Target intelligence / Profile preview

Retinoic acid receptor (RAR) and Retinoid X receptor (RXR) (RAR, RXR)

Target
RAR, RXR
Molecular classification
Nuclear receptor, Transcription factor
01

Overview

The retinoid-dependent intracellular signaling pathway refers to a set of mechanisms in which retinoids (oxidized derivatives of vitamin A, such as all-trans retinoic acid) bind to nuclear receptors called retinoic acid receptor (RAR) and retinoid X receptor (RXR). Upon ligand binding, these receptors form heterodimers, translocate to the nucleus, and bind to specific DNA sequences called retinoic acid response elements (RAREs). This leads to the activation or repression of target genes controlling cellular differentiation, proliferation, and organogenesis. Non-canonical retinoid signaling can also involve rapid kinase-mediated signaling cascades and intercellular communication. Defects or manipulations of these receptors are implicated in a variety of diseases, especially developmental disorders and cancer[1][2][3][4][5][6][7].

Other names
Retinoic acid receptorRARRetinoid X receptorRXRNuclear retinoid receptorRA receptorRexinoid receptor
02

Mechanism of action

Agonism of RAR or RXR to induce or repress gene transcription by binding to retinoic acid response elements (RARE) in DNA[2][3][4][5][7] Modulation of cell differentiation and proliferation via altered transcriptional programs

03

Biological functions

Gene transcription regulationEmbryonic developmentCell differentiationCell cycle regulationApoptosisImmune responseVisual cycle (for specific retinoids)
04

Disease associations

CancerNeurodegenerative diseaseCardiovascular diseaseInflammationDevelopmental defectsVisual disorders (Retinal degeneration, etc.)
05

Safety considerations

Teratogenicity (birth defects)HepatotoxicityMucocutaneous toxicityHyperlipidemiaCentral nervous system effects (pseudotumor cerebri)
06

Interacting drugs

All-trans retinoic acid (ATRA)

5 more in the full profile.

07

Biomarkers

Expression of RAR and RXR in tumor tissue or affected cellsPresence/levels of retinoic acid–regulated gene expression (e.g., HOX gene expression)Detection of atRA or retinol in serum/plasma (for deficiency or therapy monitoring)

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