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These data indicate that m-TRbeta1 can act as a tumor suppressor in hepatocarcinoma and its role was significantly better than that of TRbeta1.
Thyroid hormone receptor beta and NCOA4 regulate terminal erythrocyte differentiation.
Report of a novel mutation T273R in the THRB gene of patients exhibiting signs of the syndrome of resistance to thyroid hormone. Authors propose that the trans-activating function of TRbeta is likely dominantly hindered in these patients.
Authors previously shown that Nuclear Receptor Corepressor 1 (NCoR) and the thyroid hormone receptor beta1 (TRbeta) inhibit tumor invasion. Here they show that these molecules repress VEGF-C and VEGF-D gene transcription in breast cancer cells, reducing lymphatic vessel density and sentinel lymph node invasion in tumor xenografts.
The results emphasized the importance of TRB1 in the regulation of HSV-1 replication in differentiated environment with neuronal phenotype.
In certain contexts, Rb loss enables TRbeta1-dependent suppression of SKP2 as a safeguard against RB1-deficient tumorigenesis. TRbeta2 counteracts TRbeta1, thus disrupting this safeguard and promoting development of RB1-deficient malignancies.
A relatively stable genome in retinoblastoma tumor cells is maintained by TRb1 and TRb2-mediated PTTG1 inhibition, counteracting Rb-deficiency-related genomic instability.
the actions of R429Q-TRbeta1 in Resistance to Thyroid Hormone (RTH)-Syndrome most likely reflect the reduced hormone affinity observed for this mutant rather than an alteration in target gene repertoire.
The present studies uncovered a novel mechanism by which thyroid hormone receptor beta could function as a tumor suppressor through modulation of TNF alpha-IkappaB alpha-NFkappaB pathway.
Novel THRB single nucleotide substitution-C to G in codon 340 in resistance to thyroid hormone syndrome.
THRA predominates in multipotent human adipose derived stem cells (hADSC) whereas THRB is expressed at lower levels and is upregulated during hADSC differentiation.
TRbeta suppressed Runx2 transcriptional activities, thus confirming TRbeta regulation of Runx2 at functional thyroid hormone-response elements. Significantly, these findings indicate that a ratio of the tumor-suppressor TRbeta and tumor-promoting Runx2 may reflect tumor aggression and serve as biomarkers in biopsy tissues. The discovery of this TRbeta-Runx2 signaling supports the emerging role of TRbeta as a tumor supp...
results revealed that microRNA 200a inhibits erythroid differentiation by targeting PDCD4 and THRB
it was observed that ER stimulated gene expression by interacting with MEIS1 and FOXP3, and ER inhibited gene expression by interacting with THRB and GRHL1.
presents 1 pedigree of thyroid hormone resistance syndrome with heterozygous A317T mutation in THRbeta gene in the proband and his mother, which is the first reported mutation in Chinese and provides a comprehensive review of available literature
Molecular cloning and detection of TR beta isoform 4 in pituitary cells.
The expression of thyroid receptor beta is linked to fertility status.
p.H271D mutation associated with resistance thyroid hormone syndrome
diagnosis was confirmed by direct THRB sequencing that revealed 2 novel mutations: the heterozygous p.Ala317Ser in subject 1 and the heterozygous p.Arg438Pro in subject 2
Down-regulation of THRbeta correlates with the reduction of all markers of differentiation and is associated with overexpression of some miRNAs supposed to play a role in thyroid tumorigenesis.
Data suggest that gestational/maternal endocrine disruptor DEHP [di-(2-ethylhexyl) phthalate] exposure dose-dependently causes fetal IUGR (intrauterine growth restriction); mRNA levels of placental Thra1 and Thrb1 are reduced and nuclear translocation of placental Thra1 and Thrb1 is suppressed in DEHP-exposed mice.
Genetic Repression in Hypothyroidism Is Mediated by Thrb1.
TRbeta protein, target gene expression, and metabolic adaptive changes can occur in individual tissues without necessarily being reflected by circulating TH and TSH concentrations
Using domain exchanges and individual amino acid switches between THRA1 and THRB2, three amino acids were identified in helix 10 of the THRB2 ligand-binding domain that are required for negative regulation and are absent in THRA1.
Data suggest a novel role for THRbeta1 in secondary ossification at the epiphysis that involves transcriptional upregulation of Ihh gene.
In thyroid receptor-deficient mice, hair follicle stem cells present a clear defect in their mobilization (exit of their quiescent state and migration out of the niche), associated with increased activation of Smad signaling.
Data show that TRbeta deficiency causes dysfunction of the monoaminergic system, accompanied by epigenetic disruption during the brain maturation process.
