Pathway candidateNCBI-verifiedprotein-coding

SETD2

SET domain containing 2, histone lysine methyltransferase

NCBI Gene: 29072 Ensembl GeneCards UniProt: Q9BYW2

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

SETD2 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 SETD2 is not, by itself, evidence of anything related to post-drug syndromes.

Gene summary

A protein-coding gene on chromosome 3 (epigenetic regulation). Huntington's disease (HD), a neurodegenerative disorder characterized by loss of striatal neurons, is caused by an expansion of a polyglutamine tract in the HD protein huntingtin. This gene encodes a protein belonging to a class of huntingtin interacting proteins characterized by WW motifs.

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

Protein reference (UniProt)

Protein: Histone-lysine N-methyltransferase SETD2
Function (excerpt): Histone methyltransferase that specifically trimethylates 'Lys-36' of histone H3 (H3K36me3) using dimethylated 'Lys-36' (H3K36me2) as substrate. It is capable of trimethylating unmethylated H3K36 (H3K36me0) in vitro. Represents the main enzyme generating H3K36me3, a specific tag for epigenetic transcriptional activation (By similarity). Plays a role in chromatin structure modulation during elongation by coordinating recruitment of the FACT complex and by interacting with hyperphosphorylated POLR2A. Acts as a key regulator of DNA mismatch repair in G1 and early S phase by generating H3K36me3, a mark required to recruit MSH6 subunit of the MutS alpha complex: early recruitment of the MutS alpha complex to chromatin to be replicated allows a quick identification of mismatch DNA to initiate the mismatch repair reaction.
Subcellular location: Nucleus; Chromosome.
Tissue specificity: Ubiquitously expressed.
Associated conditions: Renal cell carcinoma (RCC); Luscan-Lumish syndrome (LLS); Leukemia, acute lymphoblastic (ALL); Leukemia, acute myelogenous (AML); Intellectual developmental disorder, autosomal dominant 70 (MRD70); Rabin-Pappas syndrome (RAPAS).

Source: UniProtKB/Swiss-Prot Q9BYW2, 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 SETD2 specifically.

Mentioned in 0 corpus records

No corpus record names SETD2 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 SETD2
Function (excerpt): Histone methyltransferase that specifically trimethylates 'Lys-36' of histone H3 (H3K36me3) using dimethylated 'Lys-36' (H3K36me2) as substrate. It is capable of trimethylating unmethylated H3K36 (H3K36me0) in vitro. Represents the main enzyme generating H3K36me3, a specific tag for epigenetic transcriptional activation (By similarity). Plays a role in chromatin structure modulation during elongation by coordinating recruitment of the FACT complex and by interacting with hyperphosphorylated POLR2A. Acts as a key regulator of DNA mismatch repair in G1 and early S phase by generating H3K36me3, a mark required to recruit MSH6 subunit of the MutS alpha complex: early recruitment of the MutS alpha complex to chromatin to be replicated allows a quick identification of mismatch DNA to initiate the mismatch repair reaction.
Subcellular location: Nucleus; Chromosome.
Tissue specificity: Ubiquitously expressed.
Associated conditions: Renal cell carcinoma (RCC); Luscan-Lumish syndrome (LLS); Leukemia, acute lymphoblastic (ALL); Leukemia, acute myelogenous (AML); Intellectual developmental disorder, autosomal dominant 70 (MRD70); Rabin-Pappas syndrome (RAPAS).