Thyroid Hormone Receptor Alpha (TRα; NR1A1)
| Product Family | Product Number | Product Description | Technical Manual |
| IB0100 TRα (NR1A1) |
IB01001-32 | Human TRα Reporter Assay System, 3 x 32 assays in 96-well format | Technical Manual |
| IB01001 | Human TRα Reporter Assay System, 1 x 96-well format assays | Technical Manual | |
| IB01002 | Human TRα Reporter Assay System, 1 x 384-well format assays |
Thyroid Hormone Receptor Alpha Assay Kit 
This Thyroid Hormone Receptor Alpha (TRα) assay kit is an all-inclusive assay system that includes, in addition to TRα Reporter Cells, two optimized media for use during cell culture and (optionally) in diluting the test samples, a reference agonist, Luciferase Detection Reagent, a cell culture-ready assay plate, and a detailed protocol.
TRα Reporter Cells are prepared using INDIGO’s proprietary CryoMite™ process. This cryo-preservation method yields high cell viability post-thaw, and provides the convenience of immediately dispensing healthy, division-competent reporter cells into assay plates. There is no need for intermediate spin-and-wash steps, viability determinations, or cell titer adjustments.
INDIGO’s TR alpha reporter assay kits feature a luciferase detection reagent specially formulated to provide stable light emission between 5 and 90+ minutes after initiating the luciferase reaction. Incorporating a 5-minute reaction-rest period ensures that light emission profiles attain maximal stability, thereby allowing assay plates to be processed in batch. By doing so, the signal output from all sample wells, from one plate to the next, may be directly compared within an experimental set.
TR alpha assay kits are offered in different assay formats to accommodate researchers’ needs: 3x 32, 1x 96, and 1x 384 assay formats for screening small numbers of test compounds, as well as custom bulk reagents for HTS applications.
Bulk assay reagents can be custom manufactured to accommodate any scale of HTS. Please inquire.
Thyroid Hormone Receptor Alpha Assay Services
The primary application of INDIGO’s cell-based nuclear receptor assays are to quantitatively assess the bioactivity of a test compound as an agonist (activator) or antagonist (inhibition of an agonist response) of a given receptor. Service assays include a positive control reference compound and ‘vehicle’ control for every experiment. A formal study report and all data files are provided to the client upon completion of the study. To receive a quote for your proposed study, complete & submit the online “Request a Quote” form or contact an INDIGO Customer Service Representative to discuss your desired study parameters.
Thyroid Hormone Receptor Alpha Background
Thyroid hormone receptor alpha (TR-alpha) (erythroblastic leukemia viral (v-erb-a) oncogene homolog, avian), also known as NR1A1, is nuclear receptor protein encoded by the THRA gene. 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.
The Human TRα Reporter Assay Systems utilize proprietary human cells engineered to provide constitutive, high-level expression of Human Thyroid Hormone Receptor Alpha (NR1A1), a ligand-dependent transcription factor commonly referred to as TRα. Additionally, these cells contain a TRα-responsive luciferase reporter gene. Thus, quantifying luciferase activity provides a surrogate measure of TRα activity in the treated reporter cells.
For more information on TRα, visit the Nuclear Receptor Resource.
Synonyms: Thyroid Hormone Receptor Alpha, TRα, TRa TR alpha, Human Thyroid Hormone Receptor Alpha, NR1A1)
Thyroid Hormone Receptor Alpha Assay Data
Thyroid Hormone Receptor Alpha Assay Research Areas
Dyslipidemia; NASH/NAFLD; Obesity; CNS, Circadian and Basal Metabolism; Metabolic Disease; Toxicology; Environmental Toxicology