Ccna2 antibody - C-terminal region (ARP30159_P050)
- Known as:
- Ccna2 (anti-) - C-terminal region (ARP30159_P050)
- Catalog number:
- arp30159_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Ccna2 antibody - C-terminal region (ARP30159_P050)
Ask about this productRelated genes to: Ccna2 antibody - C-terminal region (ARP30159_P050)
- Gene:
- CCNA2 NIH gene
- Name:
- cyclin A2
- Previous symbol:
- CCNA, CCN1
- Synonyms:
- -
- Chromosome:
- 4q27
- Locus Type:
- gene with protein product
- Date approved:
- 1990-04-09
- Date modifiied:
- 2015-08-28
Related products to: Ccna2 antibody - C-terminal region (ARP30159_P050)
Related articles to: Ccna2 antibody - C-terminal region (ARP30159_P050)
- The widely used chemotherapeutic drug cisplatin (CDDP) is an integral part of the preoperative chemotherapy protocol for high-grade osteosarcoma (OS). However, despite an aggressive treatment regimen, drug refractoriness is a major hindrance to successful therapy. We previously identified key transcriptomic alterations that support the survival of OS cells following CDDP exposure. In the present study, our analyses further demonstrate that CDDP treatment promotes an adaptive, ROS-dependent enrichment of the repressive histone mark H3K27me3 at the upstream promoter regions of growth-associated genes such as CCNA2, as well as at the promoter of LATS1, a negative regulator of Yes-Associated Protein (YAP). This enrichment contributes to the transcriptional repression of these genes and is associated with growth arrest; notably, quenching of reactive oxygen species with -acetyl cysteine (NAC) reversed this effect. Furthermore, reduced LATS1 expression was associated with increased nuclear localization of YAP. Importantly, pharmacological inhibition or genetic ablation of YAP attenuated the CDDP-induced accumulation of repressive marks. Mechanistically, YAP was found to colocalize and coimmunoprecipitate with EZH2, the catalytic member of the Polycomb Repressive Complex 2 (PRC2), suggesting a potential role for YAP in facilitating EZH2-mediated transcriptional repression. Consistent with these observations, inhibition of YAP or pharmacological reversal of the repressive chromatin state using a histone deacetylase (HDAC) inhibitor enhanced the sensitivity of the OS cells to low-dose CDDP treatment. Overall, the present study demonstrates an interplay among oxidative stress, epigenetics, and YAP in modulating OS cell fate post-CDDP exposure. - Source: PubMed
Publication date: 2026/04/14
Daiya AnkitaNayak ChinmayChowdhury RajdeepChowdhury ShibasishMukherjee Sudeshna - Yak (Bos grunniens) is a unique bovine species native to the Qinghai-Tibetan Plateau. Yak rely on their long hair to survive cold and snowy conditions at high altitudes. Flank hair or skirt hair is among the symbolic features that distinguish yak from other bovine species, yet the cellular and genetic basis underlying this unique trait remains unexplored. In this study, by comparing the transcriptomic data of skin tissues from the flank regions of adult yak and closely related low-altitude taurine cattle (Bos taurus), we identified 2521 differentially expressed genes (DEGs) in the flank hair of yak. Among them, fibroblast growth factor 21 (FGF21) is upregulated 10.3-fold in the flank hair follicles of yak. Functional experiments using primary cultures of dermal papilla cells demonstrated that treatment with recombinant FGF21 protein significantly increased the proliferation rate of yak cells. Immunofluorescence assays revealed significant increases in the percentage of PCNA and Mki67 cells after FGF21 treatment. The expression of cell cycle-related genes (CCND1, CCNA2, CCND3, CCNE1, CDK2, and CDK4) was also stimulated by FGF21 supplementation. The inhibition of FGF signaling decreased the index of cell proliferation and suppressed the expression of cell cycle-related genes. These findings demonstrate that the FGF21-FGFR signaling axis promotes hair follicle cell proliferation and is likely involved in regulating the substantial growth of flank hair in yak. This study provides novel evidence for the role of the FGF21-FGFR signaling axis in hair follicle development and offers new insights into the molecular control of adaptive traits in animals that live in extremely cold environments. - Source: PubMed
Publication date: 2026/04/09
