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We found that the thyroid hormone receptor (TRalpha 3) has a differential expression profile. Thyroid hormone (show PTH ELISA Kits) is critical for normal brain development. Our results showed that there is a possible link between IGF1 (show IGF1 ELISA Kits)/IGF1R (show IGF1R ELISA Kits) and the TRalpha 3 and that over expression of IGF1R (show IGF1R ELISA Kits) in RTT cells may be the cause of neurites improvement in neural RTT-derived neurons.
THRA predominates in multipotent human adipose derived stem cells (hADSC) whereas THRB (show THRB ELISA Kits) is expressed at lower levels and is upregulated during hADSC differentiation.
8 different THRA gene abnormalities have been described in 14 patients from 9 families with phenotypes including short stature, dysmorphic syndrome, psychoneuromotor disorders, constipation and bradycardia. Review.
The current study aimed to investigate whether TRs may be specifically expressed in BRCA1 associated cancer cases.
THRA mutations may be more common than expected. In patients with clinical symptoms of mild hypothyreosis without confirmation in endocrine studies, a molecular study of THRA defects is strongly recommended.
Thyroid hormone receptor (TRalpha1) is shown to occur and determine postischemic remodeling and cardiac recovery depending on the availability of TH. [review]
Data suggest thyroid hormone (show PTH ELISA Kits) resistance syndrome can be exhibited by patients with heterozygous missense mutation (Ala263Val) in THRA1 and THRA2, isoforms resulting from alternative splicing. [CASE REPORT]
Thyroid hormone (show PTH ELISA Kits) signalling may be important in a proportion of breast cancers and THRalpha2 expression may be a regulator of signalling in this pathway.
substantial reduction in the protein expression profile of THRs (show TARS ELISA Kits) in malignant versus nonmalignant mammary epithelium suggesting a possible role in breast cancer development.
A new x-ray crystallographic structure of thyroid hormone receptor ligand-binding domains shows a second binding site for thyroid hormones.
the TR-KLF9 (show KLF9 ELISA Kits) axis is responsible for the hematopoietic dysfunction in congenital hypothyroidism
there is considerable evidence that TRalpha plays an important role in fat deposition in porcine adipose tissue.
Furthermore, molecular and transgenic studies have shown that unliganded TRalpha accomplishes these via the recruitment of histone deacetylase (HDAC (show HDAC1 ELISA Kits))-containing corepressor complexes to repress the expression of TH-inducible genes
regions of the Xenopus and mouse Klf9 (show KLF9 ELISA Kits) genes 5-6 kb upstream of the transcription start sites that supported synergistic transactivation by TH plus GC.
Type 2 iodothyronine deiodinase (show DIO2 ELISA Kits) activity is required for the death of thyroid hormone receptor (TRalpha)-transfected tail muscle cells induced by a low level of thyroid hormone (show PTH ELISA Kits).
Data provide in vivo evidence for targeted recruitment of N-CoR/SMRT-TBLR1 (show TBL1XR1 ELISA Kits) complexes by unliganded thyroid hormone (show PTH ELISA Kits) receptors in transcriptional repression during vertebrate development.
Data show that thyroid hormone (show PTH ELISA Kits) receptors directly mediate the developmental effects of thyroid hormone (show PTH ELISA Kits) in individual organs by regulating target gene expression in these organs.
investigated the role of steroid receptor coactivator (show SRA1 ELISA Kits) 3 (SRC3 (show NCOA3 ELISA Kits)) in gene activation by thyroid hormone receptor (TR) in vivo during development
Binding of liganded thyroid hormnone receptor to the target promoter is reduced when arginine methyltransferase 1 (show DNMT1 ELISA Kits) was overexpressed, accompanied by a slight reduction in histone methylation.
PRMT1 functions transiently as a coactivator in thyroid hormone (show PTH ELISA Kits) (T3) receptor (TR)-mediated transcription by enhancing TR-T3 response element binding and further suggest that PRMT1 has tissue-specific roles in regulating the rate of metamorphosis.
T(3) acts to induce cell proliferation in the tadpole brain predominantly, if not exclusively, via TRalpha.
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.
zebrafish uses both alternative splicing and differential expression of TRalpha genes to diversify the cellular response to thyroid hormones.
Study demonstrated an anxiety-related phenotype in mice expressing a neuron-specific TRalpha (show GNAT1 ELISA Kits) mutation. This provides evidence that altered thyroid hormone (show PTH ELISA Kits) signaling in the brain impacts adult behavior.
the Gata-1 (show GATA1 ELISA Kits) gene was a T3-directly regulated gene and that TRa1PV could impair erythropoiesis via repression of the Gata-1 (show GATA1 ELISA Kits) gene and its regulated genes. These results provide new insights into how TRa1 (show HSP90B1 ELISA Kits) mutants acted to cause erythroid abnormalities in patients with mutations of the THRA gene.
Using domain exchanges and individual amino acid switches between THRA1 and THRB2 (show THRB ELISA Kits), three amino acidswere identified in helix 10 of the THRB2 (show THRB ELISA Kits) ligand-binding domain that are required for negative regulation and are absent in THRA1.
Hippocampal transcriptome profile of persistent memory rescue in a mouse model of Thra1 mutation-mediated resistance to thyroid hormone (show PTH ELISA Kits) has been reported.
deletion of TRalpha (show GNAT1 ELISA Kits) in ApoE (show APOE ELISA Kits)(-/-) mice alters cardiac structure and contractility; both could contribute to blunted BP response to physical exercise and impaired exercise performance
Data (including data from studies in knockout mice) suggest mitochondrial T3Ralpha in brown adipose tissue is key to regulation of energy metabolism; knockout mice exhibit hypermetabolism/hyperphagia, but not cold intolerance/defective thermogenesis.
Data (including data from studies in mutant strains of mice) suggest Thra1 (but not Thrb (show THRB ELISA Kits)) plays role in myogenesis, cell proliferation, and resistance to T3 (triiodothyronine) in skeletal myoblasts; Thra1 promotes muscle regeneration after injury.
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.
These results indicate that postnatal exposure to a low dose of decaBDE on PNDs 1 through 5 lowers the testosterone level and the levels of Ar and Thra transcripts in Sertoli cells, accompanied by an imbalance in the ratios of Thra splicing variants
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. Alternatively spliced transcript variants encoding distinct isoforms have been reported.
, ERBA-related 7
, V-erbA-related protein 7
, nuclear receptor subfamily 1 group A member 1
, thyroid hormone receptor alpha
, thyroid hormone receptor, alpha (erythroblastic leukemia viral (v-erb-a) oncogene homolog, avian)
, thyroid normone nuclear receptor alpha variant 1
, triiodothyronine receptor
, thyroid hormone receptor alpha 2
, nuclear receptor subfamily 1 group A member 1-A
, thyroid hormone receptor alpha-A
, thyroid hormone receptor, alpha (erythroblastic leukemia viral (v-erb-a) oncogene homolog)
, thyroid hormone receptor alpha 1
, thyroid hormone receptor alpha-1
, Thyroid hormone receptor alpha 1 (avian erythroblastic leukemia viral (v-erb-a) oncogene homolog 1 formerly ERBA1)
, avian erythroblastic leukemia viral (v-erb-a) oncogene homolog 1
, c-erb-A thyroid hormone receptor
, TR alpha 1
, TR alpha 2
, c-erb-A protein
, thyroid hormone receptor alpha1
, thyroid hormone receptor alpha2
, Nuclear receptor subfamily 1 group A member 1-A