Ask about this productRelated genes to: EHMT2 Blocking Peptide
- Gene:
- EHMT2 NIH gene
- Name:
- euchromatic histone lysine methyltransferase 2
- Previous symbol:
- C6orf30, BAT8
- Synonyms:
- G9A, Em:AF134726.3, NG36/G9a, KMT1C
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-09
- Date modifiied:
- 2016-10-05
Related products to: EHMT2 Blocking Peptide
Related articles to: EHMT2 Blocking Peptide
- DNA methylation plays a key role in mediating the anti-aging effects of glucose-lowering drugs. This study aims to systematically explore the potential anti-aging effects of target genes of FDA-approved glucose-lowering drugs and the underlying epigenetic mediators. - Source: PubMed
Publication date: 2026/05/21
Sun YuqiZheng HaonanHuang LanhuiMa MinGu RongrongWang ManqingFang SiSun YangboYang QianBi YufangZheng Jie - 5-Fluorouracil (5-FU) is a first-line chemotherapy commonly used to treat colorectal cancer (CRC). However, the development of acquired resistance to 5-FU remains a significant clinical challenge, and the underlying epigenetic mechanisms are not fully understood. In this study, we demonstrate that euchromatic histone lysine methyltransferase 2 (EHMT2) is significantly upregulated in CRC patients with poor responses to 5-FU, directly correlating with lower overall survival rates. Using established 5-FU resistant (5-FUR) HCT116 and HT29 cell lines, RNA-sequencing confirmed robust EHMT2 overexpression compared with wild-type cells. Mechanistically, siRNA-mediated knockdown of EHMT2 restored 5-FU sensitivity by upregulating protein phosphatase 1B (PPM1B), a key downstream target. This EHMT2-PPM1B axis disruption effectively induced G1 phase cell cycle arrest and triggered apoptosis in 5-FUR cells, fundamentally impairing their proliferation. Furthermore, we validated the therapeutic potential of targeting this pathway using in vivo and ex vivo models. Combination treatment with 5-FU and the specific pharmacological EHMT2 inhibitor (BIX-01294) synergistically suppressed tumor growth in a 5-FUR cell-derived xenograft mouse model. Importantly, these therapeutic effects were faithfully recapitulated in 5-FUR patient-derived colorectal cancer organoid (PDO) models. Together, our findings elucidate a critical epigenetic mechanism where EHMT2 promotes 5-FU drug resistance. Targeting EHMT2 represents a promising and translatable therapeutic strategy for overcoming chemoresistance and improving clinical outcomes in CRC patients. - Source: PubMed
Publication date: 2026/05/18
Tae In HwanKang YunsangLee JinkwonLee Jeong MinKim JinsanLee Su-GiPark KunhyangRyu Tae YoungKim KwanghoKim GyeonghwaSon TaesangLee Hye WonKim SolbiLee Hyo JinJung Cho-RokLim Jung HwaLee Moo-SeungHur KeunHan Tae-SuKim Dae-SooSon Mi-YoungCho Hyun-Soo - This study investigated the antitumor effects of BIX01294, a pharmacological inhibitor of euchromatic histone-lysine N-methyltransferase 2 (EHMT2), in retinoblastoma and explored the underlying mechanisms. EHMT2 expression was evaluated using Gene Expression Profiling Interactive Analysis (GEPIA), human retinoblastoma specimens, publicly available Gene Expression Omnibus (GEO) datasets, and cultured cell lines. Cell proliferation was assessed using Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) incorporation assays. Cell cycle distribution and apoptosis were analysed by flow cytometry. RNA sequencing (RNA-seq), quantitative real-time polymerase chain reaction (qRT-PCR), and western blotting were performed to investigate downstream molecular changes. An orthotopic xenograft model was established to assess the in vivo pharmacological effects of BIX01294. EHMT2 was upregulated in retinoblastoma tissues and in retinoblastoma cell lines. BIX01294 reduced EHMT2 expression, inhibited proliferation, induced apoptosis, and caused cell cycle arrest, accompanied by downregulation of cyclin A, cyclin-dependent kinase 2 (CDK2), cyclin B, and phosphorylated