Ask about this productRelated genes to: CCNB1 antibody
- 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
Related products to: CCNB1 antibody
Related articles to: CCNB1 antibody
- Traditional Chinese medicine QingYiHuaJi formula (QYHJ) has anti-tumor effect in Pancreatic adenocarcinoma (PAAD). However, the potential mechanism and key targets of QYHJ have not been fully elucidated. - Source: PubMed
Han JintaoQian FuchuShi Jiemin - Hepatocellular carcinoma (HCC) ranks among the most lethal cancers, and its dismal prognosis underscores the urgent need to elucidate the underlying carcinogenic mechanisms. Endoplasmic reticulum lipid rafts associated protein 2 (ERLIN2), an endoplasmic reticulum protein, has been implicated in various malignant tumors. However, its functional role in HCC remains poorly understood. Here, we found elevated ERLIN2 expression and N-glycosylation modification at asparagine 106 (N106) in HCC. We identify site-specific N-glycosylation as a crucial advantage of ERLIN2 that may result in aberrant cancer cell growth. Overexpression of either N-glycosylated ERLIN2 (wild-type, WT) or an asparagine-to-glutamine mutant (N106Q) in HCC cell lines indicated that N106 N-glycosylation of ERLIN2 acts as an important advantage in the tumorigenesis and triggers aberrant cell proliferation, migration, and invasion. Furthermore, we found that E3 ubiquitin ligase membrane-associated ring-CH-type finger protein 6 (MARCHF6) can mediate the ubiquitination degradation of ERLIN2, and this effect is more significant after the N-glycosylation at the N106 site is inhibited. In addition, excessive N-glycosylation at this site enhanced the interaction between ERLIN2 and cyclin B1 (CCNB1), leading to dysregulated CCNB1 expression and further accelerating the progression of HCC. Comprehensive studies confirm that N-glycosylation is a significant post-translational modification of ERLIN2 in HCC, and elucidating this mechanism may pave the way for the development of novel therapeutic strategies in the future. - Source: PubMed
Publication date: 2026/05/21
Li SijieHuang HuanhuanFeng JiahuiGu QiangSun Daquan - 23-Hydroxybetulinic acid (23-HBA), a key bioactive compound in the traditional Chinese herb , has garnered substantial scientific interest due to its potent antitumor activity. However, the inhibitory effects of 23-HBA on esophageal cancer growth have not been fully elucidated. - Source: PubMed
Publication date: 2026/05/05
Yang HuiSi GaoZhou XiSong XuejieDu HaiyangSi Fuchun - Bisphenol A (BPA), an environmental endocrine disruptor, is implicated in hepatocellular carcinoma (HCC), but its molecular mechanisms are unclear. This study employed an integrative computational framework to identify potential BPA-related molecular targets in HCC, assess their statistical clinical value, and generate hypotheses regarding their roles within the tumor microenvironment. BPA and HCC targets were retrieved from public databases and intersected with differentially expressed genes in HCC, identifying fifteen overlapping genes statistically enriched in cell cycle regulation, p53 signaling, and viral carcinogenesis. Six hub genes (MKI67, CCNA2, EZH2, CCNB1, CDK1, BIRC5) were significantly upregulated in HCC with high internal cross-validated diagnostic accuracy (AUC > 0.96), although these estimates may be susceptible to overfitting and require external validation. Molecular docking and dynamics simulations predicted stable BPA binding to six proteins (Ki67, Cyclin A2, EZH2, Cyclin B1, CDK1, Survivin), with van der Waals forces calculated as the primary driving energy contribution by MM-PBSA. The two-gene (CCNB1/EZH2) risk model showed statistical associations with patient survival, validated internally and externally, although its generalizability remains limited. Mendelian randomization provided genetic evidence consistent with a potential risk-associated role for CCNB1 and a protective-associated role for EZH2. Single-cell analysis localized high CCNB1 and EZH2 expression to malignant and proliferative T-cells, correlating with specific immune infiltration patterns and checkpoint expression. In conclusion, these computational findings suggest a statistical and structural association between BPA exposure and HCC-related core cell-cycle regulators (e.g., CCNB1/EZH2). The data generate the hypothesis that CCNB1 and EZH2 may serve as prognostic biomarkers and potential contributors to HCC biology, possibly through coordinated effects on cell cycle dysregulation and immune microenvironment remodeling, though direct evidence of in vivo molecular targeting by BPA or causal pathway activation is not established by this study. These findings provide novel insights into BPA's putative role in hepatocarcinogenesis and offer clues for future experimental validation regarding risk assessment and therapeutic strategies. - Source: PubMed
Publication date: 2026/05/12
Zeng FulingLai FuyanZeng Jiaxin - The grass carp reovirus (GCRV) infection poses a severe threat to grass carp because it triggers hemorrhagic disease using complex host-virus interactions but research on the early phases of GCRV infection is still lacking. To evaluate host responses to GCRV infection, in the current study we used Ctenopharyngodon idella kidney (CIK) cells as in vitro model infected with GCRV-I to conduct comparative experiments at different time points 0, 3, 6, 12, and 24h. GCRV infection caused cytopathic effects (CPEs) in (CIK) cells. Significant temporal variations in host gene expression were found by targeted qPCR studies and qPCR analysis demonstrated dynamic modulation of host gene expression. Significant variations between treated and control cells were shown by comparative expression profiling across different time points. High-throughput RNA sequencing (RNA-seq) revealed transcriptional reprogramming during infection, reflected by progressive elevation in differentially expressed genes, followed by qPCR validation. Notably, GO/KEGG enrichment analysis showed that GCRV-I activated the cholesterol, steroid, cell cycle, immune related and circadian regulation across all time points. Important genes with time-dependent expression patterns included dhcr7, cdk1 and irf3. Cell cycle regulators (ccnb1, cdc25b, wee1, cdc20) modulate cdk1 activity, separating transcriptional programs into irf3/tlr19 centered antiviral modules and dhcr7-centered cholesterol metabolism during early GCRV infection in CIK cells, according to our time-series RNA-seq and Weighted Gene Co-expression Network Analysis (WGCNA). These results provide possible targets for antiviral treatments in aquaculture and clarify complex host response to GCRV and provide a novel antiviral potential through cholesterol pathway. - Source: PubMed
Publication date: 2026/05/08
Younas WaqarZhang LeiShi MijuanYang HongCheng YingyinZhang WantingWang YapingXia Xiao-Qin