ARID1A
AT-rich interaction domain 1A
Theoretical — per Powers
Gene summary
A protein-coding gene on chromosome 1 (epigenetic regulation). Encodes a member of the SWI/SNF family, whose members have helicase and ATPase activities and are thought to regulate transcription of certain genes by altering the chromatin structure around those genes. The protein is part of the large ATP-dependent chromatin remodeling complex SNF/SWI, which is required for transcriptional activation of genes normally repressed by chromatin.
Source: NCBI Gene, accessed 2026-10-07.
Protein reference (UniProt)
- Protein
AT-rich interactive domain-containing protein 1A
- Function (excerpt)
Involved in transcriptional activation and repression of select genes by chromatin remodeling (alteration of DNA-nucleosome topology). Component of SWI/SNF chromatin remodeling complexes that carry out key enzymatic activities, changing chromatin structure by altering DNA-histone contacts within a nucleosome in an ATP-dependent manner. Binds DNA non-specifically. Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). During neural development a switch from a stem/progenitor to a postmitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to postmitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes.
- Subcellular location
Nucleus.
- Tissue specificity
Highly expressed in spleen, thymus, prostate, testis, ovary, small intestine, colon, and PBL, and at a much lower level in heart, brain, placenta, lung, liver, skeletal muscle, kidney, and pancreas.
- Associated conditions
Coffin-Siris syndrome 2 (CSS2).
Source: UniProtKB/Swiss-Prot O14497, 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 ARID1A specifically.
Powers’ note (his unpublished theorizing)
Named by Powers (2026 summit interview, unpublished): among epigenetic-monitoring genes showing recurring “glitches” in whole-genome sequencing of ~100 PFS patients, more often than expected; he theorizes failed removal of epigenetic flags after drug discontinuation.
Narrative library record
Function
Core DNA-binding subunit of the mammalian SWI/SNF (BAF) chromatin-remodeling complex; uses an ARID domain to bind AT-rich DNA and targets the remodeling complex to chromatin, regulating transcription, DNA repair, and differentiation. Frequently mutated in cancers; germline variants cause Coffin-Siris syndrome.
Corpus relevance
One of three epigenetic-regulator genes Powers reports recurring across PFS patient genomes in his 2026 summit interview (iWFDBRTgT3g), offered as candidate genetic-susceptibility loci for post-drug syndromes. If validated, it would connect PFS susceptibility to chromatin-remodeling machinery - consistent with the corpus's epigenetic theme (Traish PFS-002, HDAC findings). Attribution: theoretical-per-Powers (unpublished interview claim, pending formal publication).
Powers’ claims naming ARID1A
- Powers gene claim
ARID1A; CHD8; HDAC10 — recurring "glitches" (unspecified)
Confidence: interview
In whole-genome sequencing of ~100 PFS patients, glitches in epigenetic monitoring genes — ARID1A, CHD8, HDAC10 — appear "more than they should" statistically. Epigenetic flags (e.g., for AR upregulation) may fail to be removed after drug discontinuation.
ARARID1ACHD8HDAC10PGL-ARID1A-CHD8-HDAC102026-04-29PFS
Mentioned in 8 corpus records
- Video
Dr. Will Powers Interview [PFS / PAS / PSSD Summit 2026]
Dr. Will Powers · SIDEfxHUB - PFS & PSSD Patient Organisation · 21:27 (1287s)
PFS, PAS, PSSD mechanism theory; Powers' unifying model; vulnerability screening
ARARID1ACHD8HDAC10YT-iWFDBRTgT3g2026-04-29PFSPSSDPRSDCore corpus - Timeline event
Richest primary source on his mature model: androgen-metabolism genomes 'broken at baseline,' glucuronidation-defect selection bias, three phenotypes (neurosteroid vs androgenic-silencing), window/crash dynamics, chemical-castration trials, epigenetic genes…
ARID1ACHD8HDAC10TL-2026-04-29-powers-summit-interview-uploaded-recorded-at-2026-pfs2026-04-29PFSPSSDPRSDCore corpus - 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 - Powers · Reddit commentCurated Powers pick
Re: Im going to be taking the week off next week to…
u/drwillpowers · r/DrWillPowers
Replying to a post-letrozole case with PFS-identical symptoms (a Klinefelter patient), Powers frames PFS and PSSD as the same mechanism in different flavors — inborn metabolic error plus drug, with recovery blocked by an epigenetic glitch — and notes…
ARID1AHDAC10KDM6APRH-15042026-04-19T00:13:31ZPFSPSSDPowers Reddit history - Glossary term
ARID1A / CHD8 / HDAC10
epigenetic
Chromatin-remodeling/epigenetic-regulator genes that Powers reports recurring across PFS patient genomes in his summit interview — offered as candidate genetic-susceptibility loci for post-drug syndromes, pending formal publication.
ARID1ACHD8HDAC10GL-arid1a-chd8-hdac10PFSCore corpus - Gene recordPowers’ theory
ATP-dependent chromatin-remodeling enzyme of the CHD family (SNF2-like ATPase plus chromodomains); regulates transcription both up and down depending on recruited cofactors, interacting with beta-catenin/Wnt signaling, p53, CTCF, and histone-methylation…
ARID1ACHD8CTCFHDAC10GENE-CHD8PFSCore corpus - Gene recordPowers’ theory
HDAC10 — histone deacetylase 10
22q13.33
Class IIb histone deacetylase that removes acetyl groups from lysine residues on core histones (and polyamines such as N8-acetylspermidine), producing a tag for epigenetic repression; acts in large multiprotein complexes to regulate transcription, cell-cycle…
ARARID1ACHD8HDAC10GENE-HDAC10PFSCore corpus - Gene recordPowers’ theory
Rate-limiting enzyme of folate metabolism that converts 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, the methyl donor for remethylating homocysteine to methionine and ultimately producing S-adenosylmethionine - the universal methyl donor for…
ARID1ACHD8HDAC10MTHFRGENE-MTHFRPFSCore corpus
Also in epigenetic regulation
All 130 genes- HDAC10Powers
histone deacetylase 10
chr 22· Epigenetic regulation· 11 records - CHD8Powers
chromodomain helicase DNA binding protein 8
chr 14· Epigenetic regulation· 9 records - CHD4
chromodomain helicase DNA binding protein 4
chr 12· Epigenetic regulation· 1 record - CHD5
chromodomain helicase DNA binding protein 5
chr 1· Epigenetic regulation· 1 record - CHD6
chromodomain helicase DNA binding protein 6
chr 20· Epigenetic regulation· 1 record - CHD7
chromodomain helicase DNA binding protein 7
chr 8· Epigenetic regulation· 1 record - CHD9
chromodomain helicase DNA binding protein 9
chr 16· Epigenetic regulation· 1 record - CREBBP
CREB binding lysine acetyltransferase
chr 16· Epigenetic regulation· 1 record
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