Qin XiangZhang Lu-YaoZhang KeXie Wen-JieWan Rui-DongZhang Yi-WenTao Hai-PingYang Qi-En - Ribosomal RNA processing 9 (RRP9) encodes a WD‑repeat domain‑containing protein, which is a potential carcinogenic biomarker for various tumors. As a key structural component of small nucleolar ribonucleoproteins, RRP9 serves a key role in ribosome biogenesis by facilitating 18S rRNA processing. Despite its association with the pathogenesis of various malignancies, its function and molecular mechanisms in hepatocellular carcinoma (HCC) remain unknown. The present study aimed to examine the biological role of RRP9 in HCC progression and the underlying regulatory mechanisms. Immunohistochemical and western blot analyses revealed a significant downregulation of RRP9 expression in patients with HCC compared with matched adjacent non‑tumorous tissues. To investigate RRP9 biological functions in HCC, stable RRP9‑knockdown and ‑overexpressing isogenic HCC cell line models were established using lentiviral transduction and puromycin selection. Functional assays, including Cell Counting Kit‑8 viability, colony formation, wound healing migration and Transwell invasion experiments, consistently demonstrated that RRP9 significantly suppressed HCC cell viability, proliferation, invasion and migration. Transcriptome sequencing and western blot analyses indicated that RRP9 inhibited the PI3K/AKT/mTOR pathway. Furthermore, functional rescue assays using the PI3K activator 740 Y‑P and the inhibitor PI3K/AKT/mTOR‑IN‑2 verified that RRP9 exerts its tumor‑suppressive role via this pathway. Protein‑protein interaction analysis revealed an association between RRP9 and cyclin A2 (CCNA2). Western blotting confirmed that RRP9 downregulated CCNA2 expression. Additionally, subcutaneous tumorigenesis in mice showed that RRP9 inhibits liver cancer progression via the PI3K/AKT/mTOR signaling pathway. - Source: PubMed
Publication date: 2026/04/09
Fu ZhengkangLi ManDong KeshuaiFeng JiaruiWang Weixing - To investigate the prognostic value of cell cyclin A2 (CCNA2) in lung adenocarcinoma (LUAD) and to explore its mechanisms in promoting cancer progression. - Source: PubMed
Publication date: 2026/01/29
Li Jian-PingZhang Meng-YuLi RuiHuo ChenQu Jia-JiaQu Yi-Qing - Circular RNAs (circRNAs) are emerging as pivotal regulators of skeletal muscle development, a process critical to meat production in livestock. However, the specific functions of most circRNAs in bovine myogenesis remain unexplored. This study investigates the role of a novel circRNA, circFOXN3, in the proliferation and differentiation of bovine myoblasts. We first confirmed the circular nature of circFOXN3 by identifying its specific back-splice junction via divergent primers and Sanger sequencing, and its resistance to RNase R digestion as well as stability under actinomycin D treatment were confirmed. Subcellular fractionation assays revealed that circFOXN3 is predominantly localized in the cytoplasm. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis showed that circFOXN3 was highly and specifically expressed in muscle tissues and exhibits dynamic expression patterns during myoblast proliferation and differentiation. Functional knockdown of circFOXN3 using specific small interfering RNAs (siRNAs) during the proliferation phase significantly enhanced myoblast proliferation, as evidenced by elevated expression of proliferation marker genes (PCNA, CCND2) and increased 5-ethynyl-2'-deoxyuridine (EdU) incorporation. RNA-seq analysis following circFOXN3 knockdown revealed a comprehensive set of differentially expressed genes (DEGs). Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis reveal the significant enrichment in critical pathways, most notably the cell cycle pathway. Furthermore, protein-protein interaction (PPI) analysis of DEGs identified several core nodes in the cell cycle pathway, including CDC20, CDK1, BUB1, and CCNA2. Conversely, knockdown during the differentiation phase promoted myogenic differentiation, confirmed by the upregulation of differentiation markers (MyoG, MyoD1) and enhanced myotube formation. Our findings provide the first functional evidence that circFOXN3 acts as a potent negative regulator of bovine myogenesis. Its silencing promotes myoblast expansion and terminal differentiation, likely by modulating key cell cycle pathways and gene expression networks via its cytoplasmic localization. These results position circFOXN3 as a promising molecular target for genetic strategies aimed at improving muscle growth and efficiency in cattle production. - Source: PubMed
Publication date: 2026/03/24
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