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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.
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Genetic Repression in Hypothyroidism Is Mediated by Thrb1.
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Thyroid hormone receptor beta and NCOA4 regulate terminal erythrocyte differentiation.
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TRbeta protein, target gene expression, and metabolic adaptive changes can occur in individual tissues without necessarily being reflected by circulating TH and TSH concentrations
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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.
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Data suggest a novel role for THRbeta1 in secondary ossification at the epiphysis that involves transcriptional upregulation of Ihh gene.
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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.
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Data show that TRbeta deficiency causes dysfunction of the monoaminergic system, accompanied by epigenetic disruption during the brain maturation process.
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Results suggest mutually shared roles for thyroid hormone receptor beta isoforms TRbeta1 and TRbeta2 in cochlear development.
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Our findings indicated that synergistic signaling of KRAS(G12D) and TRbetaPV led to increased MYC expression.
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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.
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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.
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TRbeta-related deafness originates outside of hair cells and that TRalpha and TRbeta play opposing, non-redundant roles in hair cells.
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Luciferase expression driven by the midwavelength sensitive opsin intron 3-4 region was only slightly increased by THRB2, and rather enhanced by COUP-TFII.
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these data indicate that interactions between NCoR1 and TR control a specific pathway involved in regulation of cholesterol metabolism and clearance.
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Taken together, the results of this study provide new insights into the mechanisms of transcriptional regulation by TRbeta1 in vivo.
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Recruitment of the NRF1 and THRB to the promoters of genes.
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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.
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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.
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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.
