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Retinoic acid receptors (RARs) are ligand-activated transcription factors and nuclear hormone receptors. There are three canonical subtypes: RARα, widely expressed in tissue; RARβ, expressed in brain, CNS, intestine, liver, kidney, and limbs; and RARγ, strongly expressed in skin. They are encoded by distinct genes (RARA, RARB, RARG), exist as multiple isoforms, and mediate the cellular effects of retinoids, particularly all-trans and 9-cis retinoic acid. RARs heterodimerize with retinoid X receptors (RXRs) to regulate gene transcription relevant to embryonic development, organogenesis, and cell differentiation. Dysregulation or mutation of these receptors is implicated in a variety of diseases, notably cancers and developmental disorders. Many drugs target specific RAR subtypes via agonist, antagonist, or inverse agonist mechanisms. "Other RAR subtypes" is a non-specific label and should be replaced by the actual subtype names for clarity and scientific accuracy
Agonists activate RAR, promote coactivator recruitment, and induce gene transcription. Antagonists block RAR activation, maintain corepressor binding, and prevent target gene transcription. Some compounds act as inverse agonists, suppressing basal transcriptional activity
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