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1 and SMRT (silencing mediator of retinoid and thyroid hormone receptors).
2 nd SMRT (silencing mediator for retinoid and thyroid hormone receptors).
3 epressor silencing mediator for retinoid and thyroid hormone receptor.
4 t but essential for repression by unliganded thyroid hormone receptor.
5 proteins that facilitate the function of the thyroid hormone receptor.
6 anner but not with retinoic acid receptor or thyroid hormone receptor.
7 expression in the liver are mediated via the 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 MRT (silencing mediator of retinoic acid and thyroid hormone receptor), a nuclear corepressor involve
17 ozygous nonsense mutation in a gene encoding thyroid hormone receptor alpha (THRA) and generating a m
20 generated mice with a point mutation in the thyroid hormone receptor alpha (TRalpha) gene producing
21 family, liver X receptor beta (LXRbeta) and thyroid hormone receptor alpha (TRalpha), have been foun
23 evidence from patients with mutations of the thyroid hormone receptor alpha gene (THRA) indicates tha
26 mmaturity markers anti-Mullerian hormone and thyroid hormone receptor alpha in adults and fail to exp
27 ter with either the ligand-binding domain of thyroid hormone receptor alpha or its viral relative, vE
28 hra(tm2)) in the related Thra gene, encoding thyroid hormone receptor alpha suppresses these phenotyp
32 was localized to a 41-amino acid segment of thyroid hormone receptor alpha1 between the second zinc
33 Mice heterozygous for a point mutation in thyroid hormone receptor alpha1 display increased thermo
35 using isolated tail arteries, that defective thyroid hormone receptor alpha1 signaling impairs acetyl
36 ear localization signal in the A/B domain of thyroid hormone receptor alpha1 that is absent in thyroi
37 in mice heterozygous for a point mutation in thyroid hormone receptor alpha1 was reversed with the se
41 noic acid receptor, retinoid X receptor, and thyroid hormone receptor and induced silencing mediator
42 ed by estrogen, whereas its interaction with thyroid hormone receptor and retinoic acid receptor is l
43 findings define an important function of the thyroid hormone receptors and suggest TR ligands could h
44 sor SMRT (silencing mediator of retinoid and thyroid hormone receptors) and with histone deacetylase
45 expression analysis and the use of different thyroid hormone receptor antagonists suggest thyroid hor
46 the JCI, Mittag et al. provide evidence that thyroid hormone receptors are essential for the formatio
47 tinoic acid receptors (RARs or rars) and the thyroid hormone receptors are members of the steroid rec
48 cing mediator for retinoic acid receptor and thyroid hormone receptor) as a potential STAT5-binding p
51 ost prominent of these are components of the thyroid hormone receptor-associated protein (TRAP)/Media
52 P is an integral component of a multiprotein thyroid hormone receptor-associated protein (TRAP)/vitam
53 of the gene encoding the Mediator component thyroid hormone receptor-associated protein (TRAP)230/ME
54 eceptor-binding protein (PBP), also known as thyroid hormone receptor-associated protein 220/vitamin
56 xploiting the specificity of the coactivator thyroid hormone receptor-associated protein 80 (TRAP80).
