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1 ia SMRT (silencing mediator for retinoid and thyroid hormone receptor).
2 and SMRT (silencing mediator of retinoid and thyroid hormone receptors).
3 expression in the liver are mediated via the thyroid hormone receptor.
4 epressor silencing mediator for retinoid and thyroid hormone receptor.
5 t but essential for repression by unliganded thyroid hormone receptor.
6 proteins that facilitate the function of the thyroid hormone receptor.
7 anner but not with retinoic acid receptor or thyroid hormone receptor.
8 nding to a receptor homologous to vertebrate thyroid hormone receptors.
9 and silencing mediator of retinoic acid and thyroid hormone receptors.
10 ar receptors (NRs), such as the retinoid and thyroid hormone receptors.
11 and was thought not to be a coactivator for thyroid hormone receptors.
12 thyroid hormone inactivation proximal to the thyroid hormone receptors.
13 ses of pomc promoter sequences revealed that thyroid hormone receptor 1beta-binding motif insertions
14 MRT (silencing mediator of retinoic acid and thyroid hormone receptor), a nuclear corepressor involve
17 yroid hormone triiodothyronine and synthetic thyroid hormone receptor agonists, such as sobetirome (G
19 ozygous nonsense mutation in a gene encoding thyroid hormone receptor alpha (THRA) and generating a m
22 generated mice with a point mutation in the thyroid hormone receptor alpha (TRalpha) gene producing
23 family, liver X receptor beta (LXRbeta) and thyroid hormone receptor alpha (TRalpha), have been foun
26 evidence from patients with mutations of the thyroid hormone receptor alpha gene (THRA) indicates tha
29 mmaturity markers anti-Mullerian hormone and thyroid hormone receptor alpha in adults and fail to exp
30 ter with either the ligand-binding domain of thyroid hormone receptor alpha or its viral relative, vE
34 was localized to a 41-amino acid segment of thyroid hormone receptor alpha1 between the second zinc
35 Mice heterozygous for a point mutation in thyroid hormone receptor alpha1 display increased thermo
38 using isolated tail arteries, that defective thyroid hormone receptor alpha1 signaling impairs acetyl
39 ear localization signal in the A/B domain of thyroid hormone receptor alpha1 that is absent in thyroi
40 in mice heterozygous for a point mutation in thyroid hormone receptor alpha1 was reversed with the se
44 noic acid receptor, retinoid X receptor, and thyroid hormone receptor and induced silencing mediator
45 processes through modulation of the nuclear thyroid hormone receptors and several other proteins.
46 findings define an important function of the thyroid hormone receptors and suggest TR ligands could h
47 sor SMRT (silencing mediator of retinoid and thyroid hormone receptors) and with histone deacetylase
48 expression analysis and the use of different thyroid hormone receptor antagonists suggest thyroid hor
49 the JCI, Mittag et al. provide evidence that thyroid hormone receptors are essential for the formatio
50 tinoic acid receptors (RARs or rars) and the thyroid hormone receptors are members of the steroid rec
54 ost prominent of these are components of the thyroid hormone receptor-associated protein (TRAP)/Media
55 P is an integral component of a multiprotein thyroid hormone receptor-associated protein (TRAP)/vitam
56 of the gene encoding the Mediator component thyroid hormone receptor-associated protein (TRAP)230/ME
57 eceptor-binding protein (PBP), also known as thyroid hormone receptor-associated protein 220/vitamin
59 We show that the RNA-binding protein THRAP3 (thyroid hormone receptor-associated protein 3) regulates
60 xploiting the specificity of the coactivator thyroid hormone receptor-associated protein 80 (TRAP80).
