CCNB1 & CDC25A Protein Protein Interaction Antibody Pair
- Known as:
- CCNB1 & CDC25A Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0023
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CCNB1 & CDC25A Protein Interaction Antibody Pair
Ask about this productRelated genes to: CCNB1 & CDC25A Protein Protein Interaction Antibody Pair
- Gene:
- CCNB1 NIH gene
- Name:
- cyclin B1
- Previous symbol:
- CCNB
- Synonyms:
- -
- Chromosome:
- 5q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-10
- Date modifiied:
- 2016-10-05
- Gene:
- CDC25A NIH gene
- Name:
- cell division cycle 25A
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1992-07-31
- Date modifiied:
- 2017-12-06
Related products to: CCNB1 & CDC25A Protein Protein Interaction Antibody Pair
Related articles to: CCNB1 & CDC25A Protein Protein Interaction Antibody Pair
- This study aims to systematically investigate the molecular mechanisms through which parabens may contribute to head and neck squamous cell carcinoma (HNSCC) carcinogenesis using integrated network toxicology and molecular docking. - Source: PubMed
Publication date: 2026/03/23
Zhao LeiYang JianwangLiu TaoCao HuanYu MiaomiaoWang Baoshan - This study assessed the effect of cellular senescence-related genes in the development of osteoporosis (OP) via the databases, which may be the potential targeted biomarkers of the OP. The development of OP is significantly influenced by cellular senescence (CS). However, the exact mechanism of CS in OP is unknown. Hence, it is imperative to uncover the molecular mechanisms and therapeutic targets implicated in CS-associated OP. In the Gene Expression Omnibus (GEO) and GeneCards databases, we identified differential genes (DEGs) that are associated with OP and CS. Subsequently, their function was assessed through GO, KEGG, and GSEA analysis. The protein-protein interaction (PPI) network was correlated and analyzed to obtain key genes. Finally, animal models were employed for experimental validation. Eight genes, CDK1, CCNB1, TOP2A, FEN1, CDC6, FOXM1, CDC25A, and MCM2, were recognized as potential biomarker genes. FEN1 and CDC6, as new potential markers, have not been reported yet. We found that cell cycle regulation has an important role in aging-induced OP, which provides new ideas for the further development of targeted therapies. - Source: PubMed
Publication date: 2025/12/09
Wang PeiwenHu XipingHan ChunqingChang YuanjinXie RuijinYe JunxingWu Yu - Non-obstructive azoospermia (NOA) is among the most severe type of male infertility, which is characterized by the absence of sperm in the ejaculate of affected individuals. The underlying causes of NOA remain largely unidentified, leading to a dearth of effective clinical interventions. This study aimed to explore a potential biomarker for NOA, and to elucidate the underlying mechanisms involved. The RNA-sequencing of the testis tissue revealed that miR-34a-5p increased, while CDC25A mRNA decreased in NOA patients compared to obstructive azoospermia (OA) controls. RT-qPCR confirmed that miR-34a-5p was upregulated in the seminal plasma of NOA patients compared to healthy individuals, demonstrating its potential as a discriminatory marker for distinguishing between NOA and healthy individuals. The dual-luciferase assay demonstrated that miR-34a-5p directly targets CDC25A and inhibits the cell proliferation of TM4, GC-1 and GC-2 cells by arresting the cell cycle at the G1 phase. Both in vitro and in vivo experiments, the overexpression of miR-34a-5p led to a reduction in the level of CDC25A and CCNB1, accompanied by an elevation in the level of CDK1 phosphorylation. In mice overexpressing miR-34a-5p, the testicular size, testicular organ coefficient, total epididymal sperm count and motility were significantly decreased, the structure of seminiferous tubules was disrupted, and the abnormal tubules was significantly increased. In summary, miR-34a-5p causes cell cycle arrest by targeting CDC25A, inhibiting the expression of CDC25A and CCNB1, preventing the dephosphorylation of CDK1, which ultimately leads to male spermatogenic failure. The miR-34a-5p level in seminal plasma may have potential value for the diagnosis of NOA. - Source: PubMed
