Pathway candidateNCBI-verifiedprotein-coding

SETD1A

SET domain containing 1A, histone lysine methyltransferase

NCBI Gene: 9739 Ensembl GeneCards UniProt: O15047

Pathway candidate — not linked to PFS or PSSD by any record here

SETD1A is in the library because it belongs to the epigenetic regulation family. No study, report or commentary in the corpus names it, so a variant in SETD1A is not, by itself, evidence of anything related to post-drug syndromes.

Gene summary

A protein-coding gene on chromosome 16 (epigenetic regulation). The protein encoded by this gene is a component of a histone methyltransferase (HMT) complex that produces mono-, di-, and trimethylated histone H3 at Lys4. Trimethylation of histone H3 at lysine 4 (H3K4me3) is a chromatin modification known to generally mark the transcription start sites of active genes.

Source: NCBI Gene, accessed 2026-10-07.

Protein reference (UniProt)

Protein: Histone-lysine N-methyltransferase SETD1A
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, forms H3K4me1, H3K4me2 and H3K4me3 methylation marks at active chromatin sites where transcription and DNA repair take place. Responsible for H3K4me3 enriched promoters and transcriptional programming of inner mass stem cells and neuron progenitors during embryogenesis (By similarity). Required for H3K4me1 mark at stalled replication forks. Mediates FANCD2-dependent nucleosome remodeling and RAD51 nucleofilaments stabilization at reversed forks, protecting them from nucleolytic degradation. Does not methylate 'Lys-4' of histone H3 if the neighboring 'Lys-9' residue is already methylated. Binds RNAs involved in RNA processing and the DNA damage response.
Subcellular location: Nucleus speckle; Chromosome; Cytoplasm.
Associated conditions: Epilepsy, early-onset, 2, with or without developmental delay (EPEO2); Neurodevelopmental disorder with speech impairment and dysmorphic facies (NEDSID).

Source: UniProtKB/Swiss-Prot O15047, 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 SETD1A specifically.

Mentioned in 0 corpus records

No corpus record names SETD1A 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

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Gene summary

Source: NCBI Gene, accessed 2026-10-07.

Protein reference (UniProt)

Protein: Histone-lysine N-methyltransferase SETD1A
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, forms H3K4me1, H3K4me2 and H3K4me3 methylation marks at active chromatin sites where transcription and DNA repair take place. Responsible for H3K4me3 enriched promoters and transcriptional programming of inner mass stem cells and neuron progenitors during embryogenesis (By similarity). Required for H3K4me1 mark at stalled replication forks. Mediates FANCD2-dependent nucleosome remodeling and RAD51 nucleofilaments stabilization at reversed forks, protecting them from nucleolytic degradation. Does not methylate 'Lys-4' of histone H3 if the neighboring 'Lys-9' residue is already methylated. Binds RNAs involved in RNA processing and the DNA damage response.
Subcellular location: Nucleus speckle; Chromosome; Cytoplasm.
Associated conditions: Epilepsy, early-onset, 2, with or without developmental delay (EPEO2); Neurodevelopmental disorder with speech impairment and dysmorphic facies (NEDSID).