Abstract:Retinoic acid (RA) and its congeners mediate their biologic effects after binding to nuclear transcription factors called retinoic acid receptors. Biological effects and binding affinities to various receptors vary widely. Activation of transcription ability for selected retinoids was investigated using a standardized model system. CV‐1 cells were cotransfected with a retinoic acid responsive reporter plasmid and expression vectors for retinoic acid receptors (RARs, α, β or γ) and/or retinoic X receptor (RXRα), and were treated with a retinoid (all‐tran‐RA, 13‐cis‐RA, Ro 12‐4894, SRI 5898‐21, or Ro 13‐7410). Gene transcription for all retinoids tested was activated in a dose‐dependent manner. All‐trans‐RA was the most potent activator of RARα while SRI 5898‐21 was the least active. RARa and RARβ showed similar levels of activation with all the retinoids tested, Ro 12‐4894 and Ro 13‐7410 induced little transcription in the presence of RARγ. Cotransfection of RXRα with the RARs changed the ability of the retinoids to activate transcription. Transcriptional activation in cells cotransfected with RXR and RARβ or RARγ was lower than in cells cotransfected with RARβ alone or RARγ alone. Such models with specific responsive elements may be useful for evaluating the relative activity of various retinoidsin vitro, however, complex interactions are likely depending on the choice of the reporter construct and other tran