependent AF-2 transcriptional activation.
237         PRMT2 enhanced both ERalpha AF-1 and AF-2 transcriptional activity, and the potential methylt
238 FP) chimeras with full-length VDR (VDR-GFP), AF-2-truncated VDR (AF-2del-VDR-GFP), and ligand-binding
239 on activity of physically separated AF-1 and AF-2 using a novel hybrid reporter assay.
240 ) of RARgamma but not the C-terminal domain (AF-2) was required for association with beta-catenin, wh
241 n transcriptional synergism between AF-1 and AF-2, we expressed the amino terminal (AF-1-containing)
242 ion with beta-catenin, whereas both AF-1 and AF-2 were necessary for inhibition of beta-catenin trans
243 at the N terminus (AF-1) and the C terminus (AF-2) which work synergistically to confer full HNF-4 ac
244  transcription activation functions AF-1 and AF-2, which act in a promoter- and cell-specific manner.
245 transactivation domains, designated AF-1 and AF-2, which activate transcription in a cell type-indepe
246 -mediated activity from the separated mutant AF-2, which differed from the intact protein.
247 l activation domains, tau1 (AF-1), tau2, and AF-2, which were initially defined using transiently tra
248 istinct activation functions (AFs), AF-1 and AF-2, whose respective involvement varies in a cell type
249 f an estrogen-dependent activation function (AF-2) with p160 coactivators.
250 oxy-terminal transactivation function termed AF-2 within the last 15 amino acids of the ligand bindin

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