RSF1
remodeling and spacing factor 1
Pathway candidate — not linked to PFS or PSSD by any record here
Gene summary
A protein-coding gene on chromosome 11 (epigenetic regulation). Encodes a nuclear protein that interacts with hepatitis B virus X protein (HBX) and facilitates transcription of hepatitis B virus genes by the HBX transcription activator, suggesting a role for this interaction in the virus life cycle. This protein also interacts with SNF2H protein to form the RSF chromatin-remodeling complex, where the SNF2H subunit functions as the nucleosome-dependent ATPase, and this protein as the histone chaperone.
Source: NCBI Gene, accessed 2026-10-07.
Protein reference (UniProt)
- Protein
Remodeling and spacing factor 1
- Function (excerpt)
Regulatory subunit of the ATP-dependent RSF-1 and RSF-5 ISWI chromatin-remodeling complexes, which form ordered nucleosome arrays on chromatin and facilitate access to DNA during DNA-templated processes such as DNA replication, transcription, and repair. Binds to core histones together with SMARCA5, and is required for the assembly of regular nucleosome arrays by the RSF-5 ISWI chromatin-remodeling complex. Directly stimulates the ATPase activity of SMARCA1 and SMARCA5 in the RSF-1 and RSF-5 ISWI chromatin-remodeling complexes, respectively. The RSF-1 ISWI chromatin remodeling complex has a lower ATP hydrolysis rate than the RSF-5 ISWI chromatin-remodeling complex. The complexes do not have the ability to slide mononucleosomes to the center of a DNA template. Facilitates transcription of hepatitis B virus (HBV) genes by the pX transcription activator. In case of infection by HBV, together with pX, it represses TNF induced NF-kappa-B transcription activation.
- Subcellular location
Nucleus.
- Tissue specificity
Ubiquitously expressed. Highly expressed in the heart, skeletal muscle, kidney and placenta. Expressed at low levels in the brain and colon.
Source: UniProtKB/Swiss-Prot Q96T23, 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 RSF1 specifically.
Mentioned in 0 corpus records
No corpus record names RSF1 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- HDAC10Powers
histone deacetylase 10
chr 22· Epigenetic regulation· 11 records - ARID1APowers
AT-rich interaction domain 1A
chr 1· Epigenetic regulation· 10 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
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