Ask about this productRelated genes to: SETD4 antibody
- Gene:
- SETD4 NIH gene
- Name:
- SET domain containing 4
- Previous symbol:
- C21orf27, C21orf18
- Synonyms:
- -
- Chromosome:
- 21q22.12
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-23
- Date modifiied:
- 2018-12-21
Related products to: SETD4 antibody
Related articles to: SETD4 antibody
- 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 - Carbonyl reductase 1 (CBR1), a member of the short-chain dehydrogenase/reductase (SDR) superfamily, is implicated in tumor progression and treatment resistance. However, its role in non-small cell lung cancer (NSCLC) remains unclear. This study examined CBR1 expression in NSCLC tissues and cell lines, using gene interference and pharmacological inhibition to assess its impact on stemness, chemosensitivity, and quiescence, and to explore underlying mechanisms. Our findings indicate that CBR1 expression is elevated in NSCLC tissues and cell lines, and further increases in the presence of cisplatin (CDDP). Gene interference reducing CBR1 expression significantly decreased the percentage of cluster of differentiation 133 (CD133)-positive cells and the expression of octamer-binding transcription factor 4 (OCT4) and SRY (sex determining region Y)-box 2 (SOX2), while enhancing CDDP chemosensitivity. The CBR1-specific inhibitor hydroxy-PP-Me (PP-Me) markedly increased CDDP cytotoxicity and reduced stemness. Additionally, CBR1 inhibition via short hairpin RNA (shRNA) CBR1 (sh-CBR1) or PP-Me disrupted NSCLC cell quiescence, as shown by a decrease in G0 phase cells and p27 expression, alongside an increase in cyclin D1 and phospho-retinoblastoma (pRb) expression. Furthermore, SET domain-containing protein 4 (SETD4), which mediates stemness, chemosensitivity, and quiescence in NSCLC cells, was downregulated by sh-CBR1 or PP-Me treatment. The overexpression of SETD4 counteracted the enhanced chemosensitivity resulting from CBR1 inhibition. In A549 xenografts, combined PP-Me and CDDP therapy significantly inhibited tumor growth compared to either treatment alone. In conclusion, CBR1 inhibition enhances CDDP chemosensitivity by suppressing stemness and quiescence in NSCLC. - Source: PubMed
Publication date: 2025/12/17
Li WeiwenZhao JialuLan WeihongYe XiaofeiYing Kejing - Perirenal fat deposition significantly impacts sheep carcass quality and economic efficiency. To elucidate the underlying genetic regulation, we performed a genome-wide association study (GWAS) on 556 Hu sheep and a comparative transcriptome analysis on 24 Hu sheep (12 with high- and 12 with low-perirenal fat deposition), all with accurate phenotypic records. Furthermore, hub genes and tissue-specific genes (TSGs) were discerned through weighted gene co-expression network analysis (WGCNA) and by leveraging RNA-Seq data from 12 tissues, respectively. qRT-PCR is used to validate the accuracy of RNA-Seq data. GWAS identified significant SNPs near genes including SETD4, TIMP2, SOCS3, and DNAH17. Comparative transcriptome analysis of HPF and LPF groups identified 2072 differentially expressed genes (DEGs), which were significantly associated with lipid storage (LPL), fatty acid homeostasis (APOE, GOT1), and biosynthesis (ACACA). A total of 2333 differential alternative splicing events were identified in 1169 genes, with skipped exons (SE, 30.65 %) being the most common. GO analysis of these SEs showed links to RNA splicing and lipid metabolism, with genes like BSCL2, DGAT1, PLIN5, and PNPLA2 involved in lipid droplet organization and triglyceride storage. WGCNA revealed key modules that were positively and negatively correlated with perirenal fat deposition, emphasizing hub genes (SAR1B, THRSP, ACSS2, KIF5B) associated with lipid droplet organization and metabolism. The integrated analysis of GWAS and RNA-seq identified TIMP2, SOCS3, and DNAH17 as potential key genes involved in regulating perirenal fat deposition in sheep. An association analysis of 372 Hu sheep populations identified significant links (P < 0.05) between perirenal fat deposition traits and mutations in the TIMP2 (g.9759169 G > A) and DNAH17 (g.9494469C > T) genes. Crucially, tissue-specific gene analysis across 12 tissues identified 448 perirenal fat TSGs, of which 75 were also differentially expressed genes (e.g., LPL, THRSP, LEP, ADRB3). In conclusion, our multi-omics study identified key genes influencing perirenal fat deposition in sheep. Notably, mutations in TIMP2 and DNAH17 could serve as candidate markers for enhancing carcass quality through marker-assisted selection. - Source: PubMed
Publication date: 2025/12/24
Fu XiaoyuZhao LimingTian HuibinZhang DeyinZhang YukunZhao YuanCheng JiangboLi XiaolongXu QuanzhongXu DanYang XiaobinMa ZongwuWu WeiweiLi FadiWang WeiminZhang Xiaoxue - Trisomy 21 (T21) is the genetic cause of Down syndrome (DS), and the presence of extra genetic material causes altered expression of genes located on chromosome 21 (Hsa21) and others, with effects as altered levels of metabolic reaction products. The one‑carbon pathway plays a central role in correct human neurodevelopment and was found to be altered in DS and neurological impairments of different entities. In this work, the expression of 42 genes involved in the one‑carbon cycle was analyzed in blood samples from 10 subjects with T21 and 10 euploid (N) subjects. Additionally, plasmatic concentration of methylcobalamin (MeCbl) was evaluated in 10 subjects with T21 and 7 N subjects. The results showed that 13 genes out of 42 were differentially expressed: 11 were over-expressed (ABCC3, ABCC4, ARMT1, CTH, FOLR2, GART, ICMT, PRMT2, SETD4, SLC19A1, and NSD2) and 2 were under-expressed (NSUN3 and TRMT112). Among these, 4 over-expressed genes are located on Hsa21 (GART, PRMT2, SETD4, and SLC19A1). Statistical analyses revealed significant correlations between gene expression data, highlighting interconnections among genes. Finally, MeCbl shows a slight statistically significant reduction in the T21 group. In conclusion, the presence of three copies of Hsa21 leads to the dysregulation of gene expression associated with the one‑carbon cycle. This dysregulation affects genes located on both Hsa21 and other chromosomes resulting in metabolic alterations. Additionally, new gene interconnections were discovered that have not been previously reported in the literature. - Source: PubMed
Publication date: 2025/11/27
Vione BeatriceGaudesi Alessandro MariaAntonaros FrancescaCicilloni MichelaVitale LorenzaPiovesan AllisonPelleri Maria ChiaraStrippoli PierluigiSperti GiacomoRamacieri GiuseppeCatapano FrancescaParadisi PietroPirazzoli Gian LucaCorvaglia Luigi TommasoLocatelli ChiaraCaracausi Maria - Chronic liver injury and its progression to disease often extend beyond exposure to toxic metabolites or xenobiotics. Recovery from chronic injury, when achieved, depends on de novo regeneration, the underlying mechanisms of which remain poorly understood. Herein, we investigate a specific cell population proposed to be fundamental for de novo regeneration and recovery following chronic injury, aiming to elucidate its regulatory mechanisms. - Source: PubMed
Publication date: 2025/11/01
Jia Xi-ZhengZhuang Tian-TianYang Ri-ShengGu Yun-WenZeng Yi-ZheWood ChristopherYang Jin-ShuYang Wei-Jun