57 that mouse BMAL1 complexes include TRAP150 (thyroid hormone receptor-associated protein-150; also kn
58 d as an integral component of a multiprotein thyroid hormone receptor-associated protein/vitamin D(3)
63 evels are primarily due to its action at the thyroid hormone receptor beta (THR-beta) in the liver, w
64 ion of a cis-regulatory module (CRM) for the thyroid hormone receptor beta (Thrb) gene, an early cone
65 suggest that UCP1 is primarily dependent on thyroid hormone receptor beta (TR beta) while the normal
67 Mice harbouring a dominant-negative mutant thyroid hormone receptor beta (TRbeta(PV/PV) mice) spont
68 boring a knock-in dominantly negative mutant thyroid hormone receptor beta (TRbeta(PV/PV) mouse) spon
69 mouse harboring a dominantly negative mutant thyroid hormone receptor beta (TRbeta(PV/PV) mouse) that
74 utations in the ligand-binding domain of the thyroid hormone receptor beta (TRbeta) lead to resistanc
75 required for induction of FGF21 expression: thyroid hormone receptor beta (TRbeta), retinoid X recep
77 ction with the transcription factors CRX and thyroid hormone receptor beta 2, it enhances M-opsin exp
80 re, we have identified two binding sites for thyroid hormone receptor beta in the promoter of the rat
83 tor repression was conserved with respect to thyroid hormone receptor beta-1, whereas cyclin D1 activ
85 Mice harboring a dominant-negative mutant thyroid hormone receptor-beta (TRbeta(PV/PV) mice) spont
86 tracellular dynamics and distribution of the thyroid hormone receptor-beta (TRbeta) in living cells,
92 id hormone receptor alpha1 that is absent in thyroid hormone receptor beta1 and inactive in the oncop
93 thyroid hormone receptor antagonists suggest thyroid hormone receptor beta1 as the major player media
94 on NES-H12 suggest that altered shuttling of thyroid hormone receptor beta1 may be a contributing fac
95 ediated by estrogen receptor alpha and beta, thyroid hormone receptor beta1, androgen receptor, gluco
101 Thyroid hormone, and one of its receptors [thyroid hormone receptor beta2 (TRbeta2)], is an importa
102 and we found a mutation of the gene encoding thyroid hormone receptor beta2 associated with a decreas
103 two of these potential targets, the Jak2 and thyroid hormone receptor beta2 genes, was lost in the ne
106 These benzamides generally lack undesirable thyroid hormone receptor binding and COX-1 inhibition ac
107 ding domain was necessary and sufficient for thyroid hormone receptor binding to the steroid receptor
111 ociates with coactivator as tightly as human thyroid hormone receptor bound to thyroid hormone and is
113 improvement of pharmacological properties of thyroid hormone receptor coactivator binding inhibitors.
114 he SMRT (silencing mediator for retinoid and thyroid hormone receptor) corepressor that blocks this s
115 ow that MED1 phosphorylation by ERK enhances thyroid hormone receptor-dependent transcription in vitr
120 methyltransferase Dot1L is a coactivator for thyroid hormone receptor during Xenopus development.
121 FP) chimeras of estrogen, retinoic acid, and thyroid hormone receptors (ERs, RARs, and TRs, respectiv
123 eptor (CAR), a member of the nuclear steroid/thyroid hormone receptor family, activates transcription
126 cid receptors (RARs), members of the steroid/thyroid hormone receptor gene family, are ligand-depende
129 omplex, that interacts directly with VDR and thyroid hormone receptor in response to ligand and ancho
131 sor SMRT (silencing mediator of retinoid and thyroid hormone receptors) in C57BL/6 mice (SMRTmRID) pr
132 nd SMRT (silencing mediator for retinoid and thyroid hormone receptors) interact with unliganded nucl
137 Affected mice had a nonsense mutation in the thyroid hormone receptor interactor 11 gene (Trip11), wh
138 nments, thyroid hormone levels, and liganded thyroid hormone receptor interference with estrogen rece
139 how that activation by androgen receptor and thyroid hormone receptor is associated with the promoter
140 al synaptic activity, we also examined which thyroid hormone receptor is involved in the expression o
141 ransactivation dose-response curves for both thyroid hormone receptor isotypes, designated TRalpha an
142 we prepared mutant mice by targeting mutant thyroid hormone receptor kindred PV (PV) mutation to the
