CCNB1 antibody
- Known as:
- CCNB1 (anti-)
- Catalog number:
- orb107010
- Product Quantity:
- 20 ug(Trial size)
- Category:
- -
- Supplier:
- 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 investigate the mechanism of Shengmai San (SMS) in the treatment of lung adenocarcinoma (LUAD) based on an integrated strategy combining "network pharmacology, bioinformatics, molecular docking, and molecular dynamics simulation," aiming to provide a precise combination therapy strategy and identify potential bioactive compounds. Differentially expressed genes in LUAD were identified from the Gene Expression Omnibus database using R (originally developed at Bell Laboratories and currently managed by Lucent Technologies). SMS components (ginseng, Ophiopogon japonicus, and Schisandra chinensis) were retrieved from encyclopaedia of traditional Chinese medicine, with Lipinski-compliant compounds selected. Compound targets were predicted via SwissTargetPrediction and Similarity Ensemble Approach. Intersecting targets between differentially expressed genes and compound targets were identified for "herbs-compounds-targets-disease" network construction. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed. Hub targets were identified by analyzing the protein-protein interaction network. High-prognostic relevance targets were screened from The Cancer Genome Atlas. Compounds targeting these were identified through the herbs-compounds-targets-disease network, and absorption, distribution, metabolism, excretion, and toxicity-compliant compounds were selected using SwissADME (a web-based tool provided by the Molecular Modeling Group of the Swiss Institute of Bioinformatics). Core regulatory targets were identified through molecular docking, with complex stability assessed by molecular dynamics simulations. The key bioactive compounds of SMS for treating LUAD were identified as 7-hydroxy-2,5-dimethyl-4H-1-benzopyran-4-one, N-trans-feruloyltyramine, paprazine, and (E)-N-[(2S)-2-hydroxy-2-(4-hydroxyphenyl)ethyl]-3-(4-hydroxyphenyl)prop-2-enamide. Hub targets included AURKA, CCNA2, CCNB1, CDK1, CHEK1, KIF11, NEK2, PLK1, TTK, and TYMS. Among these, CDK1, CHEK1, and PLK1 demonstrated both high-prognostic relevance and strong binding affinity with SMS, emerging as core regulatory targets for SMS in LUAD treatment. Mechanistically, SMS exerts its anticancer effects primarily by modulating the tumor necrosis factor, interleukin-17, cell cycle, and Lipid and atherosclerosis signaling pathways. The active components of SMS, such as paprazine, may exert antitumor effects partly through downregulating CDK1, CHEK1, and PLK1 expression. Although the present study did not examine drug-resistance models or combination regimens, our findings raise the possibility that, in patients with high expression of these genes, combining SMS with standard chemotherapy or targeted therapy could potentially enhance chemosensitivity and mitigate the development of resistance. This hypothesis, however, requires formal testing in appropriate preclinical models and functional validation studies. - Source: PubMed
Zhou XiaolingWu DiyaoZhang XiaohuiZhang Xinyou - Forsythiae Fructus, a classic heat-clearing and detoxifying herb in traditional Chinese medicine (TCM), is widely used for inflammatory conditions. Its primary bioactive component, Forsythoside A (FTA), exhibits potent anti-inflammatory and antioxidant activities. Given that hypertensive nephropathy is characterized by chronic inflammation, oxidative stress, and fibrosis-hallmarks that correspond to "heat" and "toxin" pathologies in TCM theory-Forsythiae Fructus represents a rational candidate for HN therapy. However, the precise mechanisms by which FTA inhibits HN progression remain incompletely elucidated. - Source: PubMed
Publication date: 2026/08/28
