CCNB1 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- CCNB1 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00000891-T01
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CCNB1 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: CCNB1 293T Cell Transient Overexpression Lysate(Denatured)
- 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 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: CCNB1 293T Cell Transient Overexpression Lysate(Denatured)
- Meniscus is vital for maintaining knee homeostasis and function, and its degeneration is linked to knee osteoarthritis (OA) progression. However, the pathological mechanism of meniscus degeneration remains elusive. This study aimed to identify the molecular biological role of Cyclin B1 (CCNB1) in meniscus degeneration. Meniscal transcriptome sequencing of OA/non-OA was performed, and CCNB1 expression was verified in human and experimental mouse meniscal samples. The mice were administered with lentiviruses with CCNB1 overexpression via intra-articular injection after anterior cruciate ligament transection (ACLT) surgery, and the extracellular matrix (ECM) components and catabolic indicators were detected by immunohistochemistry. The in vitro and transcriptome sequencing of overexpressed CCNB1 was used to explore the mechanism of CCNB1 in meniscal degeneration. NOD-like receptor pyrin domain containing three (NLRP3) and its inhibitor were tested in explants induced by interleukin 1β. CCNB1 was significantly downregulated in meniscus cells of patients with OA and ACLT mouse models. CCNB1 overexpression restored homeostasis in meniscus cells, leading to markedly attenuated ACLT-induced meniscal degeneration. Furthermore, target prediction using bioinformatics and transcriptome sequencing analysis identified NLRP3 as a target of CCNB1. The cellular and molecular analyses showed that the inhibitor of CCNB1 effectively protected meniscal explants from degeneration by inhibiting inflammatory processes. Conclusions: Our findings indicated an essential role of CCNB1 in the pathogenesis of meniscal degeneration. Targeting the CCNB1/NLRP3 axis may serve as a practical therapeutic strategy to delay meniscal degeneration. - Source: PubMed
Publication date: 2026/06/04
Guan HongCheng JiangwenYuan XinghongCai DaozhangZhang HaiyanLiu Liangliang - Canine mammary tumours (CMTs) are the most common malignancies in female dogs and represent a valuable comparative model for human breast cancer. This study aimed to characterise the molecular and functional profiles of three CMT cell lines: CMT-U27, CMT-U131 and CMT-U229, using a zebrafish xenograft model. Gene ex-pression analysis targeted proliferation markers (MKI67, CCNB1, MYBL2, BIRC5, AURKA), receptor signalling (ESR1, PGR, AR, ERBB2, GRB7, EGFR), apoptosis and survival (BCL2, BAG1), and angiogenesis (VEGFA). Zebrafish larvae were xenotransplanted with tumour cells into either the Perivitelline Space or the Duct of Cuvier to assess larval survival and metastatic spread. The CMT-U27 displayed the most aggressive phenotype, with high expression of proliferation-associated genes and the highest metastatic frequency (60%). CMT-U229 exhibited moderate proliferation, accompanied by overexpression of VEGFA. In contrast, CMT-U131 exhibited lower proliferation, correlating with reduced survival in circulation and limited metastasis (<20%). This study provides the first comprehensive molecular characterisation of CMT cell lines in a zebrafish xenograft model. The findings underline the distinct biological profiles of these lines and demonstrate the utility of this platform for testing targeted therapies in veterinary oncology with translational relevance to human breast cancer. - Source: PubMed
Publication date: 2026/05/12
Chmielewska-Krzesińska MałgorzataDybalska-Szczepanek Joanna - Cancer is characterized as a multifactorial disease due to their complex genetic and molecular mechanisms that often converge across tissue types. Shared oncogenic pathways can help us understand these functions and discover broad-spectrum therapeutics. Earlier, most studies focused on finding specific drivers for individual cancer types. However, researchers are now more interested in identifying common molecular patterns across different cancers and developing therapies that can target multiple pathways at once. This study aimed to understand the common oncogenic pathways between breast, ovarian and colorectal (BOC) cancers and identify possible multitargeted therapeutic drug molecules. To