CCNB ELISA kit
- Known as:
- CCNB Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CCNB-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CCNB ELISA kit
Related genes to: CCNB ELISA kit
- 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: CCNB ELISA kit
Human ELC ELISA KIT 96 TEST
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Size(1-3)-beta-D-glucan Sandwich ELISA, Double Antibody(1-Kit )11,12-EET DHET Immunoassay Kit(1-Kit )11,12-EET_DHET Immunoassay Kit(1-Kit) 11,12-DHET Immunoassay Kit(1-Kit) 14,15-DHET Human Urine ELISA Kit(1-Kit) 14,15-DHET Hypertension ELISA Kit(1-Kit) 14,15-DHET sEH activity ELISA Kit(1-Kit) 14,15-EET DHET Hypertension ELISA Kit Related articles to: CCNB ELISA kit
- 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 - Ovarian cancer is one of the most lethal gynecological malignancies, characterized by late diagnosis, frequent recurrence, and high mortality. PDZ-binding kinase (PBK), a serine/threonine kinase of the mitogen-activated protein kinase kinase (MAPKK) family, has been implicated in the tumorigenesis of multiple cancers, yet its role in ovarian cancer remains incompletely characterized. This study aimed to investigate the effect of PBK on the proliferation and invasion of ovarian cancer cells. - Source: PubMed
Publication date: 2026/08/27
Awuti GuzhanuerWang JiapoLu YunJiang HaonanGuo Xiaoqing - Triple-negative breast cancer (TNBC) is a highly aggressive and treatment-resistant subtype, lacking HER2, progesterone, and estrogen receptors. Systemic chemotherapy remains the primary treatment due to the absence of molecular targets, often leading to poor prognosis and high recurrence. This study used an integrated transcriptomic and network-based bioinformatics approach to identify TNBC key genes (TKGs) and explore potential therapeutic candidates. Four TNBC microarray datasets (GSE36295, GSE38959, GSE45827, and GSE65194) were analyzed with the LIMMA algorithm in GEO2R, revealing 315 TNBC-shared differentially expressed genes (TSDEGs). Eight strongly connected TKGs were identified via topological analysis and protein-protein interaction (PPI) network construction across the STRING and IMEx databases from TSDEGs: CDK1, TOP2A, CCNB1, CDK2, FN1, UBC, PRKDC, and PARP1. Enrichment analysis of biological processes, molecular functions, cellular components, and KEGG pathways, combined with regulatory network analysis involving transcription factors and microRNAs, identified pathogenic roles of these genes. CDK1 and CDK2 were identified as the top pharmacological targets for molecular docking studies. Finally, TKG-guided top-ranked two drug molecules (Alsterpaullone and BLU-222) emerged as promising repurposed therapeutic candidates for TNBC. The absorption, distribution, metabolism, excretion, and toxicity (ADMET) and drug-likeness analyses showed these molecules have favorable pharmacokinetic properties. Molecular dynamics simulations over 100 nanoseconds demonstrated stable binding interactions and favorable behavior for the complexes CDK1-Alsterpaullone and CDK2-BLU-222, as indicated by root mean square deviation, fluctuation, and molecular interactions generalized Born surface area. Overall, these findings may aid in diagnosing and treating TNBC, providing valuable resources for future therapeutic strategies. - Source: PubMed
Publication date: 2026/09/07
Zarin NaziaTanha Tasnim HosenNishad MimunaParvin RehanaAshad RedwanIslam Md SajedulHaque Shaila - During early mammalian embryogenesis, totipotent zygotes and early blastomeres undergo extensive post-transcriptional regulation during the establishment of the first cell lineages; however, the functional contribution of alternative splicing to embryonic compaction and blastulation remains poorly understood. Here, we show that SF3B1, a core component of the spliceosome, is upregulated from the 4-cell stage and mediates highly dynamic splicing programs. Depletion of SF3B1 results in developmental arrest at the morula stage, accompanied by widespread transcriptomic dysregulation characterized by aberrant expression of transcription factors that impede pluripotency transition. Alternative splicing analysis further identifies that aberrantly spliced transcripts were significantly enriched in genes involved in cell cycle regulation, such as Cdk11b and Ccnb1. Importantly, we demonstrate that SF3B1 undergoes intrinsic, IDR-driven liquid-liquid phase separation both in vitro and in vivo, forming nuclear condensates in oocytes and early embryos, which is essential for successful development to the blastocyst stage. Together, our findings reveal that phase separation mediated SF3B1 splicing activity is a critical regulator of early mouse embryonic development. - Source: PubMed
Publication date: 2026/09/08
Zhao KangHan Ting-YuCheng Yan-LiZhang Yi-DanZhang Yu-WeiGuo JinJianZhang ShaoJunHuang WenZeZhang JingLiao Pei-YuXin YingChu ChuanChenSun Qing-YuanLiu ZhiZhenOu Xiang-HongXie Jun - Podocyte injury and loss in diabetic nephropathy (DN) are driven by mitotic catastrophe (MC), a disastrous cell death caused by aberrant cell cycle re-entry. Ten-eleven translocation 2 (TET2), a 5-methylcytosine (m5C) RNA demethylase, was upregulated in DN and regulated cell proliferation. Here, we explored whether TET2 mediates podocyte MC in DN using Adriamycin (ADM) and high glucose (HG) in vitro, and both STZ-induced and db/db diabetic mouse models in vivo. TET2 was upregulated in human diseased kidneys and injured podocytes, and its expression correlated with disease severity and podocyte loss. EdU staining and flow cytometry verified that ADM/HG facilitated cell proliferation and G2/M phase transition via elevated CDK1-cyclin B1 phosphorylation; meanwhile, ADM/HG increased reactive oxygen species and malondialdehyde levels. TET2 overexpression further enhanced ADM/HG-induced podocyte MC and oxidative stress, whereas TET2 knockdown had the opposite effect. Mechanistically, TET2 reduced Wee1 mRNA stability in an m5C-dependent manner, leading to CDK1-cyclin B1 activation. Rescue experiments confirmed that Wee1 reintroduction rescued TET2-driven MC and oxidative stress, while Wee1 silencing abolished the protection from TET2 knockdown. In vivo, TET2 depletion or Wee1 overexpression alleviated podocyte MC, renal injury, and apoptotic podocytes in both diabetic models. Collectively, TET2 promotes podocyte MC and aggravates DN via TET2-mediated m5C demethylation that suppresses Wee1 expression and activates CDK1-cyclin B1, suggesting that this axis may represent a candidate pathway in the context of DN. - Source: PubMed
Publication date: 2026/09/05
Feng JieDong HongjuanYang YiXie LiyiLu WanhongGuo YuruiKong Ranran