cell division cycle 2 (p-CDC2). Under the same 48 h treatment conditions, ARPE-19 cells showed minimal changes in viability and no obvious alterations in apoptosis or cell-cycle distribution, supporting a degree of pharmacological selectivity. Transcriptomic profiling and protein analysis indicated that BIX01294 treatment was associated with attenuation of mitogen-activated protein kinase (MAPK) signalling. In the orthotopic xenograft model, BIX01294 reduced tumour burden and Ki-67 staining. These findings support EHMT2 as a potential pharmacological target in retinoblastoma; however, additional mechanistic studies are required to define the causal link between EHMT2 inhibition and MAPK pathway modulation. - Source: PubMed
Publication date: 2026/05/12
Chen YijiaLiu JingchaoChen TingtingZhang YanyanYao ChunyueChen ShuyiHuang Guofu - Simian immunodeficiency viruses (SIVs) have crossed from apes to humans at least four times, but only one event gave rise to the AIDS pandemic. The host barriers that pandemic HIV-1 group M () strains overcame to spread efficiently in humans remain poorly understood. To identify such barriers, we performed CRISPR-Cas9 screens driven by the replication efficiency of SIVcpz, the chimpanzee precursor of HIV-1. Guide RNA libraries targeting more than 500 human genes encoding potential antiviral factors were inserted into the replication-competent SIVcpz MB897 molecular clone, which is phylogenetically closely related to HIV-1 group M strains. Propagation in Cas9-expressing human SupT1 T cells significantly enriched for sgRNAs targeting and . These hits only partially overlapped with those identified in analogous HIV-1-based screens, indicating virus-specific restriction profiles. Functional analyses confirmed that IFITM2 (interferon-induced transmembrane protein 2), PCED1B (PC-esterase domain-containing protein 1B), MEFV (Mediterranean fever protein, pyrin/TRIM20), and AXIN1 (Axis inhibition protein 1) restrict replication of the analyzed SIVcpz strains but not HIV-1 group M strains in primary human CD4 T cells. These findings reveal previously unrecognized host factors that limit SIVcpz replication in human cells and highlight barriers that at least some HIV-1 group M strains overcame during adaptation for pandemic spread. - Source: PubMed
Publication date: 2026/05/07
Xie QinyaWang QingxingNoettger SabrinaGosálbez GuillermoBetzler Annika CVolcic MetaKmiec DorotaKrebs StefanGraf AlexanderGülensoy DilaWeidinger GilbertSparrer Konstantin M JKirchhoff Frank - Extensive evidence suggests overlapping pathological mechanisms in the brain of individuals with Parkinson's disease dementia, Down syndrome dementia, and Alzheimer's disease. For these neurodegenerative dementias, we observed that the chronological age did not align with their biological age, which was determined based on hippocampal transcript levels (i.e., transcriptional age). Subsequently, we performed a transcriptomic analysis that corrected for the transcriptional age in the hippocampus of affected individuals, highlighting common underlying pathogenic mechanisms. There were 45 common differentially expressed genes (DEGs), whereas enriched functional terms were related to lysine -methyltransferase activity and intermediate filament. Co-expression network analysis displayed a module that was significantly downregulated in the non-demented control group only. This module identified and as hub genes, which were also common DEGs. Overall, these findings uncover shared functional insights in the hippocampus, while specifically highlighting and as potential universal biomarkers or disease-altered targets across neurodegenerative dementias. - Source: PubMed
Publication date: 2026/04/29
Crans René A JFructuoso MartaBascón-Cardozo KarenRecaioglu HaticeSotelo-Fonseca JesusVermeiren YannickStrydom AndréVan Dam DebbyDe Deyn Peter PRodríguez-Martín BernardoPotier Marie-ClaudeDierssen Mara