|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for THRA(NM_001190919.2) Search again
Product ID:
HQP162004
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AR7, CHNG6, EAR7, ERB-T-1, ERBA, ERBA1, NR1A1, THRA1, THRA2, THRalpha, THRalpha1, THRalpha2, TRalpha, TRalpha1, TRalpha2, c-ERBA-1, c-erbA
Gene Description:
thyroid hormone receptor alpha
Target Gene Accession:
NM_001190919.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
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
- neurodevelopmental functions of thyroid hormone signaling.
- affected receptor amino acid sequences. lost their trans-activation function and exhibited dominant negative activity.
- Our results reveal specific alterations in the expression of TRbeta and TRalpha genes in a subset of breast cancer patients, suggesting that deregulation of thyroid hormone target genes may be involved in the generation of this neoplasia.
- Less aggressive thyroid cancer was found to be linked to increased thyroid hormone receptor-alpha1 expression and an expanded THRA1 microsatellite.
- allosteric changes resulting from binding of T3Ralpha to different response elements, i.e. pHREs versus nHREs, dictate whether a cofactor will function as a coactivator or a corepressor
- the nTRE (negative thyroid hormone response element) is responsible for binding of thyroid hormone receptor alpha to the promoter in HeLa cells
- Crucial in vivo functions of mutant TRalpha1s during mouse fetal development. Expression of dominant negative mutant TRalpha1 in extensive tissues from early embryonal stages might be lethal.
- acquisition of altered nuclear export capabilities contributes to the oncogenic properties of v-ErbA
- X-ray diffraction studies of isoform alpha1 of the human thyroid hormone receptor ligand-binding domain
- Age-related hypo-activation of retinoic acid and triiodothyronine nuclear receptors in peripheral blood mononuclear cells.
- T3 receptor mutants selectively impair beta2 isoform function in providing pituitary resistance to thyroid hormone syndrome
- 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.
- Immunohistochemistry (demonstrated no overt difference between CDH, hypoplastic, and control lungs, either in the localization nor the timing of the first expression of glucocorticoid, retinoid, and thyroid hormone receptors
- defects in adipogenesis could contribute to the phenotypic manifestation of reduced body weight in TRalpha1(PV/+) mice
- the two systems, TRs and IGF1/IGF1R could be functionally associated.
- These results suggest that inactivation of p44/42 MAPK enhances T(3)-induced GLUT5 gene expression in Caco-2 cells through increasing TRalpha-1 transactivity and binding activity to the GLUT5-TRE, probably due to de-phosphorylation of TRalpha-1.
- We also found no methylation of the TRalpha gene in thyroid adenomas
- both SMRT and N-CoR are limited in cells and knocking down either of them results in co-repressor-free TR and consequently de-repression of TR target genes
- Furin overexpression in some types of hepatocellular carcinomas is TR dependent.
- The DNA-binding domain of thyroid hormone receptor alpha plays a key role in direct DNA binding on positively but not on negatively triiodothyronine-regulated target genes.
- TRalpha may follow a cooperative export pathway in which both calreticulin and CRM1 play a role in facilitating efficient translocation of TRalpha from the nucleus to cytoplasm
- Two SNPs in the 3' untranslated region of THRA were genotyped: a novel SNP (2390A/G) and 1895C/A (rs12939700).