61 that mouse BMAL1 complexes include TRAP150 (thyroid hormone receptor-associated protein-150; also kn
65 evels are primarily due to its action at the thyroid hormone receptor beta (THR-beta) in the liver, w
66 ion of a cis-regulatory module (CRM) for the thyroid hormone receptor beta (Thrb) gene, an early cone
68 a (PPARG), glucocorticoid receptor (GR), and thyroid hormone receptor beta (THRB), when exposed to 14
69 suggest that UCP1 is primarily dependent on thyroid hormone receptor beta (TR beta) while the normal
70 Mice harbouring a dominant-negative mutant thyroid hormone receptor beta (TRbeta(PV/PV) mice) spont
71 boring a knock-in dominantly negative mutant thyroid hormone receptor beta (TRbeta(PV/PV) mouse) spon
72 mouse harboring a dominantly negative mutant thyroid hormone receptor beta (TRbeta(PV/PV) mouse) that
76 utations in the ligand-binding domain of the thyroid hormone receptor beta (TRbeta) lead to resistanc
77 required for induction of FGF21 expression: thyroid hormone receptor beta (TRbeta), retinoid X recep
79 ction with the transcription factors CRX and thyroid hormone receptor beta 2, it enhances M-opsin exp
82 ing in KO mice, likely a result of decreased thyroid hormone receptor beta expression without Mdr2.
83 re, we have identified two binding sites for thyroid hormone receptor beta in the promoter of the rat
84 (RTH) disorders, due to mutations in either thyroid hormone receptor beta or alpha (beta: female n =
86 ated that PI3K/Akt signaling is important in thyroid hormone receptor beta(PV/PV) knock-in (PV) mice
89 tor repression was conserved with respect to thyroid hormone receptor beta-1, whereas cyclin D1 activ
92 Mice harboring a dominant-negative mutant thyroid hormone receptor-beta (TRbeta(PV/PV) mice) spont
93 tracellular dynamics and distribution of the thyroid hormone receptor-beta (TRbeta) in living cells,
95 s a liver-directed, orally active, selective thyroid hormone receptor-beta agonist designed to improv
99 id hormone receptor alpha1 that is absent in thyroid hormone receptor beta1 and inactive in the oncop
100 thyroid hormone receptor antagonists suggest thyroid hormone receptor beta1 as the major player media
101 on NES-H12 suggest that altered shuttling of thyroid hormone receptor beta1 may be a contributing fac
107 mponent of the cone precursor circuitry, the thyroid hormone receptor beta2 (TRbeta2), enables the ab
108 Thyroid hormone, and one of its receptors [thyroid hormone receptor beta2 (TRbeta2)], is an importa
109 and we found a mutation of the gene encoding thyroid hormone receptor beta2 associated with a decreas
110 two of these potential targets, the Jak2 and thyroid hormone receptor beta2 genes, was lost in the ne
113 These benzamides generally lack undesirable thyroid hormone receptor binding and COX-1 inhibition ac
114 ding domain was necessary and sufficient for thyroid hormone receptor binding to the steroid receptor
117 ociates with coactivator as tightly as human thyroid hormone receptor bound to thyroid hormone and is
118 improvement of pharmacological properties of thyroid hormone receptor coactivator binding inhibitors.
119 he SMRT (silencing mediator for retinoid and thyroid hormone receptor) corepressor that blocks this s
120 rotein, vitellogenin, estrogen receptor, and thyroid hormone receptor, demonstrated that blood is a u
121 ow that MED1 phosphorylation by ERK enhances thyroid hormone receptor-dependent transcription in vitr
126 methyltransferase Dot1L is a coactivator for thyroid hormone receptor during Xenopus development.