identify the common differentially expressed genes (DEGs), we analyzed three transcriptomic datasets and found a total of 128 DEGs. The protein-protein interaction (PPI) network study reveals the top-ranked, most significant hub targets, AURKA, CDK1 and CCNB1, as drug targets. Enrichment analysis with GO and KEGG pathways, as well as regulatory network (TFs and mRNAs) analysis, revealed common pathogenetic processes among BOC cancers. The AMG-900 exhibits the highest binding affinity scores of -10.8, -9.40, and -9.7 kcal/mol with the target proteins AURKA, CCNB1, and CDK1, respectively. The stability and structural flexibility of the selected protein-ligand complexes were validated by a large-scale (500 ns) molecular dynamics and MM-GBSA analyses, and the results indicate stable interactions for AURKA and CCNB1, while CDK1 showed comparatively reduced stability. The pharmacokinetic analysis revealed favorable drug-likeness and a manageable toxicity profile typical of anticancer agents. Therefore, the findings of this study propose that AMG-900 may serve as a promising multi-targeted candidate for further investigation in multi-target therapeutic strategies within precision oncology. Furthermore, these results require additional experimental (in vivo and in vitro) and clinical validation to confirm the potentiality and efficiency of this (AMG-900) lead compound. - Source: PubMed
Publication date: 2026/06/01
Sarker HriddhiFarid Farhad BinKamrun MargubaMasud EshaAhmed AsifMiah MamunRoy Neladre ShakerKumar NeerajAli Md Ahad - Pancreatic cancer mortality remains high due to late diagnosis and therapeutic resistance. The present study investigated acylglycerol kinase (AGK), which has been implicated in other tumors, in pancreatic cancer. Quantitative PCR, western blotting and immunohistochemistry analyses showed that AGK was markedly upregulated in pancreatic cancer tissues and cell lines and its expression associated with poor prognosis. Furthermore, functional studies using AGK knockdown and overexpression models demonstrated that AGK promoted cancer cell proliferation by upregulating proliferation‑associated genes, such as and . Mechanistically, AGK activates NF‑κB signaling pathway by facilitating p65 nuclear translocation and enhancing its phosphorylation. Additionally, CCK‑8 and colony formation assays further indicated that elevated AGK levels reduced sensitivity to therapeutic drugs and irradiation in pancreatic cancer cells. These findings revealed the critical role of AGK in pancreatic cancer progression and treatment resistance, identifying it as a potential novel therapeutic target and diagnostic marker. - Source: PubMed
Publication date: 2026/05/29
Han KunkunZhang QianyunGao ShengnanZhang JigangMei XiaoLi FeiXu XinLi ShuChen Guodong - Hepatocellular carcinoma (HCC) is one of the most common types of liver cancer, with a high mortality rate. Despite significant advances in HCC detection and treatment, problem remain persistence. Plant-derived natural products have always been a boon for novel medication development; in this case, is a traditional medicinal plant recognised for its therapeutic usefulness in a variety of diseases. However, its efficacy against HCC has never been tested. Therefore, this study was initiated using an integrated in-silico approach to determine whether -derived compounds could target hub genes associated in HCC. Extracted Differentially expressed genes from two GEO database and TCGA-LIHC using GEO2R tool and R software. Overlapped DEG, were then utilised to conduct cluster analysis and performed three centrality techniques which were then intersected to obtain hub genes. The compounds extracted from bark of using ethyl acetate and identified via mass spectrometry. These hub genes were then docked with the selected compounds obtained from the bark extract of and Simultaneous drug-likeness was assessed through ADMET followed by validation using MD simulation. Six hub genes BUB1, BUB1B, CCNA2, CCNB1, CDK1 and KIF11 were seen significantly upregulated in hepatocellular carcinoma. Out of 64 compounds only C2, C55, and C65 of displayed strong binding affinity as well as favourable drug-likeness. Molecular dynamics simulation validated the stability of these complexes' structures, but localised loop flexibility facilitated adaptation. At last, this pioneer study shown the potential of as promising leads to HCC open avenue for future research. - Source: PubMed
Publication date: 2026/05/26
Das TanusreeChoudhury ShuvasishChoudhury Manabendra Dutta