Ask about this productRelated genes to: SMYD2 Blocking Peptide
- Gene:
- SMYD2 NIH gene
- Name:
- SET and MYND domain containing 2
- Previous symbol:
- -
- Synonyms:
- HSKM-B, ZMYND14, KMT3C
- Chromosome:
- 1q32.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-28
- Date modifiied:
- 2014-11-19
Related products to: SMYD2 Blocking Peptide
Related articles to: SMYD2 Blocking Peptide
- Members of the KDM5 family of Jumonji histone demethylases have been implicated in a variety of human diseases including multiple cancers and neurological disorders. The regulation of KDM5 enzyme levels and activity, however, are poorly understood. Here we report that KDM5A is methylated by SMYD2 and that this methylation decreases histone demethylase activity and partly alters the KDM5A protein interactome. A mutant KDM5A that can no longer be modified at K1063 exhibits unique genomic sites of action, demethylates H3K4me3 more robustly across the genome and at new loci, has stronger and unique transcriptional effects, and distinct protein-protein interactions. As a result, a number of cell proliferation pathways are affected and cancer cell growth is blunted. This study illustrates the functional consequences of post-translational modifications of lysine residues in KDM enzymes impacting genomic histone demethylation, gene expression, protein-protein interactions and growth signaling, and establishes lysine methylation as a regulatory event in KDM5A action. - Source: PubMed
Publication date: 2026/04/08
Tran Tram AnhGopinathan GokulNuñez Clarissa GGoodavish FrankWu Shwu-YuanTran RandyLemoff AndrewGirard LucMartinez Elisabeth D - Acute lymphoblastic leukemia (ALL) is the most common childhood malignancy worldwide. Despite a good rate of treatment success, the poor prognosis underscores the urgent need for new prognostic markers and effective therapeutic strategies. The SET family of lysine methyltransferases (KMTs) has been implicated in several cancers. While the KMT has been identified as a prognostic marker in ALL, remains poorly characterized. The present study analyzed the expression patterns of in 83 pediatric ALL patients at diagnosis and during treatment using reverse transcription-quantitative PCR. Kaplan-Meier analysis was employed to evaluate survival outcomes between the high and basal expression groups. It was found that expression is markedly upregulated in bone marrow (BM) samples derived from ALL patients compared with non-neoplastic BM (median fold-change of 5.14 P=0.0095) and expression is correlated with leukemic burden. Importantly, the levels of decreased in chemotherapy-responsive patients. The present study further investigated whether levels are associated with those of . Notably, a positive correlation between both genes was observed at diagnosis (Spearman ρ=0.759, P<0.0001), with a substantial correlation persisting throughout treatment (Spearman ρ=0.925; P<0.01). Furthermore, patients classified in the high-risk category exhibited elevated expression, with those displaying high transcription exhibiting the poorest survival outcomes. The findings revealed the involvement of in leukemogenesis and highlighted its potential as a promising prognostic marker. - Source: PubMed
Publication date: 2026/03/24
Telles Luis Augusto MunizDe Loyola Mariana BraccialliSakamoto Luis Henrique ToshihiroRabello Doralina Do Amaral RamosMotoyama Andrea BarrettoPittella-Silva Fabio - - Source: PubMed
Publication date: 2026/03/09
Mahmud Md AshiqMohyeldin Mohamed MTarun Md Towhidul IslamSiddique Abu BakarSingh Sitanshu SEl Sayed Khalid A - - Source: PubMed
Li JunhongHong ZheZhang JunyuZheng ShengfengWan FangningLiu ZhengDai Bo - In epigenetic research, abnormalities in protein methylation modifications are closely related to the development of various diseases. The protein lysine methyltransferase SMYD2 has been extensively studied in cancer and age-related diseases due to its broad substrate specificity. However, SMYD2 as a promising small molecule inhibitor target, the biological functions have not been fully elucidated, and reports on related inhibitors are limited. Here, we will focus on studies about the mechanisms of SMYD2 on the treatment for different cancers and aging-related diseases and clarify the specific SMYD2 inhibitors' effects on different diseases. Moreover, we will also briefly discuss the contradiction points in existing studies, provide novel ideas about further study on SMYD2 structure and inhibitor development and finally, discuss the new aspects in further studies of SMYD2. Hopefully, this review stimulates new ideas in drug development for the treatment of cancer and aging-related diseases, maximizes human life, and benefit society. - Source: PubMed
Publication date: 2026/01/19
Gu MengZhu MenglinCai JianghongDing QianHu WeiHu QingwenZhang HaoZhu XuanzheZhu Yi Zhun