127 FP) chimeras of estrogen, retinoic acid, and thyroid hormone receptors (ERs, RARs, and TRs, respectiv
129 eptor (CAR), a member of the nuclear steroid/thyroid hormone receptor family, activates transcription
132 cid receptors (RARs), members of the steroid/thyroid hormone receptor gene family, are ligand-depende
136 sor SMRT (silencing mediator of retinoid and thyroid hormone receptors) in C57BL/6 mice (SMRTmRID) pr
137 nd SMRT (silencing mediator for retinoid and thyroid hormone receptors) interact with unliganded nucl
142 CIP4 (Cdc42-interacting protein 4)/TRIP10 (thyroid hormone receptor interactor 10) was identified a
143 Affected mice had a nonsense mutation in the thyroid hormone receptor interactor 11 gene (Trip11), wh
144 how that activation by androgen receptor and thyroid hormone receptor is associated with the promoter
145 We conclude that TRbeta2-46 is an oncogenic thyroid hormone receptor isoform that promotes SKP2 expr
146 ransactivation dose-response curves for both thyroid hormone receptor isotypes, designated TRalpha an
147 stance occurs when a genetic mutation in the thyroid hormone receptor leads to reduced hormone bindin
148 with the ligand-binding domain of the human thyroid hormone receptor led to specific thyroid hormone
151 and SMRT (silencing mediator of retinoid and thyroid hormone receptors; NCoR2) are well-recognized co
152 ncluding silencing mediator for retinoid and thyroid hormone receptors, nuclear receptor coreceptor,
156 In this report, we demonstrate that the thyroid hormone receptor/retinoblastoma-interacting prot
157 n of appropriate reporter genes and that the thyroid hormone receptor RNA-binding domain is important
159 rs SMRT (silencing mediator for retinoid and thyroid hormone receptors), SHARP (SMRT and histone deac
160 s in the anterior hypothalamus that requires thyroid hormone receptor signaling for proper developmen
163 ning silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) and nuclear receptor cor
164 proteins silencing mediator for retinoid and thyroid hormone receptor (SMRT) and the nuclear receptor
165 n as silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) are essential components
166 epressor silencing mediator for retinoid and thyroid hormone receptor (SMRT) associates with the DNA-
167 the silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressor functions wi
168 and silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressors and is larg
169 and silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressors establish r
170 the silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) gene that maps at chromo
172 Silencing mediator for retinoic acid and thyroid hormone receptor (SMRT) is a transcriptional cor
173 ssor silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) or histone deacetylase 1
174 that silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) represses the expression
175 the silencing mediator for retinoic acid and thyroid hormone receptor (SMRT)-histone deacetylase 3 (H
176 inal silencing mediator of retinoic acid and thyroid hormone receptor (SMRT)-interacting domain.
179 t of the silencing mediator for retinoid and thyroid hormone receptor (SMRT)/histone deacetylase 3 (H
180 repressor silencing mediator of retinoid and thyroid hormone receptors (SMRT(mRID)) produced a transp
181 R and the silencing mediator of retinoid and thyroid hormone receptors (SMRT) and determined the role
183 epressor silencing mediator for retinoid and thyroid hormone receptors (SMRT) from the vitamin D rece
184 The silencing mediator of retinoic acid and thyroid hormone receptors (SMRT) is an established histo
186 The silencing mediator for retinoid and thyroid hormone receptors (SMRT) serves as a platform fo
187 sor silencing mediator for retinoic acid and thyroid hormone receptors (SMRT) suppressed AP-1 activit
188 el termed silencing mediator of retinoid and thyroid hormone receptors (SMRT)(mRID1) in which targete
189 epressor, silencing mediator of retinoid and thyroid hormone receptors (SMRT), is recruited by a plet
190 uced silencing mediator of retinoic acid and thyroid hormone receptors (SMRT)-receptor interaction.
195 CoR1) and silencing mediator for retinoid or thyroid-hormone receptors (SMRT) are the best characteri
196 1 (NCoR1)/silencing mediator for retinoid or thyroid-hormone receptors (SMRT) corepressors in skin ke
197 1 (NCoR1)/silencing mediator for retinoid or thyroid-hormone receptors (SMRT) corepressors or histone
201 (VDR) belongs to the superfamily of steroid/thyroid hormone receptors that is activated by 1alpha,25
202 restingly, EBI was found to be a very potent thyroid hormone receptor (THR) agonist, while NH-3 is an
203 rofile in maternal serum for activity at the thyroid hormone receptor (THR) and ryanodine receptor (R
