Loading
KMT2B (Histone-lysine N-methyltransferase 2B) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a drug target, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Hepatocellular carcinoma, Vulvar cancer, Melanoma and 1 more.
Histone methyltransferase that catalyses 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.
CIViC holds 2 clinical evidence items and 0 assertions across 1 variant, naming Immune Checkpoint Inhibitor. IntOGen calls it a driver in 2 cohorts (0 activating, 2 loss-of-function), covering Hepatocellular Carcinoma, Vulva/Vagina.
In plain words · KMT2B (Histone-lysine N-methyltransferase 2B) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a drug target, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Hepatocellular carcinoma, Vulvar cancer, Melanoma and 1 more.
KMT2B (Histone-lysine N-methyltransferase 2B) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a drug target, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Hepatocellular carcinoma, Vulvar cancer, Melanoma and 1 more.
Histone methyltransferase that catalyses 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.
No product in this corpus aims at KMT2B yet. Because the protein is lost rather than overactive, drugs either restore its function or exploit the weakness its loss leaves (synthetic lethality).
Tumour-specific alteration: the catalogues call it a tumour suppressor (IntOGen finds it knocked out more often than chance); what a medicine would aim at or exploit is the altered form or its loss, absent from normal cells; no corpus medicine is aimed at it yet. HPA KMT2B: RNA low tissue specificity; no normal tissue stained high. Distribution: 4 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Hepatocellular carcinoma, Vulvar cancer, Skin cancer (all types), Lung cancer (all types)); Open Targets associates it with 0 specific cancer types at or above 0.5. (Rule 6 of scripts/fetch-target-specificity.ts.)
Sources: UniProt Q9UMN6; CIViC gene KMT2B; IntOGen KMT2B; Human Protein Atlas KMT2B tissue; Open Targets ENSG00000272333 associations
First described 1997. Earliest sequence paper UniProt cites for the protein: Nagase et al, DNA Res, 1997, "Prediction of the coding sequences of unidentified human genes. VII. The complete sequences of 100 new cDNA clones from brain which can code for large proteins in vitro". Source.
Sources: HGNC HGNC:15840 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt Q9UMN6 (protein name, function text, keywords and locations (REST API)); CIViC gene KMT2B (2 evidence items, 0 assertions, 1 variants; diseases: Melanoma, Lung Non-small Cell Carcinoma (GraphQL API, CC0)); IntOGen KMT2B (driver in 2 cohorts (Act 0, LoF 2); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Histone methyltransferase that catalyses 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. 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. Location: Nucleus (UniProt). Locus 19q13.12 (HGNC).
RNA: low tissue specificity, detected in all normal tissues.
No normal tissue stained high.
No cancer sample stained medium or high.
Human Protein Atlas version 25.1, antibody staining at reliability approved, enhanced or supported; used under CC BY-SA 3.0. Staining counts are patients per level in the atlas cohort, not population prevalence.
Query for this target: (TITLE:"KMT2B" OR ABSTRACT:"KMT2B" OR TITLE:"lysine methyltransferase 2B" OR ABSTRACT:"lysine methyltransferase 2B" OR TITLE:"Histone-lysine N-methyltransferase 2B" OR ABSTRACT:"Histone-lysine N-methyltransferase 2B" OR TITLE:"KIAA0304" OR ABSTRACT:"KIAA0304" OR TITLE:"MLL2" OR ABSTRACT:"MLL2" OR TITLE:"TRX2" OR ABSTRACT:"TRX2") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about KMT2B, not a curated reading list.
Shares Vulvar cancer, IntOGen.
Shares Vulvar cancer, Hepatocellular carcinoma, IntOGen.
Shares Vulvar cancer, IntOGen, Non-small-cell lung cancer.
Shares Vulvar cancer, IntOGen.
Shares Vulvar cancer, Melanoma.
Shares Vulvar cancer, Melanoma.
Shares Vulvar cancer, Melanoma.