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Panel of Human RAR Reporter Assays: RARa, RARb & RARg

each in-1 x-32-96 well format
each in-1 x-32-96 well format

Product Description and Product Data

INDIGO’s Retinoic Acid Receptors Panel (RAR alpha, RAR beta, and RAR gamma) assay kit is an all-inclusive firefly luciferase reporter assay system that includes in addition to reporter cells for each RAR, optimized cell culture medium, a medium for diluting test compounds, a control agonist for each RAR, stable-glow luciferase detection reagent, detailed protocol, Protocol Quick Guide, and a cell culture-ready assay plate in strip-well format so that (if preferred) RAR alpha, RAR beta, and RAR gamma assays may be performed at different times. This panel contains sufficient materials to perform 32 RAR alpha assays, 32 RAR beta assays, and 32 RAR gamma assays in 96-well plate format.


  • Clear, Reproducible Results

  • All-Inclusive Assay Systems
  • Exceptional Cell Viability Post-Thaw
  • Consistent Results Lot to Lot

Product Specifications

Target TypeNuclear Hormone Receptor
Receptor FormHybrid
Assay ModeAgonist, Antagonist
Kit Components
  • RARa Reporter Cells
  • RARb Reporter Cells
  • RARg Reporter Cells
  • Cell Recovery Medium (CRM)
  • Compound Screening Medium (CSM)
  • 9 cis-Retinoic Acid, (ref. agonist RARa; in DMSO)
  • trans-Retinoic Acid, (ref. agonist RARb RARg; in DMSO)
  • Detection Substrate
  • Detection Buffer
  • White, sterile, cell-culture ready assay plate
Shelf Life6 months
Shipping RequirementsDry Ice
Storage temperature-80C


Target Background

Retinoic acid receptors (RARs) are nuclear hormone receptors of the NRB1 class, which function as heterodimers with retinoid X receptors (RXRs). There are three distinct RAR subtypes; RARalpha, RARbeta and RARgamma. RARalpha is present in most tissue types, whereas RARbeta and RARgamma expression is more selective. RXR-RAR heterodimers act as ligand-dependent transcriptional regulators by binding to the specific retinoic acid response element (RARE) found in the promoter regions of target genes. In the absence of an RAR agonist, RXR-RAR recruits co-repressor proteins such as NCoR and associated factors such as histone deacetylase to maintain a condensed chromatin structure. RAR agonist binding stimulates co-repressor release and co-activator complexes, such as histone acetyltransferase, are recruited to activate transcription. RARs transduce retinoid signals in vivo, which mediates proper embryogenesis, differentiation and growth arrest. Specifically, RXRalpha-RARgamma heterodimers are necessary for growth arrest and viseral and primitive endodermal differentiation, whereas RXRalpha-RARalpha is required for cAMP-dependent parietal endodermal differentiation. In vitro it has been difficult to elucidate the roles of individual subtypes as functional RAR knockouts generate artificial redundancies that are thought not to exist under normal conditions.

This PANEL of Retinoic Acid Receptors Reporter Assays utilizes non-human mammalian cells engineered to express distinct human RARα (NR1B1), RARβ (NR1B2), and RARγ (NR1B3) proteins.


Oral squamous cell carcinoma (OSCC) is world-wide health problem associated with high morbidity and mortality. From both the patient and socio-economic perspectives, prevention of progression of premalignant oral intraepithelial neoplasia (OIN) to OSCC is clearly the preferable outcome. Optimal OSCC chemopreventives possess a variety of attributes including high-tolerability, bioavailability, efficacy and preservation of an intact surface epithelium. Terminal differentiation, which directs oral keratinocytes leave the proliferative pool to form protective cornified envelopes, preserves the protective epithelial barrier while concurrently eliminating growth-aberrant keratinocytes. This study employed human premalignant oral keratinocytes and an OSCC cell line to evaluate the differentiation-inducing capacity of the synthetic retinoid, fenretinide (4HPR). Full thickness oral mucosal explants were evaluated for proof of concept differentiation studies. Results of this study characterize the ability of 4HPR to fulfill all requisite components for keratinocyte differentiation i.e. nuclear import via binding to CRABP-II (molecular modeling), binding to and subsequent activation of retinoic acid nuclear receptors (receptor activation assays), increased expression and translation of genes associated with keratinocyte differentiation (RT-PCR, immunoblotting) upregulation of a transglutaminase enzyme essential for cornified envelope formation (TGM3, functional assay) and augmentation of terminal differentiation in human oral epithelial explants (image-analyses quantified corneocyte desquamation). These data build upon the chemoprevention repertoire of 4HPR that includes function as a small molecule kinase inhibitor and inhibition of essential mechanisms necessary for basement membrane invasion. An upcoming clinical trial, which will assess whether a 4HPR-releasing mucoadhesive patch induces histologic, clinical and molecular regression in OIN lesions, will provide essential clinical insights.

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Retinoic Acid Receptor Alpha, Beta, & Gamma (RARa, RARb, & RARg)

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