Mouse Aurka antibody
- Known as:
- Mouse Aurka (anti-)
- Catalog number:
- orb32797
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- Mouse Aurka antibody
Related genes to: Mouse Aurka antibody
- 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
Related articles to: Mouse Aurka antibody
- Liver hepatocellular carcinoma (LIHC) is a leading cause of cancer-related mortality worldwide, with limited therapeutic options and poor prognosis, particularly at advanced stages. Identifying key molecular drivers involved in LIHC progression is critical for improving diagnosis and treatment strategies. In this study, we performed an integrated bioinformatics analysis using four independent GEO datasets (GSE19665, GSE54236, GSE55092, and GSE84598) to identify differentially expressed genes (DEGs) associated with LIHC. A total of 147 common DEGs were identified, and protein-protein interaction network analysis revealed CCNA2, MAD2L1, AURKA, and PTTG1 as central hub genes. Functional enrichment analyses indicated that these genes are primarily involved in cell cycle regulation, mitosis, and chromosomal stability. Expression analyses using TCGA-based databases demonstrated significant upregulation of these hub genes at both mRNA and protein levels in LIHC tissues compared with normal liver tissues. Elevated expression was associated with advanced tumor stage, poor overall survival, immune cell infiltration, and altered drug sensitivity, highlighting their clinical relevance. Promoter methylation analysis suggested that epigenetic regulation may contribute to gene dysregulation, while genetic alterations were infrequent. Experimental validation using RT-qPCR confirmed overexpression of hub genes in LIHC cell lines. Furthermore, siRNA-mediated knockdown of these genes significantly suppressed proliferation, colony formation, and migration in HepG2 and Huh7 cells. Collectively, these findings identify CCNA2, MAD2L1, AURKA, and PTTG1 as key oncogenic drivers and potential biomarkers and therapeutic targets in LIHC. - Source: PubMed
Publication date: 2026/05/28
Jinli WangShiping Hu - A new series of seven N-(isoxazol-3-yl)-4-(1,3,4-thiadiazol-3(2H)-yl)benzenesulfonamide derivatives (22-28) was designed, synthesized, and biologically evaluated as potential dual Aurora kinase A/B inhibitors. Cytotoxicity screening against MCF-7, PC-3, HepG-2, and HCT-116 cell lines revealed variable activities, with compound 25 emerging as the most potent derivative (IC = 7.72-9.51 μM) and exhibiting selective toxicity toward cancer cells over normal WI-38 fibroblasts. Mechanistic studies demonstrated that compound 25 significantly reduced intracellular levels of Aurora A and Aurora B kinases in MCF-7 cells, decreasing Aurora A from 53.96 to 42.21 pg/mg protein and Aurora B from 63.84 to 36.48 pg/mg protein, with a more pronounced inhibition of Aurora B. Flow cytometric analysis revealed marked induction of G2/M phase arrest (46.10% vs 26.46% in control), indicating disruption of mitotic progression. In addition, compound 25 induced significant apoptosis, increasing early and late apoptotic populations to 7.99% and 25.39%, respectively, accompanied by a substantial reduction in viable cells. This effect was further supported by activation of the intrinsic apoptotic pathway, as evidenced by a 7.6-fold increase in caspase-3 expression, upregulation of Bax, and downregulation of Bcl-2.Computational analyses were performed to rationalize the observed biological behavior. DFT calculations confirmed the structural and electronic stability of compound 25. Molecular docking revealed that compound 25 binds strongly to Aurora A and B through key hydrogen-bonding and hydrophobic interactions within the ATP-binding site. Subsequent 100 ns MD simulations, MM-GBSA analyses, Pro-LIF profiling, and PCA of trajectories collectively confirmed the dynamic stability, thermodynamic favorability, and persistence of key interactions in the complexes. In silico ADME and toxicity assessments further indicated favorable pharmacokinetic properties and low predicted toxicity for compound 25. Collectively, the experimental and computational findings establish compound 25 as a promising dual Aurora kinase A/B inhibitor, integrating potent antiproliferative activity with a mechanistically supported and computationally validated interaction profile, warranting further optimization and in vivo evaluation. - Source: PubMed
Publication date: 2026/05/25
