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KDMs in Epigenetics and Disease
Lysine Demethylase Enzymes (KDMs) are enzymes that remove methyl groups from lysine residues on histone and other proteins. Lysine methylation is a key epigenetic mark that, depending on its site and degree, can either activate or repress gene expression. KDMs are divided into two major classes:
- FAD-dependent KDMs (LSD family): For example, KDM1A (LSD1) uses FAD as a cofactor and typically removes mono- or dimethyl marks.
- JmjC domain-containing KDMs (KDM2–KDM7 families): These require Fe²⁺ and 2-oxoglutarate as cofactors and can remove mono-, di-, and trimethyl marks.
| Protein / Family | Epigenetic Function | Disease Association | Key Publications | Key Products |
|---|---|---|---|---|
| Androgen Receptor | Transcription factor. Recruits KDM1A/KDM4 to remodel chromatin. | Prostate cancers | Nataraj et al., Cell. Mol. Gastroenterol. Hepatol. 2025. | |
| Estrogen Receptor | Transcription Factors and histone acetyltransferases (p300/CBP), histone deacetylases (HDACs), and lysine demethylases ( KDM1A/LSD1, KDM4 family) to modulate chromatin structure. | Breast cancer, endometrial cancer, osteoporosis and cardiovascular disease. | Liu et al., Cell Death Disc 2025. | |
| Interactors (e.g., HDAC1/2, CTBP1, RBBP4/7) | Coregulators or scaffolds with KDMs (not demethylases). Modulate chromatin accessibility and transcription complexes. | Broadly implicated in cancer and aging. | Cursaeo et al., ChemMed. 2024. |
Antibodies
Proteins Kits |
| KDM1A (LSD1) | Flavin-dependent lysine demethylase, Demethylates H3K4me1/2 and H3K9me1/2, and modulates transcriptional repression/activation. | Multiple cancers ( prostate, breast), neurodevelopmental disorders. | Martin-Gonzalez et al., Cell Rep. 2025 | |
| KDM1B (LSD2) | LSD family, similar catalytic mechanism to KDM1A. Demethylates H3K4me1/2 and H3K9me1/2. | Overexpression/mutation in cancers (bladder, ovarian, melanoma). | Gacek-Matthews et al., PLoS Genet. 2016 | |
| KDM2A (FBXL11) | JmjC domain demethylase. Part of FBXL family. H3K36me1/2 demethylase. Affects transcription elongation and chromatin structure | Gastric cancer, breast cancer, and others. | Sultana et al., Science Direct. 2026. | |
| KDM2B (FBXL10) | JmjC, demethylates H3K36me2 and H3K4me3. Regulates ribosomal gene repression and cell growth control. | AML (leukemia), and solid tumors. | Yan et al., AMJ Transl Res. 2018. | |
| KDM6A (UTX) | Part of chromatin remodeling. Removes repressive H3K27 methyl marks, enabling gene activation. | Kabuki syndrome, and cancer. | Tran et al., Mol. Cell. Biol. 2020 | |
| KDM7A / PHF8 & KDM7B / PHF8 & KDM7C / PHF2 | KDM7 subfamily. Multifunctional demethylases. Disrupted chromatin recognition and demethylation affects target gene regulation during development. | Mental retardation syndromes; cancer. | Fan et al., Epigenomes. 2024 Liu et al., CIMB. 2025 |
|
| MYC | Interacts with multiple KDMs to regulate proliferation | Most frequently dysregulated oncogenes in human cancers, including breast, lung, colorectal, lymphoma, and many others. | Santarelli et al., Molecules. 2025 | |
| p53 | Functional interactions with KDM1A, KDM5, and KDM6 family members | Various cancers (lung, breast, colorectal, ovarian, liver. | Paluszczak et al., Cancers. 2025 | |
| RCOR1 / CoREST | Scaffold protein; essential for KDM1A/LSD1 activity. Partners with KDM1A to demethylate histone marks and repress transcription. | Involved in cancers and neurological disorders. | Kalin et al., Nat. Commun. 2018. | |
| SIN3A | Transcriptional corepressor scaffold. Switch independent transcription regulator family member. | Cancers, neurodevelopmental disorders, and metabolic disorders. | Monziani et al.., Nucleic Acids Res. 2025. |
Additional Resources
- [Blog] KDM5 Inhibitors: A Potential Tumor-specific Epigenetic Therapy that Functions through Viral Mimicry
- [Blog] The Critical Role of Iron Metabolism in KDM3A-mediated Epigenetic Determination of Male Sex
