KMT2B
lysine methyltransferase 2B
Pathway candidate — not linked to PFS or PSSD by any record here
Gene summary
A protein-coding gene on chromosome 19 (epigenetic regulation). Encodes a protein which contains multiple domains including a CXXC zinc finger, three PHD zinc fingers, two FY-rich domains, and a SET (suppressor of variegation, enhancer of zeste, and trithorax) domain. The SET domain is a conserved C-terminal domain that characterizes proteins of the MLL (mixed-lineage leukemia) family.
Source: NCBI Gene, accessed 2026-10-07.
Protein reference (UniProt)
- Protein
Histone-lysine N-methyltransferase 2B
- Function
Histone methyltransferase that catalyzes methyl group transfer from S-adenosyl-L-methionine to the epsilon-amino group of 'Lys-4' of histone H3 (H3K4) via a non-processive mechanism. Part of chromatin remodeling machinery predominantly forms H3K4me1 and H3K4me2 methylation marks at active chromatin sites where transcription and DNA repair take place. Likely plays a redundant role with KMT2C in enriching H3K4me1 marks on primed and active enhancer elements. Plays a central role in beta-globin locus transcription regulation by being recruited by NFE2. Plays an important role in controlling bulk H3K4me during oocyte growth and preimplantation development (By similarity). Required during the transcriptionally active period of oocyte growth for the establishment and/or maintenance of bulk H3K4 trimethylation (H3K4me3), global transcriptional silencing that preceeds resumption of meiosis, oocyte survival and normal zygotic genome activation (By similarity).
- Subcellular location
Nucleus.
- Tissue specificity
Widely expressed. Highest levels in testis. Also found in brain with higher expression in the cerebellum than in any other region, bone marrow, heart, muscle, kidney, placenta, spleen, thymus, prostate, ovary, intestine, colon, peripheral blood lymphocytes and pancreas. Often amplified in pancreatic carcinomas.
- Associated conditions
Dystonia 28, childhood-onset (DYT28); Intellectual developmental disorder, autosomal dominant 68 (MRD68).
Source: UniProtKB/Swiss-Prot Q9UMN6, 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 KMT2B specifically.
Mentioned in 0 corpus records
No corpus record names KMT2B 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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