Results suggest mutually shared roles for thyroid hormone receptor beta isoforms TRbeta1 and TRbeta2 in cochlear development.
Our findings indicated that synergistic signaling of KRAS(G12D) and TRbetaPV led to increased MYC expression.
T3 induces FGF21 in cultured hepatocytes and this effect involves direct actions of TRbeta1, which binds a TRE within intron 2 of FGF21. But T3 induced most gene expression in liver independently of FGF21.
TRbeta acts as a cytoplasmic, phosphotyrosine-dependent scaffold for the p85 regulatory subunit of PI3K and the Src kinase Lyn in the absence of thyroid hormone.
TRbeta-related deafness originates outside of hair cells and that TRalpha and TRbeta play opposing, non-redundant roles in hair cells.
Luciferase expression driven by the midwavelength sensitive opsin intron 3-4 region was only slightly increased by THRB2, and rather enhanced by COUP-TFII.
these data indicate that interactions between NCoR1 and TR control a specific pathway involved in regulation of cholesterol metabolism and clearance.
Taken together, the results of this study provide new insights into the mechanisms of transcriptional regulation by TRbeta1 in vivo.
Recruitment of the NRF1 and THRB to the promoters of genes.
A combination of isoform-specific recruitment and tissue-specific expression of these newly identified coregulator candidates serves to customize TR function for different biological purposes in different cell types.
For the first time, we show an opposing effect of the two TR isoforms, TRalpha1 and TRbeta, in the regulation of state anxiety, with alpha1 knockout animals (alpha1KO) showing higher levels of anxiety and betaKO males showing less anxiety compared to wild-type mice.
Findings indicate that diet-induced obesity exacerbates thyroid cancer progression in Thrb(PV/PV)Pten(+/-) mice and suggest that the STAT3 signaling pathway could be tested as a potential target for the treatment of thyroid cancer.
Data provide evidence that zebrafish represents a valid model to study in vivo the thyroid hormone (TH) action, and the molecular mechanisms underlying the two syndromes of TH resistance, RTHa and RTHb.
Loss- and gain-of-function experiments show that L-opsin expression requires trbeta2 activity before cone differentiation. Ectopic expression of trbeta2 after cone differentiation produces cones with mixed opsins.
Data suggest that the embryonic to larval transitory phase is characterized by its dependency on the timely synthesis of thyroid hormone and the concomitant autoinductive increase in thyroid hormone receptor beta mRNA levels.
Increased expression of mammary TRbeta1 and DIO2, and decreased RXRalpha, provide a mechanism to increase thyroid hormone activity within the mammary gland during lactation.
Precocious exposure to the thyroid hormone antagonist NH-3 or impaired thyroid receptor beta function led to severe malformations related to neurocristopathies.
Data show that forced expression of Kruppel-like factor 9 (Klf9) in the brain of thyroid-intact tadpoles increased baseline thyroid hormone receptor-beta (trb) mRNA and enhanced trb autoinduction.
Expression analysis of TRalpha and TRbeta, and studies with TRalpha and TRbeta selective ligands support the hypothesis that the action of thyroid hormone on neurogenesis in the tadpole brain may be cell autonomous, and is mediated by the TRalpha.
The protein encoded by this gene is a nuclear hormone receptor for triiodothyronine. It is one of the several receptors for thyroid hormone, and has been shown to mediate the biological activities of thyroid hormone. Knockout studies in mice suggest that the different receptors, while having certain extent of redundancy, may mediate different functions of thyroid hormone. Mutations in this gene are known to be a cause of generalized thyroid hormone resistance (GTHR), a syndrome characterized by goiter and high levels of circulating thyroid hormone (T3-T4), with normal or slightly elevated thyroid stimulating hormone (TSH). Several alternatively spliced transcript variants encoding the same protein have been observed for this gene.
nuclear receptor subfamily 1 group A member 2
, oncogene ERBA2
, thyroid hormone nuclear receptor beta variant 1
, thyroid hormone receptor beta
, thyroid hormone receptor, beta (erythroblastic leukemia viral (v-erb-a) oncogene homolog 2, avian)
, TR beta
, thyroid hormone receptor beta 1
, thyroid hormone receptor beta 2
, thyroid hormone receptor beta-1
, beta-thyroid hormone receptor
, thyroid hormone receptor beta isoform
, thyroid hormone receptor beta 3
, thyroid hormone receptor beta2delta
, thyroid hormone receptor, beta (avian erythroblastic leukemia viral (v-erb-a) oncogene homolog 2)
, thyroid hormone receptor beta2
, nuclear receptor subfamily 1 group A member 2-B
, thyroid hormone receptor beta-B
, LOW QUALITY PROTEIN: thyroid hormone receptor beta