204 H expression, presumably by interacting with thyroid hormone receptors (THRs) bound to TSH subunit ge
205 otein and silencing mediator of retinoid and thyroid hormone receptors to a newly identified putative
208 g four decades, the therapeutic potential of thyroid hormone receptor (TR) agonists as lipid-lowering
212 to elevated expression of genes regulated by thyroid hormone receptor (TR) and liver X receptor (LXR)
213 oduct (Hr) acts as a corepressor of both the thyroid hormone receptor (TR) and the orphan nuclear rec
214 ed that a knock-in mouse harboring a mutated thyroid hormone receptor (TR) beta (PV; TRbeta(PV/PV) mo
216 wth and metastatic progression in vivo using thyroid hormone receptor (TR) beta(PV/PV) knock-in (PV)
218 t mediates ligand-independent actions of the thyroid hormone receptor (TR) during development and in
219 potency and efficacy of different ligands of thyroid hormone receptor (TR) for regulating the recruit
220 multimeric complex that copurifies with the thyroid hormone receptor (TR) from HeLa cells and marked
223 triiodo-l-thyronine, T3) inhibits binding of thyroid hormone receptor (TR) homodimers, but not TR-ret
226 ivators implicated in gene activation by the thyroid hormone receptor (TR) include members of the p16
228 ransporters, corepressors, and coactivators; thyroid hormone receptor (TR) isoform-specific action; a
233 e only a modest affinity and potency for the thyroid hormone receptor (TR) that limits studies of the
234 ors, including nuclear receptors such as the thyroid hormone receptor (TR) that targets the TRAP220 s
236 formed malignant hepatic cell lines in which thyroid hormone receptor (TR) was over-expressed by co-t
237 cute response of the Xenopus TRbetaA gene to thyroid hormone receptor (TR), an extensively studied me
238 d of the VDR DBD resembles that found in the thyroid hormone receptor (TR), and suggests a mechanism
239 show that another nuclear hormone receptor, thyroid hormone receptor (TR), can suppress ABCA1 transc
240 (COUP-TF1), retinoid X receptor (RXR)-gamma, thyroid hormone receptor (TR)-beta2, and guanylyl cyclas
241 gene through this interaction, and enhances thyroid hormone receptor (TR)-driven transcription in a
242 nuclear receptor corepressor (NCoR) enhances thyroid hormone receptor (TR)-mediated basal transactiva
249 ator-1) has been previously shown to enhance thyroid hormone receptor (TR)/retinoid X receptor-mediat
251 a nonpermissive heterodimer, such as that of thyroid hormone receptor (TR)/RXR, where it has been ref
253 is alternatively spliced to generate either thyroid hormone receptor (TR)alpha1 or a non-hormone-bin
256 are mediated by their respective receptors: thyroid hormone receptors (TR) and peroxisome proliferat
257 for transcriptional repression by unliganded thyroid hormone receptors (TR) but not essential for tra
259 ed a direct interaction of cytosol-localized thyroid hormone receptor TRalpha1 and the p85alpha subun
260 Thyroid hormone (T(3)) signaling through the thyroid hormone receptor (TRalpha1) regulates hepatoma c
261 oD, myocyte enhancer factor-2 (MEF2) and the thyroid hormone receptor (TRalpha1) that takes place in
262 mitogen-activated protein kinase (MAPK) and thyroid hormone receptor TRbeta1 (TR) in the cell nucleu
263 ells transfected with wild-type (wt) nuclear thyroid hormone receptor TRbeta1 (TR), L-thyroxine (T(4)
265 that express a dominant negative form of the thyroid hormone receptor (TRDN) controlled by the cardia
266 xpression of a dominant negative form of the thyroid hormone receptor (TRDN) driven by the elastase p
267 xpression of a dominant negative form of the thyroid hormone receptor (TRDNalpha) was restricted to t
269 entified in humans as a coactivator bound to thyroid hormone receptors (TRs) and essential for thyroi
270 hyroid hormone action is mediated by nuclear thyroid hormone receptors (TRs) and is dependent upon th
286 orm-selective agonists or antagonists of the thyroid hormone receptors (TRs) might be therapeutically
287 these T(3) -induced changes are mediated via thyroid hormone receptors (TRs) or by non-genomic mechan
289 pite the well documented broad expression of thyroid hormone receptors (TRs), analysis of different T
290 with the transcription activity of wild-type thyroid hormone receptors (TRs), leading to dysregulatio
295 II nuclear hormone receptor subfamily (e.g., thyroid hormone receptors [TRs], retinoic acid receptors
296 By inducing a dominant negative form of the thyroid hormone receptor under the control of doxycyclin
297 criptional regulator of MyHC expression, the thyroid hormone receptor, was pharmacologically manipula
299 metabolic homeostasis by binding to nuclear thyroid hormone receptors, which regulate target gene ex
300 effect is mediated via the genomic action of thyroid hormone receptors, with little evidence for non-