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Using domain exchanges and individual amino acid switches between THRA1 (show THRA ELISA Kits) 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 ELISA Kits).
Data suggest a novel role for THRbeta1 in secondary ossification at the epiphysis that involves transcriptional upregulation of Ihh (show IHH ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) expression.
T3 induces FGF21 (show FGF21 ELISA Kits) in cultured hepatocytes and this effect involves direct actions of TRbeta1, which binds a TRE (show TREH ELISA Kits) within intron 2 of FGF21 (show FGF21 ELISA Kits). But T3 induced most gene expression in liver independently of FGF21 (show FGF21 ELISA Kits).
TRbeta acts as a cytoplasmic, phosphotyrosine-dependent scaffold for the p85 (show ECM1 ELISA Kits) regulatory subunit of PI3K and the Src kinase (show CSK ELISA Kits) Lyn (show LYN ELISA Kits) in the absence of thyroid hormone (show PTH ELISA Kits).
TRbeta-related deafness originates outside of hair cells and that TRalpha (show GNAT1 ELISA Kits) 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 (show NR2F2 ELISA Kits).
Data provide evidence that zebrafish represents a valid model to study in vivo the thyroid hormone (show PTH ELISA Kits) (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 ELISA Kits) and the concomitant autoinductive increase in thyroid hormone receptor beta mRNA levels.
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 ELISA Kits) syndrome.
THRA (show THRA ELISA Kits) predominates in multipotent human adipose derived stem cells (hADSC) whereas THRB is expressed at lower levels and is upregulated during hADSC differentiation.
TRbeta (show TXNRD2 ELISA Kits) suppressed Runx2 (show RUNX2 ELISA Kits) transcriptional activities, thus confirming TRbeta (show TXNRD2 ELISA Kits) regulation of Runx2 (show RUNX2 ELISA Kits) at functional thyroid hormone (show PTH ELISA Kits)-response elements. Significantly, these findings indicate that a ratio of the tumor-suppressor TRbeta (show TXNRD2 ELISA Kits) and tumor-promoting Runx2 (show RUNX2 ELISA Kits) may reflect tumor aggression and serve as biomarkers in biopsy tissues. The discovery of this TRbeta (show TXNRD2 ELISA Kits)-Runx2 (show RUNX2 ELISA Kits) signaling supports the emerging role of TRbeta (show TXNRD2 ELISA Kits) as a tumor supp...
results revealed that microRNA 200a inhibits erythroid differentiation by targeting PDCD4 (show PDCD4 ELISA Kits) and THRB
it was observed that ER stimulated gene expression by interacting with MEIS1 (show MEIS1 ELISA Kits) and FOXP3 (show FOXP3 ELISA Kits), and ER inhibited gene expression by interacting with THRB and GRHL1 (show GRHL1 ELISA Kits).
presents 1 pedigree of thyroid hormone (show PTH ELISA Kits) 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.
p.H271D mutation associated with resistance thyroid hormone (show PTH ELISA Kits) 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
Increased expression of mammary TRbeta1 and DIO2 (show DIO2 ELISA Kits), and decreased RXRalpha (show RXRA ELISA Kits), provide a mechanism to increase thyroid hormone (show PTH ELISA Kits) 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