EZH2 Blocking Peptide
- Known as:
- EZH2 Blocking Peptide
- Catalog number:
- 3242BP-50
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- Biovis
- Gene target:
- EZH2 Blocking Peptide
Related genes to: EZH2 Blocking Peptide
- Gene:
- EZH2 NIH gene
- Name:
- enhancer of zeste 2 polycomb repressive complex 2 subunit
- Previous symbol:
- -
- Synonyms:
- EZH1, ENX-1, KMT6, KMT6A
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-12-21
- Date modifiied:
- 2019-04-23
Related products to: EZH2 Blocking Peptide
Related articles to: EZH2 Blocking Peptide
- Occupational pesticide exposure is a significant environmental health concern associated with genomic instability. Histone methyltransferases including SMYD2, SMYD3, EZH2, and SETD8 participate in chromatin regulation and DNA damage responses, but their transcriptional profiles in exposed populations remain poorly understood. To evaluate chromosomal instability and expression of histone methyltransferase genes in agricultural workers. A cross-sectional biomonitoring study included 137 participants classified as directly exposed (n = 62), indirectly exposed (n = 41), or putative non-exposed (n = 34). Buccal epithelial cells were collected for micronucleus (MN) analysis and gene expression profiling. Relative mRNA expression levels of SMYD2, SMYD3, EZH2, and SETD8 were quantified by RT-qPCR. Statistical analyses included ANOVA, correlation analyses, and multivariable regression models. MN frequency increased significantly according to exposure status, with directly exposed workers exhibiting the highest levels of chromosomal damage (7.0 ± 1.2 MN/2000 cells), followed by indirectly exposed individuals (3.9 ± 1.0 MN/2000 cells) and putative non-exposed participants (2.1 ± 0.6 MN/2000 cells) (p < 0.001). Consistent use of personal protective equipment was associated with lower MN frequencies among directly exposed workers (p < 0.001). Gene expression analyses demonstrated increased EZH2 and SETD8 expression in exposed groups, whereas SMYD3 exhibited greater transcriptional variability than SMYD2. Significant positive correlations between MN frequency and expression levels of EZH2, SETD8, SMYD3, and SMYD2 were observed among directly exposed workers (all p < 0.05). Chronic occupational pesticide exposure is associated with chromosomal instability and altered expression of genes involved in chromatin regulation. These findings support their utility as potential exposure biomarkers. - Source: PubMed
Rodrigues Renato Arthur FrancoFernandes Eduardo VignotoBocchi MayaraNeto Fermino Sanches Lizartede Oliveira Fábio Morato - Polycomb Repressive Complex 2 (PRC2), containing homologous EZH1 or EZH2 as the catalytic subunit, is a conserved methyltransferase complex that represses gene transcription by transferring methyl group from SAM to H3K27. Gain-of-function mutations of EZH2 and aberrant H3K27 methylation have been linked to human cancers. SAM-competitive EZH1 and EZH2 dual inhibitors have been approved by the FDA for treating B-cell lymphoma and other cancers. Here, we characterized a small molecule C36, which potently inhibits EZH2/PRC2, but not EZH1/PRC2, with a novel SAM non-competitive mechanism. Cryo-EM structures revealed that C36 binds to a pocket at the interface of SET-Activation-Loop (SAL), stimulation-responsive motif (SRM), and I-SET domain of EZH2, and WD40 domain of EED. C36 binding induces conformational changes and disrupts allosteric communication between EZH2 and ligand-bound EED. C36 efficiently inhibits H3K27 trimethylation and PRC2 target gene expression in tumor cells and xenograft tumors with low hematotoxicity. Multi-omics analyses employing C36 uncovered the direct regulation of IFNB1 by EZH2/PRC2. The combined treatment of syngeneic LLC lung cancer with C36 and a PD-1 antibody significantly enhances anti-tumor efficacy. Our study identifies a new allosteric mechanism of PRC2 inhibition and paves the way for the development of highly selective EZH2/PRC2 inhibitors for combination therapy. - Source: PubMed
