Mouse Aurka Antibody (N-term)
- Known as:
- Mouse Aurka Antibody (N-terminus)
- Catalog number:
- AP14609a
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- Mouse Aurka Antibody (N-term)
Related genes to: Mouse Aurka Antibody (N-term)
- Gene:
- AURKA NIH gene
- Name:
- aurora kinase A
- Previous symbol:
- STK15, STK6
- Synonyms:
- BTAK, AurA, STK7, ARK1, PPP1R47, AIK
- Chromosome:
- 20q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-02
- Date modifiied:
- 2016-10-05
Related products to: Mouse Aurka Antibody (N-term)
Related articles to: Mouse Aurka Antibody (N-term)
- Chemotherapy resistance remains a major challenge in colorectal cancer (CRC) treatment, necessitating novel adjuvant strategies. This study employed an integrated analytical strategy combining network pharmacology, single-cell RNA sequencing (scRNA-seq) of patient-derived organoids (PDOs) and molecular dynamics simulations to identify bioactive compounds from and elucidate their chemo-sensitizing mechanisms. Network pharmacology identified five bioactive components of , corresponding to 267 potential targets. Integration with transcriptomic data, weighted gene co-expression network analysis (WGCNA), and known CRC genes refined these to 19 core targets. Cross-referencing with scRNA-seq data from irinotecan-treated PDOs pinpointed cyclin-dependent kinase 2 () and Aurora kinase A () as pivotal targets. Molecular dynamics simulations confirmed stable binding of the key component cerevisterol to both CDK2 and AURKA proteins, with binding free energies of -120.67 kJ/mol and -134.47 kJ/mol, respectively. In vitro cell viability assays across multiple CRC cell lines (HCT116, RKO, and HT-29) and PDOs demonstrated that cerevisterol significantly sensitized CRC cells to irinotecan (SN38). Notably, we observed that CDK2 was preferentially enriched in MSI-H tumors, whereas AURKA was enriched in MSS tumors, suggesting the potential of MSI status as a biomarker for patient stratification. Collectively, these findings identify cerevisterol as a dual-targeting natural product that modulates CDK2 and AURKA to overcome chemotherapy resistance, providing a quantitative analytical framework for discovering bioactive compounds and their molecular targets from medicinal fungi. - Source: PubMed
Publication date: 2026/07/08
Pan YiWu XueweiChen LinZhang ChaoHu YuqingChang JieLou QiuwenZhang JiaqiXu ShuochenXu WenxiaWang Jianping - : Colorectal cancer (CRC) remains a heterogeneous disease, and improved biomarkers are needed to support prognostic assessment. This study aimed to characterize hub genes in CRC and evaluate whether a gene signature provides biologically meaningful and prognostic information in clinical-genomic models. : We integrated three GEO microarray datasets (GSE110223, GSE110224, and GSE23878) to identify common differentially expressed genes using adjusted p<0.05 and ∣log2FC∣>1. Hub genes and protein expression were identified through protein-protein interaction network analysis using maximal clique centrality and Human Protein Atlas, respectively. Prognostic relevance was evaluated in TCGA-COAD/READ using Kaplan-Meier analysis, multivariable Cox regression, Cox-derived prognostic indices, time-dependent ROC analysis, and regression-based machine learning for internal robustness. Principal component analysis (PCA) was used to derive a standardized PC1-based score from the 10-hub gene signature. : A ten-gene mitotic hub signature (TPX2, UBE2C, AURKA, NEK2, PRC1, CCNB1, CDK1, CEP55, FOXM1, and RRM2) was consistently upregulated across the three datasets and enriched for cell-cycle and mitotic pathways. Protein-level and survival analyses supported the biological relevance of several hub genes. In TCGA-COAD/READ, the signature showed limited standalone prognostic value and did not retain independent significance after adjustment for clinical variables, although it contributed modestly in integrated clinical-genomic models. PCA showed a one-dimensional signature, with PC1 capturing the dominant shared expression pattern. Gradient Boosting Regressor (R = 0.8035, MSE = 0.0473) supported the internal robustness of the DEG-based expression pattern. : The ten-gene mitotic hub signature represents a coherent CRC-related proliferative program with limited value as an isolated prognostic marker, but it may still be useful as part of integrated risk models that require external validation. - Source: PubMed
Publication date: 2026/07/08
Kamal EbtihalMoglad EhssanMohager Samah OAhmed MehadAldoseri Mobarak MahfodSuwayyid Barakat A AlBawadood Azizah SalimHamdan Hamdan ZAkbulut Mikail - Metabolic dysfunction-associated steatohepatitis (MASH) is a severe, progressive liver disease lacking effective therapies. Disulfiram (DSF), an FDA-approved medication for alcohol dependence, exhibits diverse biological activities beyond its primary indication. This study aimed to evaluate whether DSF holds intervention promise for MASH and to unravel the underlying molecular mechanism. The efficacy of DSF was assessed in a mouse model of MASH induced by a choline-deficient, L-amino acid-defined diet, as well as in hepatocytes exposed to free fatty acids (FFAs) to trigger lipotoxicity. RNA-seq analysis combined with bioinformatic approaches was performed to identify key pathways and hub genes. Mechanistic validation was carried out using Western blotting and qPCR. Computational predictions suggested that DSF may influence insulin resistance, inflammation, autophagy-related markers, and lipid metabolism. In FFAs-treated hepatocytes, DSF administration dose-dependently reduced lipid accumulation and lipotoxicity. Consistently, in MASH mice, DSF administration significantly lowered elevated serum ALT (35%) and AST (40%) levels and the absolute hepatic triglyceride content (reduced from 1 to 0.5 μg/mg protein), and markedly attenuated hepatic steatosis, inflammation, fibrosis, and oxidative stress. Of note, RNA-seq analysis revealed that DSF modulated autophagy-related pathways and identified Aurora kinase A (AURKA) as a central downregulated hub gene. Mechanistically, DSF suppressed AURKA expression, which in turn led to changes in autophagy-related markers. These changes in autophagy-related markers were functionally coupled to a reduction in lipotoxicity. Collectively, DSF alleviates MASH by inhibiting AURKA, thereby relieving AURKA-mediated suppression of autophagy-related markers, which was associated with diminishing lipotoxicity, and ultimately achieving broad suppression of disease progression. Thus, DSF represents a promising hepatoprotective candidate for the intervention of MASH. - Source: PubMed
Publication date: 2026/07/11
Zhou ZixiongZeng XiGuo YuqiTan ZhengyiZhang XinLiu XuyangZheng ShuyuLiu WenwenWang HaiyanQi Jing - Despite the success of CDK4/6 inhibitors (CDK4/6i) in treating HR+/HER2- breast cancer (BC), some patients experience treatment failure due to CDK4/6i resistance. This study aimed to investigate whether targeting Aurora A kinase enhances CDK4/6 inhibitor sensitivity. - Source: PubMed
Publication date: 2026/07/16
Wu JuanWang YueYan HonglinLi JuanjuanQuan ChuntaoYuan JingpingSun Shengrong - Therapy-induced senescence (TIS) is a common outcome of diverse anticancer treatments, including chemotherapy, radiation, and small-molecule inhibitors. Senescence is characterized by stable growth arrest and the senescence-associated secretory phenotype (SASP), which includes various immune mediators. As the role of the immune system in controlling cancer becomes increasingly appreciated, understanding the impact of TIS on the tumor immune microenvironment (TIME) is critically important. Here, we investigated how senescence can be leveraged to enhance antitumor immune responses. - Source: PubMed
Publication date: 2026/07/22
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