Publication date: 2025/05/26
Lin MeinaShi ZiyanChen XinrenNi XiangSui YuLi HuanGuan ChangjiTian ZhiyingJiang MiaoJiang JingyiGuo TingchaoLu Yongping - The ALDH1A1 gene encodes a cytoplasmic member of the aldehyde dehydrogenase 1 family, which plays an important role in regulating animal reproductive performance, including estrus cycle and embryonic development. The aim of this study was to characterize ALDH1A1 activity in ovaries of 3-5 year-old yaks and to determine its effects on cell proliferation, apoptosis, and progesterone secretion in luteal cells (LCs). The coding sequence (CDS) of the ALDH1A1 gene was cloned by reverse transcription-PCR and immunohistochemical analysis was used to confirm localization of the ALDH1A1 protein in the ovary. To assess the activity of ALDH1A1 in regulating progesterone secretion, si-ALDH1A1 was transfected into LCs in vitro and progesterone levels in LC supernatants were measured by ELISA. The interference efficiency was assessed by real-time quantitative PCR (RT-qPCR) and immunofluorescence staining, and cell proliferation and apoptosis were evaluated by EdU and TUNEL staining, respectively. The cloned ALDH1A1 sequence contained 1462 bp, encoding 487 amino acids. Immunohistochemical analysis showed that ALDH1A1 protein expression, which was significantly higher in LCs, was mainly found in antral follicles and the corpus luteum (CL). The expression of ALDH1A1 mRNA in LCs was effectively inhibited by si-ALDH1A1transfection, and progesterone secretion was markedly decreased along with the significant down-regulation of progesterone pathway-related genes, STAR, CYP11A1, CYP19A1, CYP17A1, 3β-HSD, and HSD17B1. Knockdown of ALDH1A1 mRNA expression decreased cell proliferation and increased apoptosis in LCs. The mRNA expression of the proliferation-related genes, PCNA, CCND1, CCNB1 and CDC25A, was significantly down-regulated, while expression of the apoptosis-promoting CASP3 gene was significantly increased. In summary, we characterized the yak ALDH1A1 gene and revealed that ALDH1A1 knockdown promoted apoptosis, repressed cell proliferation, and decreased progesterone secretion by yak LCs, potentially by regulating the mRNA expression of genes related to proliferation, apoptosis, and progesterone synthesis and secretion. - Source: PubMed
Publication date: 2024/04/30
Fei XixiZhu YanjinPan BangtingCheng YuyingYang QinhuiXie YumianXiong YanFu WeiXiong XianrongLi Jian - Hyperprolactinemia is prevalent in up to 16% of infertile males. Although the prolactin receptor (PRLR) is present on various testicular cells, the physiological role of this receptor in spermatogenesis remains elusive. The aim of this study is to delineate prolactin actions in rat testicular tissue. Serum prolactin, developmental expression of PRLR, signaling pathways associated, and gene transcription regulation in the testes were investigated. Serum prolactin and testicular PRLR expression was found to be significantly increased at pubertal and adult ages as compared to prepubertal. Further, PRLR activated the JAK2/STAT5 pathway, but not the MAPK/ERK and PI3K/AKT pathway in the testicular cells. Gene expression profiling following prolactin treatment in seminiferous tubule culture resulted in a total of 692 differentially expressed genes, of which 405 were upregulated and 287 were downregulated. Enrichment map analysis showed that prolactin target genes are involved in processes such as cell cycle, male reproduction, chromatin remodeling, and cytoskeletal organization. Novel gene targets of prolactin whose role in testes is unexplored were obtained and validated by qPCR. Additionally, 10 genes involved in cell cycle process were also validated; 6 genes (Ccna1, Ccnb1, Ccnb2, Cdc25a, Cdc27, Plk1) were found to be significantly upregulated, whereas 4 genes (Ccar2, Nudc, Tuba1c, Tubb2a) were found to be significantly downregulated in testes after treatment with prolactin. Taken together, the findings from this study suggest a crucial role of prolactin in male reproduction and identified target genes regulated by prolactin in the testes. - Source: PubMed
Raut SanketaKhambata KushaanGoffin VincentBalasinor Nafisa