RXRA
retinoid X receptor alpha
Pathway candidate — not linked to PFS or PSSD by any record here
Gene summary
A protein-coding gene on chromosome 9 (steroid and nuclear hormone receptors). Retinoid X receptors (RXRs) and retinoic acid receptors (RARs) are nuclear receptors that mediate the biological effects of retinoids by their involvement in retinoic acid-mediated gene activation. These receptors function as transcription factors by binding as homodimers or heterodimers to specific sequences in the promoters of target genes.
Source: NCBI Gene, accessed 2026-10-07.
Protein reference (UniProt)
- Protein
Retinoic acid receptor RXR-alpha
- Function (excerpt)
Receptor for retinoic acid that acts as a transcription factor. Forms homo- or heterodimers with retinoic acid receptors (RARs) and binds to target response elements in response to their ligands, all-trans or 9-cis retinoic acid, to regulate gene expression in various biological processes. The RAR/RXR heterodimers bind to the retinoic acid response elements (RARE) composed of tandem 5'-AGGTCA-3' sites known as DR1-DR5 to regulate transcription. The high affinity ligand for retinoid X receptors (RXRs) is 9-cis retinoic acid. In the absence of ligand, the RXR-RAR heterodimers associate with a multiprotein complex containing transcription corepressors that induce histone deacetylation, chromatin condensation and transcriptional suppression. On ligand binding, the corepressors dissociate from the receptors and coactivators are recruited leading to transcriptional activation. Serves as a common heterodimeric partner for a number of nuclear receptors, such as RARA, RARB and PPARA.
- Subcellular location
Nucleus; Cytoplasm; Mitochondrion.
- Tissue specificity
Expressed in lung fibroblasts (at protein level). Expressed in monocytes. Highly expressed in liver, also found in kidney and brain.
Source: UniProtKB/Swiss-Prot P19793, release 2026_03, licensed CC BY 4.0. This is the protein’s normal biology, not evidence about post-drug syndromes; associated conditions are inherited disorders of the gene, not PFS, PSSD or PRSD.
Why its pathway is in the library
Nuclear receptors transduce steroid signals into lasting gene-expression programs; persistent receptor-level remodeling (or silencing) is a leading hypothesis for symptoms that outlast drug exposure.
Written for the whole nuclear receptors / retinoid signaling family, not for RXRA specifically.
Mentioned in 0 corpus records
No corpus record names RXRA directly yet. It is in the library because it sits in a pathway the corpus tracks (Nuclear receptors, retinoid signaling).
Also in steroid and nuclear hormone receptors
All 41 genes- ARPowers
androgen receptor
chr X· Nuclear receptors· 41 records - ESR1
estrogen receptor 1
chr 6· Nuclear receptors· 1 record - ESR2
estrogen receptor 2
chr 14· Nuclear receptors· Pathway candidate - FOXA1
forkhead box A1
chr 14· Nuclear receptors· Pathway candidate - HNF4A
hepatocyte nuclear factor 4 alpha
chr 20· Nuclear receptors· Pathway candidate - HNF4G
hepatocyte nuclear factor 4 gamma
chr 8· Nuclear receptors· Pathway candidate - NCOA1
nuclear receptor coactivator 1
chr 2· Nuclear receptors· Pathway candidate - NCOA2
nuclear receptor coactivator 2
chr 8· Nuclear receptors· Pathway candidate
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