A third human retinoic acid receptor, hRAR-gamma.

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Abstract
Retinoic acid receptors (RARs) are retinoic acid (RA)-inducible enhancer factors belonging to the super-family of steroid/thyroid nuclear receptors. we have previously characterized two human RAR (hRAR-.alpha. and hRAR-.beta.) cDNAs and have recently cloned their murine cognates (mRAR-.alpha. and mRAR-.beta.) together with a third RAR (mRAR-.gamma.) whose RNA was detected predominantly in skin, a well-known target for RA. mRAR-.gamma. cDNA was used here to clone its human counterpart (hRAR-.gamma.) from a T47D breast cancer cell cDNA library. Using a transient transfection assay in HeLa cells and a reporter gene harboring a synthetic RA resonsive element, we demonstrate that hRAR-.gamma. cDNA indeed encodes a RA-inducible transcriptional trans-activator. Interestingly, comparisons of the amino acid sequences of all six human and mouse RARs indicate that the interspecies conservation of a given member of the RAR subfamily (either .alpha., .beta., or .gamma.) is much higher than the conservation of all three receptors within a given species. These observations indicate that RAR-.alpha., -.beta., and -.gamma. may perform specific functions. We show also that hRAR-.gamma. RNA is the predominant RAR RNA species in human skin, which suggests that hRAR-.gamma. mediates some of the retinoid effects in this tissue.