RAR beta is a member of the Retinoic Acid Receptor family of nuclear receptors. Retinoids, vitamin A and its natural and synthetic analogues, are a very important group of hormones that regulate a wide variety of biological functions including embryogenesis, cell growth, and cell differentiation. Retinoids have a wide variety of clinical benefit, they have uses in dermatology, oncology, diabetes, and diseases associated with HPV. Non-selective retinoids are usually associated with toxicity problems that limit their therapeutic usefulness. Currently, research is being done to find more receptor-selective retinoids, as well as function-selective retinoids, such as inverse agonists and antagonists. RAR beta is also viewed as a tumor suppressor. It is often lost or down-regulated in breast cancer and breast cancer cell lines. It is often silenced during cancer progression, and re-expression can restore RA-mediated growth control. Cotransfection experiments showed that RARs are activated by either alltrans- or 9-cis-retinoic acid at a ligand concentration of 5 X 10^-8 mmol/L. RAR beta and gamma are significantly different from RAR alpha in the way they bind to co-repressors. RAR alpha binds co-repressor SMRT in the absence of ligand, but RAR beta and gamma interact only very weakly with this co-repressor, due to the conformation of helix 12 in these two receptors. This ultimately leads to high basal levels of transcription even in the absence of ligand. This transcriptional activity can, however, be increased with the addition of the ligand all-trans retinoic acid (ATRA).
|Abbr||HEK 293T(UAS-bla)-HuRAR bata(LBD)-GAL4(DBD)|
|Host Cell||HEK 293T|
|Product Type||GPCR Expressing Cell|