Ask about this productRelated genes to: AURKC Blocking Peptide
- Gene:
- AURKC NIH gene
- Name:
- aurora kinase C
- Previous symbol:
- STK13
- Synonyms:
- AurC, ARK3
- Chromosome:
- 19q13.43
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-13
- Date modifiied:
- 2015-08-27
Related products to: AURKC Blocking Peptide
Related articles to: AURKC Blocking Peptide
- Children with intellectual disability are more likely to experience chronic and neuropathic pain, which remains frequently under-recognized due to limitations in self-reporting and objective assessment tools. Epigenetic mechanisms, particularly DNA methylation, are believed to influence pain perception. This study investigates the differences in methylation patterns between children with intellectual disability and their age- and sex-matched neurotypical controls. - Source: PubMed
Publication date: 2026/05/18
Celsi FulvioZupin LuisaSenn Francescad'Adamo PioCappellani StefaniaDe Zen LuciaCozzi GiorgioSelicorni AngeloBarbi EgidioPeri Francesca - Acute myeloid leukemia (AML) is an aggressive hematologic malignancy characterized by impaired differentiation and accumulation of immature myeloid cells. Aurora kinases and their regulatory genes play key roles in mitotic progression and may contribute to leukemogenesis. This study aimed to evaluate the expression and promoter methylation status of , , and and their regulatory genes, , , and in AML. Peripheral blood samples from 83 AML patients and 28 age- and sex-matched healthy controls were analyzed using MIQE-compliant RT-qPCR for gene expression and MSRE-qPCR for promoter methylation. Diagnostic performance was assessed using receiver operating characteristic (ROC) curve analysis. Expression levels of , , , and were significantly increased in AML patients ( < 0.001), whereas expression was significantly reduced ( = 0.001), and showed no significant difference. Promoter methylation analysis revealed significantly increased methylation in AML ( < 0.001), decreased methylation ( = 0.023), and no significant change in . ROC analysis demonstrated strong diagnostic performance, with showing the highest accuracy (AUC = 0.95), while a combined biomarker panel achieved an AUC of 0.96. Aurora kinase-related genes are dysregulated in AML and may serve as preliminary peripheral biomarker candidates. However, further validation in independent cohorts and more refined cellular models is required before clinical application. - Source: PubMed
Publication date: 2026/04/05
Yalniz Kayim ZubeydeTuncer Seref BugraCelik Demirbas BetulGezer UgurSukruoglu Erdogan OzgeKilic Erciyas SedaDalay NejatSelim Yavuz AkifYasasever Vildan - Decabromodiphenyl ethane (DBDPE), a widely used novel brominated flame retardant, has been increasingly detected across environmental matrices and human samples. Owing to its marked persistence and bioaccumulation potential, DBDPE was designated as a Substance of Very High Concern (SVHC) by the European Chemicals Agency in 2025. However, evidence regarding its potential reproductive hazards remains limited. Here, we systematically investigated the molecular mechanisms underlying DBDPE-induced spermatogenic disorder using an integrated approach that combines network toxicology, machine learning, and in vivo validation. Intersecting 564 DBDPE-associated targets with 1,743 NOA-related differentially expressed genes identified 33 overlapping candidates that may mediate DBDPE-induced spermatogenic disorder. Enrichment analyses implicated the HIF-1 signaling and gap junction pathways in DBDPE-induced spermatogenic disorder. Machine learning prioritized five core genes, including PRKACG, WDR5, AURKC, PFKP, and ASGR1, all of which were downregulated in NOA patients. Molecular docking demonstrated stable binding between DBDPE and these core targets. In vivo, DBDPE exposure disrupted testicular structure, reduced sperm concentration and motility, and decreased expression of the five core proteins, confirming the predicted mechanisms. Additionally, we proposed an adverse outcome pathway (AOP) framework describing key events leading to DBDPE-induced spermatogenic impairment. Collectively, our findings revealed the reproductive toxicity of DBDPE and provided a mechanistic foundation for developing strategies to safeguard male fertility. - Source: PubMed
Publication date: 2026/03/27
Shi WeiSun YuantengLiu KejiaZhang YingLu LuZhou QianPu YuepuSun RongliYin Lihong - Macrozoospermia is a rare cause of male infertility characterized by a high proportion of sperm with large, irregular heads. In this study, we identified a novel homozygous Aurora kinase C () missense variant (c.253G > A (p.Glu85Lys)) in a Chinese infertile man using whole-exome sequencing. Segregation of the c.253G > A variant within the family was confirmed by Sanger sequencing, and In silico prediction tools suggested that the variant is pathogenic. Sperm ultrastructural abnormalities in the patient were further examined using transmission electron microscopy. Our findings identify a novel pathogenic variant associated with macrozoospermia, providing potential value for genetic diagnosis and clinical management. - Source: PubMed
Publication date: 2026/01/13
Zhang JianZhao YijiaDeng LiwenWu YuchunLi RongWang Binbin - Aurora kinases, AURKA, AURKB, and AURKC, are serine/threonine kinases that play a vital role in regulating cell division and mitosis, particularly in the separation of chromosomes. These kinases are often overexpressed in human tumor cell lines, indicating their potential involvement in tumorigenesis. Preliminary evidence supports the use of Aurora kinase inhibitors for certain types of tumors, several AURKs inhibitors are currently under phase I and II trials. As a result, there is a growing interest in identifying small-molecule Aurora kinase inhibitors to develop as anti-cancer agents. The regulation of the cell cycle, including mitosis, is increasingly recognized as a key target in the fight against various forms of cancer. Novel drugs are being designed to inhibit the function of regulatory proteins, such as Aurora kinases, with the goal of creating personalized treatments. This review summarizes the biology of Aurora kinases in the context of cancer, integrating both preclinical and clinical data. It discusses the challenges and opportunities associated with using Aurora kinases to enhance cancer treatment. Future directions for Aurora kinase-based therapies include developing more selective inhibitors that minimize off-target effects and improve therapeutic efficacy. Researchers are also exploring combination therapies that use Aurora kinase inhibitors alongside other targeted treatments to overcome resistance and improve patient outcomes. Additionally, advancements in biomarker discovery are expected to facilitate the identification of patients most likely to benefit from Aurora kinase-targeted therapies, paving the way for more personalized approaches to cancer treatment. - Source: PubMed
Publication date: 2025/06/18
Vats PrernaSaini ChainseeBaweja BhavikaSrivastava Sandeep KKumar AshokKushwah Atar SinghNema Rajeev