CREBBP
CREB binding lysine acetyltransferase
Gene summary
A protein-coding gene on chromosome 16 (epigenetic regulation). This gene is ubiquitously expressed and is involved in the transcriptional coactivation of many different transcription factors. First isolated as a nuclear protein that binds to cAMP-response element binding protein (CREB), this gene is now known to play critical roles in embryonic development, growth control, and homeostasis by coupling chromatin remodeling to transcription factor recognition.
Source: NCBI Gene, accessed 2026-10-07.
Protein reference (UniProt)
- Protein
CREB-binding protein
- Function (excerpt)
Acetylates histones, giving a specific tag for transcriptional activation. Mediates acetylation of histone H3 at 'Lys-18' and 'Lys-27' (H3K18ac and H3K27ac, respectively). Also acetylates non-histone proteins, like DDX21, FBL, IRF2, MAFG, NCOA3, POLR1E/PAF53 and FOXO1. Binds specifically to phosphorylated CREB and enhances its transcriptional activity toward cAMP-responsive genes. Acts as a coactivator of ALX1. Acts as a circadian transcriptional coactivator which enhances the activity of the circadian transcriptional activators: NPAS2-BMAL1 and CLOCK-BMAL1 heterodimers. Acetylates PCNA; acetylation promotes removal of chromatin-bound PCNA and its degradation during nucleotide excision repair (NER). Acetylates POLR1E/PAF53, leading to decreased association of RNA polymerase I with the rDNA promoter region and coding region. Acetylates DDX21, thereby inhibiting DDX21 helicase activity. Acetylates FBL, preventing methylation of 'Gln-105' of histone H2A (H2AQ104me).
- Subcellular location
Cytoplasm; Nucleus.
- Associated conditions
Rubinstein-Taybi syndrome 1 (RSTS1); Menke-Hennekam syndrome 1 (MKHK1).
Source: UniProtKB/Swiss-Prot Q92793, 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 CREBBP specifically.
Mentioned in 1 corpus record
- Powers · Reddit commentCurated Powers pick
Re: Questions regarding current PFS theory
u/drwillpowers · r/DrWillPowers
Answering questions about variable onset and post-cessation crashes, Powers gives three linked explanations. First, milder or slower onsets reflect fewer defects — it takes longer to reach threshold. Second, people who crash on quitting had upregulated…
ARID1ACHD4CHD5CHD6CHD7+3PRH-15012026-04-18T08:57:02ZPFSPowers Reddit history
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