Alsfouk Bshra AElkady HazemElgammal Walid ENofal AhmedMahdy Hazem AHusein Dalal ZAmin Fatma GElkaeed Eslam BEissa Ibrahim HMetwaly Ahmed M - Lung cancer continues to be the primary contributor to cancer-related mortality worldwide. While immunotherapy markedly improves outcomes for many patients, clinical evidence indicates that non-small-cell lung cancer (NSCLC) patients with elevated Aurora A expression exhibit reduced therapeutic responses to immune checkpoint blockade. Elucidating the underlying mechanisms may unlock novel strategies to enhance the clinical benefits for this subset. In this study, we characterised cellular senescence and tumour microenvironment interactions using lung cancer cell lines with different Aurora A expression levels. H23 (high Aurora A expression) and A549 (low Aurora A expression) cells were selected to model tumour-immune crosstalk. Tumour-infiltrating lymphocytes (TILs) were isolated and activated via anti-CD28 costimulation. Through gain- and loss-of-function experiments, we established the optimal conditions to induce T-lymphocyte apoptosis and identified critical cell ratios and culture durations. In these co-culture systems, immune checkpoint inhibitors more effectively suppressed Aurora A-low tumour growth. Mechanistically, Aurora A overexpression exacerbated T-lymphocyte apoptosis via the NOXA-MCL-1 pathway. Further analysis revealed that Aurora A disrupts the eIF4G:eIF4E complex by suppressing p4E-BP1, thereby up-regulating the pro-apoptotic factor NOXA while down-regulating the anti-apoptotic factor MCL-1. Aurora A-driven T-lymphocyte apoptosis via the NOXA-MCL-1 axis compromises PD-1/PD-L1-mediated immune responses, providing a molecular rationale for immunotherapy resistance in Aurora A-high NSCLC patients. Targeting this pathway may restore T-cell viability and improve therapeutic outcomes. - Source: PubMed
Zhou ZiyiChen BiaoZheng KaiyueWan DewenKuang Peng - Malignant melanoma is an aggressive skin cancer with increasing incidence and poor prognosis after metastasis. Identifying key molecular drivers of melanoma progression is critical for developing novel therapeutic strategies. Therefore, in the present study, differential gene expression analysis was conducted on GSE98394 and The Cancer Genome Atlas-skin cutaneous melanoma datasets using 'limma' package and Gene Expression Profiling Interactive Analysis 2. Consistently dysregulated genes were intersected and subjected to Kaplan-Meier survival and Cox regression analyses. Functional assays, including reverse transcription-quantitative PCR, western blotting, MTT proliferation assay, wound healing, Transwell migration and small interfering (si)RNA-mediated targeting protein for Xklp2 (TPX2) knockdown assays, were performed in A375 and C32 melanoma cells and PIG1 melanocytes. Intersection of the two datasets revealed eight upregulated and five downregulated genes, and high TPX2 expression was significantly associated with short overall survival. TPX2 mRNA and protein levels were markedly higher in A375 cells than in PIG1 controls. silencing via siRNA reduced aurora kinase A mRNA and protein levels, inhibited cell proliferation and impaired cell migration in wound healing and Transwell assays. Overall, the integrated bioinformatics and experimental analyses identified as a potent oncogene promoting cell proliferation and migration, at least in part, via upregulation of aurora kinase A in melanoma. In conclusion, TPX2 may constitute a potential prognostic biomarker and therapeutic target for metastatic melanoma. - Source: PubMed
Publication date: 2026/05/08
Li FuqiYang RonghuiWu Zhixian - Autosomal dominant polycystic kidney disease (ADPKD), with a prevalence of approximately 1 in 1000, is the most common inherited cause of end-stage renal disease (ESRD). It is primarily caused by mutations in the or genes. Multiple studies have demonstrated that deficiency of polycystin proteins, dysregulation of signaling pathways, and activation of inflammatory factors contribute to the progression of ADPKD. The cAMP-targeting drug tolvaptan is currently the only approved therapy for ADPKD; however, its side effects and high cost have limited its widespread use. Meanwhile, mTOR inhibitors, AMPK-targeting agents, anti-inflammatory agents, and dietary interventions have shown promising results in treating ADPKD. Furthermore, the emergence of novel targets such as Notch3 and AURKA offers new directions for ADPKD therapy. This article aims to review the pathogenesis of ADPKD and current treatment advances, while exploring potential new targets for future research, hoping to provide a scientific theoretical foundation for disease management. - Source: PubMed
Publication date: 2026/04/30
Zhang WenzhengSun TianzeWang XinJiang Tao