143 stance occurs when a genetic mutation in the thyroid hormone receptor leads to reduced hormone bindin
144 with the ligand-binding domain of the human thyroid hormone receptor led to specific thyroid hormone
148 and SMRT (silencing mediator of retinoid and thyroid hormone receptors; NCoR2) are well-recognized co
149 ncluding silencing mediator for retinoid and thyroid hormone receptors, nuclear receptor coreceptor,
153 In this report, we demonstrate that the thyroid hormone receptor/retinoblastoma-interacting prot
154 n of appropriate reporter genes and that the thyroid hormone receptor RNA-binding domain is important
156 rs SMRT (silencing mediator for retinoid and thyroid hormone receptors), SHARP (SMRT and histone deac
157 s in the anterior hypothalamus that requires thyroid hormone receptor signaling for proper developmen
159 ning silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) and nuclear receptor cor
161 proteins silencing mediator for retinoid and thyroid hormone receptor (SMRT) and the nuclear receptor
162 n as silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) are essential components
163 epressor silencing mediator for retinoid and thyroid hormone receptor (SMRT) associates with the DNA-
164 the silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressor functions wi
165 and silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressors and is larg
166 and silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressors establish r
167 the silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) gene that maps at chromo
169 Silencing mediator for retinoic acid and thyroid hormone receptor (SMRT) is a transcriptional cor
170 ssor silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) or histone deacetylase 1
171 that silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) represses the expression
172 the silencing mediator for retinoic acid and thyroid hormone receptor (SMRT)-histone deacetylase 3 (H
173 inal silencing mediator of retinoic acid and thyroid hormone receptor (SMRT)-interacting domain.
176 t of the silencing mediator for retinoid and thyroid hormone receptor (SMRT)/histone deacetylase 3 (H
177 repressor silencing mediator of retinoid and thyroid hormone receptors (SMRT(mRID)) produced a transp
178 R and the silencing mediator of retinoid and thyroid hormone receptors (SMRT) and determined the role
180 epressor silencing mediator for retinoid and thyroid hormone receptors (SMRT) from the vitamin D rece
181 The silencing mediator of retinoic acid and thyroid hormone receptors (SMRT) is an established histo
182 The silencing mediator for retinoic acid and thyroid hormone receptors (SMRT) mediates transcriptiona
184 The silencing mediator for retinoid and thyroid hormone receptors (SMRT) serves as a platform fo
185 sor silencing mediator for retinoic acid and thyroid hormone receptors (SMRT) suppressed AP-1 activit
186 el termed silencing mediator of retinoid and thyroid hormone receptors (SMRT)(mRID1) in which targete
187 epressor, silencing mediator of retinoid and thyroid hormone receptors (SMRT), is recruited by a plet
188 uced silencing mediator of retinoic acid and thyroid hormone receptors (SMRT)-receptor interaction.
193 1 (NCoR1)/silencing mediator for retinoid or thyroid-hormone receptors (SMRT) corepressors in skin ke
194 1 (NCoR1)/silencing mediator for retinoid or thyroid-hormone receptors (SMRT) corepressors or histone
198 (VDR) belongs to the superfamily of steroid/thyroid hormone receptors that is activated by 1alpha,25
199 restingly, EBI was found to be a very potent thyroid hormone receptor (THR) agonist, while NH-3 is an
200 H expression, presumably by interacting with thyroid hormone receptors (THRs) bound to TSH subunit ge
201 otein and silencing mediator of retinoid and thyroid hormone receptors to a newly identified putative
204 g four decades, the therapeutic potential of thyroid hormone receptor (TR) agonists as lipid-lowering
208 to elevated expression of genes regulated by thyroid hormone receptor (TR) and liver X receptor (LXR)
209 oduct (Hr) acts as a corepressor of both the thyroid hormone receptor (TR) and the orphan nuclear rec
210 ed that a knock-in mouse harboring a mutated thyroid hormone receptor (TR) beta (PV; TRbeta(PV/PV) mo
