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Validated All-in-One™ qPCR Primer for THRB(NM_001252634.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
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.
Gene References into function
- TR surfaces and conformations required to bind nuclear receptor corepressor
- neurodevelopmental functions of thyroid hormone signaling
- affected receptor amino acid sequences.lost their trans-activation function and exhibited dominant negative activity.
- genetic analysis revealed a novel heterozygous missense mutation at codon 334 of thyroid hormone receptor beta1 in a family with resistance to thyroid hormone
- a point mutation, not anticipated to occur in resistance to thyroid hormone, causes variable phenotypes.
- Thrb(PV)/Thrb(PV) mice have severe hearing impairment that is already present at 3 weeks of age. This hearing loss is associated with disruption of postnatal morphogenesis of the tectorial membrane and organ of Corti.
- x-ray crystal structures of two hTRbeta ligand-binding domains, Ala 317 Thr and Arg 316 His
- expression of functionally impaired mutants of THRB1 in papillary carcinomas is rare
- The crystal structure of human thyroid hormone receptor beta at 2.8-A resolution with GC-24 bound explains its agonist activity and unique isoform specificity.
- Except for cardiac hypertrophy, the presence of a germline TR-beta mutation had surprisingly little effect on cardiac function.
- thyroid hormone receptor-beta cell cycle-dependent expression regulates variable hormone sensitivity
- partial dissociation of TR/retinoid X receptor heterodimer complex from the TRE is involved in the suppression of transcription induced by polychlorinated biphenyls
- novel point mutation, a heterozygous transition c.1031G>C in exon 9 theoretically substituting Gly344Ala results in bone development retardation
- developmental and tissue-specific expression of human thyroid hormone receptor beta1 5'-UTR mRNAs may regulate T3-responsiveness in target tissues by modulating TRbeta protein translation
- Most patients with resistance to thyroid hormone carry a mutation in this gene.
- unliganded TRbeta1 suppresses promoter activity driven by LXRalpha and its ligand, whereas transactivation by T3-bound TRbeta1 is not affected by LXRalpha in the presence or absence of oxysterols
- two novel TRbeta mutations occurring in the same nucleotide
- results suggested that T3 upregulates cellular proliferation on LNCaP cells but not other prostatic carcinoma cells and PZ-HPV-7 and CA-HPV-10 cells express the novel TRbeta1, which locates at cell nuclear membrane
- a small subset of TRbeta mutations that arise in resistance to thyroid hormone syndrome inhibit both T3 binding and formation of TRbeta homodimers on thyroid hormone response elements
- Modulation of hepatic TRbeta1, a key regulator of gene expression involved in lipid metabolism by soy proteins may be a novel mechanism by which soy components lower blood lipid level and exert their hypocholesterolemic actions.
- Pituitary and peripheral tissue responses to graded doses of liothyronine in 5 affected members of a family with thyroid hormone resistance due to the common TRbeta mutation P453T are reported.
- Association of TRbeta1 expression with growth pattern and the presence of K-ras mutations suggest that abnormalities in thyroid hormone signalling involving TRbeta1 play a role in the development of some types of colorectal adenocarcinomas
- Thyroid hormone receptor (TR) D-domain has the potential to form functionally important extensions of the DNA-binding domain (DBD) and ligand-binding domain (LBD) or unfold to permit TRs to adapt to different DNA response elements.
- The E333D TRbeta mutation is responsible for the resistance to thyroid hormone syndrome in a case report.
- apo THRBs form tetramers in solution which dissociate into dimers upon thyroid hormone T3 binding
- Mediates Akt activation by T3 in pancreatic beta cells.
- These findings provide a molecular rationale for the role of hS14 in TR-dependent transcriptional activation of the expression of specific genes.
- the two systems, TRs and IGF1/IGF1R could also be functionally associated.
- an insertion mutation in thyroid hormone receptor-beta may have a role in thyroid hormone resistance
- Generalized resistance to thyroid hormone with chronic thyroiditis with a novel mutation, G347A, of the TR beta gene.
- hypermethylation of the TRbeta gene as an alternative gene silencing mechanism is highly prevalent in thyroid cancer
- Activation of the thyroid hormone receptor beta/retinoid X receptor alpha heterodimer by T(3) stimulated expression of the hepatic leukemia factor, which increases HIF-1alpha gene expression.
- We report the first case of a woman with resistance to thyroid hormone, which was found to be caused by a missense mutation (V349M) in the TR beta gene.
- Furin overexpression in some types of hepatocellular carcinomas is TR dependent.
- Mutational analysis of the TRRB gene allows definitive diagnosis of thyroid hormone resistance syndrome, potentially avoiding the need for protracted and expensive pituitary function testing.
- As TRbeta(H435Y) has been found in both resistance to thyroid hormone and pituitary carcinoma, these results serve perhaps as the first example of chemical rescue that targets a mutant protein involved in multiple disease states.
- Analysis of the T3 receptor genes revealed 15 SNPs, including 7 novel. Only THRB-in9-G/A was associated with higher serum TSH in a large population of Danish twins.
- Our findings suggest that flexibility plays an important role in interaction between the receptor & its coregulators, & point out important aspects of experimental design that should be addressed when using TRbeta ligand binding domain & its agonists.
