Pathway candidateNCBI-verifiedprotein-coding

BRD4

bromodomain containing 4

NCBI Gene: 23476 Ensembl GeneCards UniProt: O60885

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

BRD4 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 BRD4 is not, by itself, evidence of anything related to post-drug syndromes.

Gene summary

A protein-coding gene on chromosome 19 (epigenetic regulation). The protein encoded by this gene is homologous to the murine protein MCAP, which associates with chromosomes during mitosis, and to the human RING3 protein, a serine/threonine kinase. Each of these proteins contains two bromodomains, a conserved sequence motif which may be involved in chromatin targeting.

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

Protein reference (UniProt)

Protein: Bromodomain-containing protein 4
Function (excerpt): Chromatin reader protein that recognizes and binds acetylated histones and plays a key role in transmission of epigenetic memory across cell divisions and transcription regulation. Remains associated with acetylated chromatin throughout the entire cell cycle and provides epigenetic memory for postmitotic G1 gene transcription by preserving acetylated chromatin status and maintaining high-order chromatin structure. During interphase, plays a key role in regulating the transcription of signal-inducible genes by associating with the P-TEFb complex and recruiting it to promoters. Also recruits P-TEFb complex to distal enhancers, so called anti-pause enhancers in collaboration with JMJD6. BRD4 and JMJD6 are required to form the transcriptionally active P-TEFb complex by displacing negative regulators such as HEXIM1 and 7SKsnRNA complex from P-TEFb, thereby transforming it into an active form that can then phosphorylate the C-terminal domain (CTD) of RNA polymerase II.
Subcellular location: Nucleus; Chromosome.
Tissue specificity: Ubiquitously expressed.
Associated conditions: Cornelia de Lange syndrome 6 (CDLS6).

Source: UniProtKB/Swiss-Prot O60885, 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 BRD4 specifically.

Mentioned in 0 corpus records

No corpus record names BRD4 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

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Gene summary

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

Protein reference (UniProt)

Protein: Bromodomain-containing protein 4
Function (excerpt): Chromatin reader protein that recognizes and binds acetylated histones and plays a key role in transmission of epigenetic memory across cell divisions and transcription regulation. Remains associated with acetylated chromatin throughout the entire cell cycle and provides epigenetic memory for postmitotic G1 gene transcription by preserving acetylated chromatin status and maintaining high-order chromatin structure. During interphase, plays a key role in regulating the transcription of signal-inducible genes by associating with the P-TEFb complex and recruiting it to promoters. Also recruits P-TEFb complex to distal enhancers, so called anti-pause enhancers in collaboration with JMJD6. BRD4 and JMJD6 are required to form the transcriptionally active P-TEFb complex by displacing negative regulators such as HEXIM1 and 7SKsnRNA complex from P-TEFb, thereby transforming it into an active form that can then phosphorylate the C-terminal domain (CTD) of RNA polymerase II.
Subcellular location: Nucleus; Chromosome.
Tissue specificity: Ubiquitously expressed.
Associated conditions: Cornelia de Lange syndrome 6 (CDLS6).