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The Retinoid X receptor (RXR) is a type of nuclear receptor that functions as a transcription factor. It exists as three subtypes (RXR-alpha, RXR-beta, RXR-gamma) and has a modular structure with NTD, DBD, and LBD domains. RXR primarily functions by forming heterodimers with numerous other nuclear receptors (like RAR, VDR, PPAR, etc.) and binding to specific DNA sequences (often DR-1) to regulate gene transcription. Ligand binding to RXR leads to corepressor dissociation and coactivator recruitment, activating transcription. RXRs play crucial roles in development (e.g., axial and limb patterning) and metabolism (e.g., regulating the thyroid pathway). They are considered therapeutic targets; Bexarotene is a clinically used RXR-specific activator. RXRs are described as permissive co-receptors, potentially making them interesting therapeutic targets, though treatment with RXR activators like bexarotene can have side effects such as severe hypothyroidism.
RXR functions as a nuclear receptor and transcription factor. It is activated by specific ligands (agonists). Upon ligand binding, RXR, primarily as a heterodimer with other nuclear receptors, binds to specific DNA sequences (response elements) in gene promoters. This leads to the dissociation of corepressor proteins, recruitment of coactivator proteins, and promotion of transcription of downstream target genes. Therapeutic activators like Bexarotene bind to and activate RXR.
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