CCNB1 antibody
- Known as:
- CCNB1 (anti-)
- Catalog number:
- orb107010
- Product Quantity:
- 20 ug(Trial size)
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- CCNB1 antibody
Ask about this productRelated 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
- The advancement of nanotechnology has significantly accelerated the development of antibacterial and anticancer therapeutics for biomedical applications. Among emerging nanomaterials, layered double hydroxides (LDHs) offer several advantages, including ease of synthesis and inherent therapeutic properties. In this study, the antibacterial and anticancer activities of copper-aluminum (CuAl) LDHs were assessed. - Source: PubMed
Publication date: 2026/08/26
Shi JiayanWang YueranXu MengtingJin ShunjieYin YingKhor Kai HeZhou XuanBahadur AliShameli KamyarTeow Sin-Yeang - 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
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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
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