Cui XiaoliYang DiZhang ZhihongWang ChunmeiLi HeSun JinghuiZhang TianyuWang Mengyang - Chlorophenylacetonitriles are known as one of the emerging nitrogenous disinfection byproducts (N-DBPs) in chlorinated drinking water due to their concerned cytotoxicity and genotoxicity compared to regulated carbonaceous DBPs. However, under low-dose exposure, the in vivo pathological consequences of chlorophenylacetonitriles remain largely unresolved. Here, C57BL/6J mice were exposed to 2-chlorophenylacetonitrile (2-CPAN) via drinking water (100 ug/L) for six months, and an integrated histopathological and genome-wide transcriptomic approach was employed to mechanistically characterize its multi-organ toxicological consequences. 2-CPAN ingestion significantly suppressed body weight (35.9 ± 2.0 g vs. 47.6 ± 11.6 g, < 0.05) and induced severe gastroenteropathy-including gastric lamina propria inflammatory infiltration, intestinal villous blunting, crypt disorganization, transmural mononuclear infiltration, and abrogating epithelial barrier integrity. Intestinal barrier failure drove portal translocation of luminal PAMPs, potentially triggering splenic white pulp atrophy, red/white pulp boundary dissolution, and parenchymal changes consistent with fibrotic remodeling. Splenic RNA sequencing revealed a bipartite transcriptomic reprogramming: upregulated pathways were enriched in the ribosome, MAPK signaling, cytokine-cytokine receptor interaction, and chemokine signaling pathways. A proteotoxic stress module (, 9.4-fold; , 10.2-fold) and a chemokine effector hub (, 3.43-fold; , 2.9-fold; , 2.58-fold; , 2.15-fold) were identified by the STRING network. Downregulated pathways converged on cell cycle suppression, with concurrent loss of / and (G1/S block), and (G2/M arrest), and // (dNTP and aminoacyl-tRNA starvation), collectively forcing splenic lymphocytes into irreversible proliferative failure. These findings provide the first mechanistically resolved in vivo evidence that chronic 2-CPAN exposure drives a potential gut-spleen toxicological axis, underscoring the urgent need to incorporate organ endpoints by long-term exposure into N-DBP risk assessment. - Source: PubMed
Publication date: 2026/07/23
Zhang YayunLiu FeiZhou HaoChen JingwenJiang LeiYan ChangchunLi XiaodongXue DingmingWang Jiangfei - Prostate cancer (PCa) is the second most prevalent malignancy in men worldwide, and accurate stratification of biochemical recurrence (BCR) risk remains challenging using conventional clinicopathological parameters alone. Identification of robust molecular biomarkers and integrated prognostic models is therefore of high clinical priority. - Source: PubMed
Publication date: 2026/08/12
Chen GuquanZhang JiefengZhao LinfuZhu Jianyou - Growing evidence links 2, 2', 4, 4'-tetrabromodiphenyl ether (BDE47), a common environmental pollutant, to various health risks. This study examines the shared genetic markers between BDE47 exposure and lung adenocarcinoma, analyzes their biological roles, and assesses their prognostic value for clinical outcomes. BDE47-related lung adenocarcinoma genes were identified using The Cancer Genome Atlas (TCGA) and the Comparative Toxicogenomics Database (CTD). The screen identified 406 overlapping genes potentially linking BDE47 exposure to lung adenocarcinoma pathogenesis-related processes. Network topology analysis delineated well-defined hub genes organizing into functionally coherent modules. Pathway enrichment highlighted significant involvement in cancer-related signaling (such as PI3K-AKT, IL-17), cell cycle, ECM-receptor activation and chemical carcinogenesis-receptor activation. The LASSO-derived prognostic signature comprised four genes (KIF11, CCNA2, CCNB1, TOP2A) that effectively stratified patients into distinct risk cohorts. Molecular docking suggested that BDE47 might bind with high affinity to these target proteins, with CCNB1 emerging as a potential key target. In vitro experiments demonstrated that BDE47 treatment significantly promoted cell proliferation and migration, attenuated cisplatin sensitivity, and upregulated the expression of p-AKT and CCNB1 in lung adenocarcinoma cells. Furthermore, cisplatin treatment suppressed CCNB1 protein levels, an effect that was reversed by co-incubation with BDE47. This study reveals how BDE47 exposure may influence lung adenocarcinoma and highlights the need for environmental pollutant monitoring, while also offering potential biomarkers for cancer prognosis and treatment. - Source: PubMed
Publication date: 2026/08/25
Zhao MingyuWu XiaorongMao YixinWu MeixuanDu JunZhang YujieWang Yueyuan