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Genetic Repression in Hypothyroidism Is Mediated by Thrb1.
Thyroid hormone receptor beta and NCOA4 (show NCOA4 Proteins) regulate terminal erythrocyte differentiation.
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 (show THRA Proteins) 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 (show THRA Proteins).
Data suggest a novel role for THRbeta1 in secondary ossification at the epiphysis that involves transcriptional upregulation of Ihh (show IHH Proteins) 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 (show SMAD1 Proteins) 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 (show MYC Proteins) expression.
T3 induces FGF21 (show FGF21 Proteins) in cultured hepatocytes and this effect involves direct actions of TRbeta1, which binds a TRE (show TREH Proteins) within intron 2 of FGF21 (show FGF21 Proteins). But T3 induced most gene expression in liver independently of FGF21 (show FGF21 Proteins).
Data provide evidence that zebrafish represents a valid model to study in vivo the thyroid hormone (show PTH Proteins) (TH) action, and the molecular mechanisms underlying the two syndromes of TH resistance, RTHa and RTHb.
Data suggest that the embryonic to larval transitory phase is characterized by its dependency on the timely synthesis of thyroid hormone (show PTH Proteins) and the concomitant autoinductive increase in thyroid hormone receptor beta mRNA levels.
Report of a novel mutation T273R in the THRB gene of patients exhibiting signs of the syndrome of resistance to thyroid hormone (show PTH Proteins). Authors propose that the trans-activating function of TRbeta (show TXNRD2 Proteins) is likely dominantly hindered in these patients.
Authors previously shown that Nuclear Receptor Corepressor 1 (NCoR (show NCOR1 Proteins)) and the thyroid hormone receptor (show THRA Proteins) beta1 (TRbeta (show TXNRD2 Proteins)) inhibit tumor invasion. Here they show that these molecules repress VEGF-C (show VEGFC Proteins) and VEGF-D (show Figf Proteins) 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 (show TRIB1 Proteins) 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 (show RB1 Proteins)-deficient tumorigenesis. TRbeta2 counteracts TRbeta1, thus disrupting this safeguard and promoting development of RB1 (show RB1 Proteins)-deficient malignancies.
A relatively stable genome in retinoblastoma tumor cells is maintained by TRb1 (show TRIB1 Proteins) and TRb2 (show TRIB2 Proteins)-mediated PTTG1 (show PTTG1 Proteins) 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 (show PTH Proteins) syndrome.
THRA (show THRA Proteins) predominates in multipotent human adipose derived stem cells (hADSC) whereas THRB is expressed at lower levels and is upregulated during hADSC differentiation.
Increased expression of mammary TRbeta1 and DIO2 (show DIO2 Proteins), and decreased RXRalpha (show RXRA Proteins), provide a mechanism to increase thyroid hormone (show PTH Proteins) activity within the mammary gland during lactation.
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.
thyroid hormone receptor beta
, nuclear receptor subfamily 1 group A member 2
, 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)
, TR beta
, thyroid hormone receptor beta 1
, thyroid hormone receptor beta 2
, thyroid hormone receptor beta-1
, oncogene ERBA2
, thyroid hormone nuclear receptor beta variant 1
, thyroid hormone receptor, beta (erythroblastic leukemia viral (v-erb-a) oncogene homolog 2, avian)
, thyroid hormone receptor beta2
, beta-thyroid hormone receptor