DNMT3B
DNA methyltransferase 3 beta
Pathway candidate — not linked to PFS or PSSD by any record here
Gene summary
A protein-coding gene on chromosome 20 (epigenetic regulation). CpG methylation is an epigenetic modification that is important for embryonic development, imprinting, and X-chromosome inactivation. Studies in mice have demonstrated that DNA methylation is required for mammalian development.
Source: NCBI Gene, accessed 2026-10-07.
Protein reference (UniProt)
- Protein
DNA (cytosine-5)-methyltransferase 3B
- Function
Required for genome-wide de novo methylation and is essential for the establishment of DNA methylation patterns during development. DNA methylation is coordinated with methylation of histones. May preferentially methylates nucleosomal DNA within the nucleosome core region. May function as transcriptional co-repressor by associating with CBX4 and independently of DNA methylation. Seems to be involved in gene silencing (By similarity). In association with DNMT1 and via the recruitment of CTCFL/BORIS, involved in activation of BAG1 gene expression by modulating dimethylation of promoter histone H3 at H3K4 and H3K9. Isoforms 4 and 5 are probably not functional due to the deletion of two conserved methyltransferase motifs. Functions as a transcriptional corepressor by associating with ZHX1. Required for DUX4 silencing in somatic cells.
- Subcellular location
Nucleus.
- Tissue specificity
Ubiquitous; highly expressed in fetal liver, heart, kidney, placenta, and at lower levels in spleen, colon, brain, liver, small intestine, lung, peripheral blood mononuclear cells, and skeletal muscle. Isoform 1 is expressed in all tissues except brain, skeletal muscle and PBMC, 3 is ubiquitous, 4 is expressed in all tissues except brain, skeletal muscle, lung and prostate and 5 is detectable only in testis and at very low level in brain and prostate.
- Associated conditions
Immunodeficiency-centromeric instability-facial anomalies syndrome 1 (ICF1); Facioscapulohumeral muscular dystrophy 4, digenic (FSHD4).
Source: UniProtKB/Swiss-Prot Q9UBC3, 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 DNMT3B specifically.
Mentioned in 0 corpus records
No corpus record names DNMT3B 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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