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overview of the clinical features together with the underlying molecular mechanisms in patients with resistance to thyroid hormone (zeige PTH Proteine) due to heterozygous mutations in TRalpha (Review).
We found that the thyroid hormone receptor (TRalpha 3) has a differential expression profile. Thyroid hormone (zeige PTH Proteine) is critical for normal brain development. Our results showed that there is a possible link between IGF1 (zeige IGF1 Proteine)/IGF1R (zeige IGF1R Proteine) and the TRalpha 3 and that over expression of IGF1R (zeige IGF1R Proteine) 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 (zeige THRB Proteine) 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 (zeige PTH Proteine) 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 (zeige PTH Proteine) 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 (zeige TARS Proteine) in malignant versus nonmalignant mammary epithelium suggesting a possible role in breast cancer development.
the TR-KLF9 (zeige KLF9 Proteine) 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 (zeige HDAC1 Proteine))-containing corepressor complexes to repress the expression of TH-inducible genes
regions of the Xenopus and mouse Klf9 (zeige KLF9 Proteine) genes 5-6 kb upstream of the transcription start sites that supported synergistic transactivation by TH plus GC.
Type 2 iodothyronine deiodinase (zeige DIO2 Proteine) activity is required for the death of thyroid hormone receptor (TRalpha)-transfected tail muscle cells induced by a low level of thyroid hormone (zeige PTH Proteine).
Data provide in vivo evidence for targeted recruitment of N-CoR/SMRT-TBLR1 (zeige TBL1XR1 Proteine) complexes by unliganded thyroid hormone (zeige PTH Proteine) receptors in transcriptional repression during vertebrate development.
Data show that thyroid hormone (zeige PTH Proteine) receptors directly mediate the developmental effects of thyroid hormone (zeige PTH Proteine) in individual organs by regulating target gene expression in these organs.
investigated the role of steroid receptor coactivator (zeige SRA1 Proteine) 3 (SRC3 (zeige NCOA3 Proteine)) 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 (zeige DNMT1 Proteine) was overexpressed, accompanied by a slight reduction in histone methylation.
PRMT1 functions transiently as a coactivator in thyroid hormone (zeige PTH Proteine) (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 (zeige PTH Proteine) (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 (zeige GNAT1 Proteine) mutation. This provides evidence that altered thyroid hormone (zeige PTH Proteine) signaling in the brain impacts adult behavior.
the Gata-1 (zeige GATA1 Proteine) gene was a T3-directly regulated gene and that TRa1PV could impair erythropoiesis via repression of the Gata-1 (zeige GATA1 Proteine) gene and its regulated genes. These results provide new insights into how TRa1 (zeige HSP90B1 Proteine) 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 (zeige THRB Proteine), three amino acidswere identified in helix 10 of the THRB2 (zeige THRB Proteine) 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 (zeige PTH Proteine) has been reported.
deletion of TRalpha (zeige GNAT1 Proteine) in ApoE (zeige APOE Proteine)(-/-) 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 (zeige THRB Proteine)) 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 (zeige SMAD1 Proteine) 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