212 wth and metastatic progression in vivo using thyroid hormone receptor (TR) beta(PV/PV) knock-in (PV)
214 t mediates ligand-independent actions of the thyroid hormone receptor (TR) during development and in
215 potency and efficacy of different ligands of thyroid hormone receptor (TR) for regulating the recruit
216 multimeric complex that copurifies with the thyroid hormone receptor (TR) from HeLa cells and marked
219 triiodo-l-thyronine, T3) inhibits binding of thyroid hormone receptor (TR) homodimers, but not TR-ret
222 ivators implicated in gene activation by the thyroid hormone receptor (TR) include members of the p16
224 ransporters, corepressors, and coactivators; thyroid hormone receptor (TR) isoform-specific action; a
230 e only a modest affinity and potency for the thyroid hormone receptor (TR) that limits studies of the
231 ors, including nuclear receptors such as the thyroid hormone receptor (TR) that targets the TRAP220 s
233 formed malignant hepatic cell lines in which thyroid hormone receptor (TR) was over-expressed by co-t
234 cute response of the Xenopus TRbetaA gene to thyroid hormone receptor (TR), an extensively studied me
235 d of the VDR DBD resembles that found in the thyroid hormone receptor (TR), and suggests a mechanism
236 show that another nuclear hormone receptor, thyroid hormone receptor (TR), can suppress ABCA1 transc
237 IP1, reportedly a coactivator for GR and the thyroid hormone receptor (TR), was recruited to col3A an
238 (COUP-TF1), retinoid X receptor (RXR)-gamma, thyroid hormone receptor (TR)-beta2, and guanylyl cyclas
239 gene through this interaction, and enhances thyroid hormone receptor (TR)-driven transcription in a
240 nuclear receptor corepressor (NCoR) enhances thyroid hormone receptor (TR)-mediated basal transactiva
247 ator-1) has been previously shown to enhance thyroid hormone receptor (TR)/retinoid X receptor-mediat
249 a nonpermissive heterodimer, such as that of thyroid hormone receptor (TR)/RXR, where it has been ref
250 is alternatively spliced to generate either thyroid hormone receptor (TR)alpha1 or a non-hormone-bin
253 are mediated by their respective receptors: thyroid hormone receptors (TR) and peroxisome proliferat
255 for transcriptional repression by unliganded thyroid hormone receptors (TR) but not essential for tra
257 ed a direct interaction of cytosol-localized thyroid hormone receptor TRalpha1 and the p85alpha subun
258 Thyroid hormone (T(3)) signaling through the thyroid hormone receptor (TRalpha1) regulates hepatoma c
259 oD, myocyte enhancer factor-2 (MEF2) and the thyroid hormone receptor (TRalpha1) that takes place in
260 mitogen-activated protein kinase (MAPK) and thyroid hormone receptor TRbeta1 (TR) in the cell nucleu
261 ells transfected with wild-type (wt) nuclear thyroid hormone receptor TRbeta1 (TR), L-thyroxine (T(4)
263 that express a dominant negative form of the thyroid hormone receptor (TRDN) controlled by the cardia
264 xpression of a dominant negative form of the thyroid hormone receptor (TRDN) driven by the elastase p
265 xpression of a dominant negative form of the thyroid hormone receptor (TRDNalpha) was restricted to t
267 entified in humans as a coactivator bound to thyroid hormone receptors (TRs) and essential for thyroi
268 hyroid hormone action is mediated by nuclear thyroid hormone receptors (TRs) and is dependent upon th
284 ituitary and hypothalamus when T(3) binds to thyroid hormone receptors (TRs) interacting with the pro
285 orm-selective agonists or antagonists of the thyroid hormone receptors (TRs) might be therapeutically
287 pite the well documented broad expression of thyroid hormone receptors (TRs), analysis of different T
288 with the transcription activity of wild-type thyroid hormone receptors (TRs), leading to dysregulatio
296 II nuclear hormone receptor subfamily (e.g., thyroid hormone receptors [TRs], retinoic acid receptors
297 By inducing a dominant negative form of the thyroid hormone receptor under the control of doxycyclin
298 criptional regulator of MyHC expression, the thyroid hormone receptor, was pharmacologically manipula
300 metabolic homeostasis by binding to nuclear thyroid hormone receptors, which regulate target gene ex
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