TOP2A (Phospho-Thr1343) Antibody
- Known as:
- TOP2A (Phospho-Thr1343) Antibody
- Catalog number:
- 11763
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- TOP2A (Phospho-Thr1343) Antibody
Related genes to: TOP2A (Phospho-Thr1343) Antibody
- Gene:
- TOP2A NIH gene
- Name:
- DNA topoisomerase II alpha
- Previous symbol:
- TOP2
- Synonyms:
- -
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-03-23
- Date modifiied:
- 2017-08-04
Related products to: TOP2A (Phospho-Thr1343) Antibody
Related articles to: TOP2A (Phospho-Thr1343) Antibody
- Osteosarcoma is a highly aggressive bone malignancy with a strong tendency for metastasis and poor clinical outcomes. The molecular mechanisms driving osteosarcoma progression and metastasis remain incompletely understood, highlighting the need to identify robust biomarkers and therapeutic targets. Weighted gene co-expression network analysis (WGCNA) was performed using osteosarcoma datasets from the Gene Expression Omnibus to identify metastasis-associated gene modules and hub genes. Expression, methylation, mutation, immune infiltration, and drug sensitivity analyses were conducted using multiple public databases, including TCGA, GSCA, UALCAN, and cBioPortal. A prognostic model was developed using the TARGET osteosarcoma cohort and validated in an independent GEO dataset. Functional roles of hub genes were investigated through loss- and gain-of-function experiments in sarcoma cell lines using RT-qPCR, Western blotting, proliferation, colony formation, wound-healing, and luciferase reporter assays. Four hub genes, AURKB, CDC20, KIF11, and TOP2A, were identified as strongly associated with metastasis. These genes were significantly upregulated in sarcoma tissues and cell lines and demonstrated excellent diagnostic performance. Promoter hypomethylation and frequent genomic alterations contributed to their aberrant expression. High expression of the hub genes was associated with poor overall survival, and a four-gene prognostic model showed strong predictive performance in both training and validation cohorts. Functional assays confirmed that these genes promote sarcoma cell proliferation and migration, while miRNA-mediated regulation and drug resistance associations further highlighted their biological relevance. This integrated computational and experimental study identifies AURKB, CDC20, KIF11, and TOP2A as key oncogenic drivers in osteosarcoma, with significant diagnostic, prognostic, and therapeutic implications. - Source: PubMed
Publication date: 2026/09/01
Xia QingquanMeng XiangchaoWu XuhuaLi XujunFei TengRong Ke - DNA topoisomerase II (TOP2) generates transient DNA double-strand breaks that are trapped as TOP2-DNA covalent complexes (TOP2cc) by antibiotic and chemotherapy drugs. Here, we characterize tools for study of cellular responses to TOP2cc, exploiting a mutant () that generates spontaneous and inhibitor-induced covalent complexes at elevated frequencies. This Top2-hc (for "hypercleavage") mutant protein inhibits yeast cell growth when expressed alone or with endogenous Top2, and growth defects are exacerbated in DNA-repair-deficient genetic backgrounds and/or in the presence of low doses of the Top2 poison mAMSA. We generated analogous mutations in human and mouse TOP2A and TOP2B that gave increased TOP2cc, hypersensitization to topoisomerase poisons, increased DNA damage, and decreased cell survival in cultured cells. We further established knock-in mouse models with inducible, tissue-specific expression of each TOP2-hc isoform, demonstrating overt organismal toxicity and cellular markers of DNA damage responses. To illustrate the potential of these genetic tools, we carried out proof-of-principle screens in yeast and cultured human cells for sensitivity to TOP2-hc. The yeast screen revealed strong requirements for homologous recombination, moderate roles for sister chromatid cohesion and kinetochore function, and dependencies on vesicle and vacuolar functions. The pilot shRNA screen in human cells revealed shared requirements for resistance to expression of either TOP2A-hc or TOP2B-hc as well as examples of isoform specificity. These findings establish hypercleavage mutant proteins as effective tools for studying topoisomerase isoform-specific DNA damage and offer a foundation for exploring TOP2cc toxicity and tolerance in vivo. - Source: PubMed
Publication date: 2026/09/01
Ontoso DavidMehta MonikaShabro AidinDittmar JohnReid Robert J DRothstein RodneyNitiss John LKeeney Scott - TOP2A has been implicated in the progression of multiple malignancies; however, its clinical significance and biological role in OSCC remain poorly understood. This study aimed to comprehensively investigate the expression, prognostic value, biological functions, and molecular mechanisms of TOP2A in OSCC through an integrative, multilevel approach that combined multi-cohort bioinformatics analyses, clinical immunohistochemical validation, and both in vitro and in vivo functional experiments. - Source: PubMed
Publication date: 2026/08/31
Zhang XueyingZhang ShaohongChen ChongZhou ShuhanYu HuimingZhang Wei - 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