CCNB1 antibody
- Known as:
- CCNB1 (anti-)
- Catalog number:
- orb69328
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- CCNB1 antibody
Related genes to: CCNB1 antibody
- Gene:
- CCNB1 NIH gene
- Name:
- cyclin B1
- Previous symbol:
- CCNB
- Synonyms:
- -
- Chromosome:
- 5q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-10
- Date modifiied:
- 2016-10-05
Related products to: CCNB1 antibody
Related articles to: CCNB1 antibody
- To identify psoriasis-associated candidate genes and regulatory features via integrated transcriptomic, immune and genetic analyses, and validate them in an imiquimod-induced psoriasis-like murine model. - Source: PubMed
Publication date: 2026/09/21
Yang LingyiMo WenshenWang GangWu Xiaowei - Intrauterine adhesion (IUA) represents a prevalent cause of persistent infertility and continues to be a significant unresolved challenge in reproductive medicine. However, its full pathogenic mechanisms remain incompletely elucidated. We retrieved endometrial RNA-sequencing data from IUA patients and normal controls in the Gene Expression Omnibus (GEO) database, and screened 586 differentially expressed genes (DEGs) in the endometrium of IUA patients using the R package limma. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and gene set enrichment analysis (GSEA) revealed activation of immune-related pathways, including chronic inflammatory response, complement activation, and complement and coagulation cascades in IUA. Further single-sample gene set enrichment analysis (ssGSEA)-based relative immune cell enrichment analysis revealed decreased enrichment scores of activated CD4 T cells and type 2 T helper cells, alongside increased enrichment scores of effector memory CD8 T cells, macrophages, mast cells, natural killer cells, and T follicular helper cells in IUA patients, indicating their potential involvement in IUA pathogenesis. A protein-protein interaction (PPI) network was constructed, identifying 10 hub genes associated with IUA: , , , , , , , , , and . The expression patterns of these genes were further validated in two independent external IUA cohorts, supporting a potential correlative link between these genes and IUA pathogenesis. Our findings provide exploratory insights and potential candidate molecules for subsequent mechanistic studies of IUA onset and progression. - Source: PubMed
Publication date: 2026/09/20
Feng XueYu Lili - Hepatitis C virus (HCV)-related hepatocellular carcinoma (HCC) remains a major global health challenge, with high morbidity and mortality despite recent therapeutic advances. Early detection and identification of reliable molecular biomarkers are essential to improve patient outcomes. Therefore, the present study aimed to investigate key hub genes and pathways associated with HCV-related HCC as potential diagnostic biomarkers. - Source: PubMed
Publication date: 2026/06/11
Karimi ElhamSadat Kalaki NiloufarShavandi MahnazMahlouji FargolHaidar Abed El HasanAbedi Asl AriaSafarnezhad Tameshkel FahimehZamani FarhadKarbalaie Niya Mohammad Hadi - Colorectal cancer (CRC) remains a major cause of cancer-related mortality worldwide, and patients with advanced or metastatic disease still require more effective targeted therapeutic options. N-acetyltransferase 10 (NAT10), an RNA acetyltransferase responsible for N4-acetylcytidine (ac4C) modification, has been implicated in CRC progression, metastasis, immune evasion, and therapy resistance. The recently resolved human NAT10 structure (PDB ID: 9J3C) provides a structural basis for rational discovery of NAT10-directed chemical scaffolds. We combined large-scale virtual screening, molecular simulation, and cellular testing to identify NAT10-targeting compounds. Approximately 300,000 molecules were screened by hierarchical docking, followed by ADMET prediction, 100-ns molecular dynamics simulations, and MM/PBSA analysis. G856-6814 showed a predicted binding free energy of - 26.33 ± 3.37 kcal/mol and inhibited HCT116 cell viability with an IC of 211.6 ± 14.8 nM. In a recombinant enzyme assay, G856-6814 inhibited NAT10 acetyltransferase activity with an IC of 2.3 ± 0.4 µM. G856-6814 treatment increased the apparent NAT10 melting temperature from 50.4 ± 0.5 to 56.0 ± 0.8 °C. Treatment also reduced global RNA ac4C and ac4C enrichment on c-MYC, CCNA2, and CCNB1 transcripts. G856-6814 was 19.6-fold less potent against TIP60 and more than 43-fold less potent against p300 and GCN5. Together with the attenuation of cellular effects after NAT10 knockdown, these findings support G856-6814 as a NAT10-targeting inhibitory scaffold that requires broader selectivity and in vivo evaluation. - Source: PubMed
Publication date: 2026/09/15
Xu ChaoZhao ShileiXu BingXu JiapingWu YongliZhang DanWu BenshengZhou Qing - Liposarcoma (LPS) is a common soft tissue sarcoma; however, its molecular pathogenesis and immune cell infiltration remain poorly understood. This study investigated potential driver genes and pathways in LPS and characterized immune cell infiltration patterns to identify potential markers for targeted therapy. Differentially expressed genes (DEGs) in LPS were analyzed by GO and KEGG pathway enrichment analysis. A protein-protein interaction network was constructed using the STRING database and visualized with Cytoscape. mRNA expression of genes with high |logFC| values was verified by RT-qPCR. Immune cell subsets were quantified using CIBERSORT. GO and KEGG analysis revealed significant functional clusters and pathways, and most verified genes were consistent with the bioinformatics analysis. Survival analysis showed that high expression of TYMS, KIF20A, BUB1B, LMNB1, RRM2, ZWINT, and RACGAP1 was significantly associated with poor overall survival and poor disease-free survival (DFS). High levels of TMSB15A, TPX2, PKM2, and PTTG1 were significantly associated with poor DFS alone. CIBERSORT analysis identified a significantly higher fraction of resting mast cells (MCs) in LPS tissues compared to normal fatty tissues (P < 0.05). TOP2A, IL-6, PCNA, CDK1, JUN, MYC, CCNB1, EGFR, ACACB, and BIRC5 were identified as potential diagnostic biomarkers of LPS, providing strong evidence for hub gene studies. Immune cell infiltration analysis further suggested that resting MCs may play a potential role in LPS development, although further experimental validation is warranted. Collectively, these findings clarify the molecular basis of LPS and provide a foundation for future research into its treatment. - Source: PubMed
Publication date: 2026/09/11
Liu ChunxiaoWang YanhuaLiu QiuxiaZhang Sha