Pathway candidateNCBI-verifiedprotein-coding

TRIM24

tripartite motif containing 24

NCBI Gene: 8805 Ensembl GeneCards UniProt: O15164

Pathway candidate — not linked to PFS or PSSD by any record here

TRIM24 is in the library because it belongs to the epigenetic regulation family. No study, report or commentary in the corpus names it, so a variant in TRIM24 is not, by itself, evidence of anything related to post-drug syndromes.

Gene summary

A protein-coding gene on chromosome 7 (epigenetic regulation). The protein encoded by this gene mediates transcriptional control by interaction with the activation function 2 (AF2) region of several nuclear receptors, including the estrogen, retinoic acid, and vitamin D3 receptors. The protein localizes to nuclear bodies and is thought to associate with chromatin and heterochromatin-associated factors.

Source: NCBI Gene, accessed 2026-10-07.

Protein reference (UniProt)

Protein: Transcription intermediary factor 1-alpha
Function (excerpt): Transcriptional coactivator that interacts with numerous nuclear receptors and coactivators and modulates the transcription of target genes. Interacts with chromatin depending on histone H3 modifications, having the highest affinity for histone H3 that is both unmodified at 'Lys-4' (H3K4me0) and acetylated at 'Lys-23' (H3K23ac). Has E3 protein-ubiquitin ligase activity. During the DNA damage response, participates in an autoregulatory feedback loop with TP53. Early in response to DNA damage, ATM kinase phosphorylates TRIM24 leading to its ubiquitination and degradation. After sufficient DNA repair has occurred, TP53 activates TRIM24 transcription, ultimately leading to TRIM24-mediated TP53 ubiquitination and degradation. Plays a role in the regulation of cell proliferation and apoptosis, at least in part via its effects on p53/TP53 levels. Up-regulates ligand-dependent transcription activation by AR, GCR/NR3C1, thyroid hormone receptor (TR) and ESR1.
Pathway: Protein modification; protein ubiquitination.
Subcellular location: Nucleus; Cytoplasm; Mitochondrion.

Source: UniProtKB/Swiss-Prot O15164, 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

Epigenetic persistence is the leading hypothesis for why post-drug syndromes endure after the drug is gone; chromatin regulators are therefore priority candidates in any persistence mechanism.

Written for the whole epigenetic regulation family, not for TRIM24 specifically.

Mentioned in 0 corpus records

No corpus record names TRIM24 directly yet. It is in the library because it sits in a pathway the corpus tracks (Epigenetic regulation).

Also in epigenetic regulation

All 130 genes

Browse by family on the gene families page.

Gene summary

Source: NCBI Gene, accessed 2026-10-07.

Protein reference (UniProt)

Protein: Transcription intermediary factor 1-alpha
Function (excerpt): Transcriptional coactivator that interacts with numerous nuclear receptors and coactivators and modulates the transcription of target genes. Interacts with chromatin depending on histone H3 modifications, having the highest affinity for histone H3 that is both unmodified at 'Lys-4' (H3K4me0) and acetylated at 'Lys-23' (H3K23ac). Has E3 protein-ubiquitin ligase activity. During the DNA damage response, participates in an autoregulatory feedback loop with TP53. Early in response to DNA damage, ATM kinase phosphorylates TRIM24 leading to its ubiquitination and degradation. After sufficient DNA repair has occurred, TP53 activates TRIM24 transcription, ultimately leading to TRIM24-mediated TP53 ubiquitination and degradation. Plays a role in the regulation of cell proliferation and apoptosis, at least in part via its effects on p53/TP53 levels. Up-regulates ligand-dependent transcription activation by AR, GCR/NR3C1, thyroid hormone receptor (TR) and ESR1.
Pathway: Protein modification; protein ubiquitination.
Subcellular location: Nucleus; Cytoplasm; Mitochondrion.