Publication date: 2026/06/18
Cao TingLiu DongdongGao HaishanQin ChenyangZhang WenLu ZiyunTan DongxiaQu YuxiuLiu YusongZou ZhiranYu HongtaoQi Wei - Castration-resistant prostate cancer (CRPC) lethality arises from epigenetic-driven resistance to androgen deprivation therapy (ADT). Here, we uncover a compensatory epigenetic switch between DNA methylation and H3K27me3-mediated repression as a critical barrier to epigenetic therapy in CRPC. Integrative multiomics analyses reveal that DNMT inhibitors (DNMTis) trigger EZH2-dependent H3K27me3 accumulation at the ADAMTS1 locus-a master collagenase essential for extracellular matrix (ECM) remodeling-perpetuating fibrotic niche formation and therapy resistance. Dual targeting of DNMTs and EZH2 disrupts this epigenetic plasticity, synergistically reactivating ADAMTS1 to degrade collagen-rich stroma, suppress FAK/MAPK mechanotransduction signaling, and reverse epithelial-mesenchymal transition (EMT). Crucially, in immunocompetent models, this strategy achieves >90% tumor suppression and reverses immunosuppression by enhancing cytotoxic CD8 T cell infiltration 11.4-fold while depleting immunosuppressive macrophages and Tregs. Mechanistically, dual therapy inactivates the FAK/MAPK/EMT axis via ADAMTS1-mediated ECM degradation, overcoming stromal-mediated resistance. Our work establishes epigenetic-ECM coevolution as a hallmark of CRPC and provides a rationally designed combination therapy to dismantle the therapy-resistant niche. - Source: PubMed
Publication date: 2026/06/18
Wu XiangSong XiaoyiLi BoYang YuchunLi KunyuZhu JunLi YaweiYang XinmingDai YingboZhang Zhuangzhuang - RUNX1 is one of the most commonly mutated genes in myelodysplastic neoplasms (MDS) and essential for hematopoiesis. However, clinical phenotype features of RUNX1 mutated patients and the interaction between RUNX1 and other genes mutations remains incompletely explored. We enrolled 1473 consecutive adult patients with primary MDS to investigate the laboratory, genomic characteristics, and survival of RUNX1-mutated MDS subjects. We found that RUNX1 mutations are associated with older age (median, 59 vs. 56 years, p = 0.007), lower platelet counts (median, 50 × 10/L vs. 66 × 10/L; p < 0.001), higher bone marrow blasts (median, 6.0% vs. 2.5%, p < 0.001) and a higher proportion of micro-megakaryocytes (median, 26.0% vs. 18.7%, p < 0.001). Additionally, our data showed a correlation between the variant allele frequency (VAF) of RUNX1 mutations and proportion of micro-megakaryocytes (r = 0.242, p = 0.006), suggesting RUNX1 mutations burden was associated with dysmegakaryopoiesis. Mutations in ASXL1, SRSF2, EZH2 and NRAS were significantly more frequent in RUNX1-mutated patients compared with those without RUNX1 mutations (adjusted p < 0.05). RUNX1-mutated patients exhibited poorer overall survival (median OS 18 months vs. 51 month, p < 0.001), while U2AF1 co-mutations were associated with a relatively better prognosis (median OS 34 months vs. 17 months, p = 0.003), indicating a potential modifying effect of U2AF1 on the outcome of RUNX1-mutated patients. - Source: PubMed
Liu LinlinLi BingQin TiejunXu ZefengQu ShiqiangPan LijuanGao QingyanJiao MengBao ZefeiLiu NingningJia YujiaoLi ChengwenXiao Zhijian - - Source: PubMed
Huo YanqingLi QingboWang XiqianJiao XiejiaZheng JiachunLi ZhiqiangPan Xiaohan