CCND1 ELISA kit
- Known as:
- CCND1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CCND1-Mu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CCND1 ELISA kit
Related genes to: CCND1 ELISA kit
- Gene:
- CCND1 NIH gene
- Name:
- cyclin D1
- Previous symbol:
- BCL1, D11S287E, PRAD1
- Synonyms:
- U21B31
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-06
- Date modifiied:
- 2019-04-23
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- Hepatocellular Carcinoma (HCC) remains a highly lethal malignancy with limited therapeutic options, particularly in advanced stages. Yindan Pinggan Capsule (YDPG), a Traditional Chinese Medicine (TCM) formulation with hepatoprotective properties, has shown potential in liver diseases; however, its anti-tumor effects against HCC and the underlying mechanisms remain unclear. This study aimed to evaluate the anti-tumor effects of YDPG against HCC, elucidate its molecular mechanisms, and investigate its potential synergistic effects with Sorafenib. - Source: PubMed
Publication date: 2026/09/03
Hong YilinXi WeiGuo HanshiLiang JiadiZhang FudongZhang JunjieZhang YongYu Chundong - Epigenetic clocks have been widely used to estimate biological age across various tissues, but their accuracy in breast tissue remains suboptimal. Classical models such as Horvath's and Hannum's clocks perform poorly in predicting chronological age in breast tissue, underscoring the need for a tissue-specific approach. In this study, we introduce a Breast Tissue-specific Epigenetic Clock (BTEC), developed using DNA methylation data from 553 healthy breast tissue samples across seven different studies. BTEC significantly outperformed existing clocks, demonstrating superior correlation with chronological age ( = 0.91) and lower prediction errors (MAE = 3.0 y) without requiring dataset-specific regressions adjustments. Notably, BTEC showed consistent performance across ancestry groups, in contrast to existing clocks which exhibited variable ancestry-related biases. We also found that residual-based epigenetic age acceleration, commonly used to correct for prediction bias, is highly dependent on the choice of reference dataset and does not provide a generalizable correction. BTEC's chronological age predictions for tumor-adjacent samples showed distortions, with an average deviation of -2.3 y, which was even more pronounced in tumor samples, where the average difference between predicted and chronological age was -14 to -15 y. When analyzed by molecular subtype, the distortion was greater in the more aggressive HER2+ and TNBC tumors compared to HR+ tumors. Overall, our findings indicate that breast tumors do not generally exhibit accelerated epigenetic aging. The probes used by BTEC were associated with known oncogenes such as JAK1, TP73, PDGFRA, CCND1 and STAT5B, as well as genes involved in cancer-related pathways, including Wnt, Hedgehog and ErbB signaling. Importantly, extreme deviations in epigenetic age, as measured by BTEC-derived epigenetic age acceleration (EAA), were associated with patient survival in HR+ breast cancer patients in an exploratory analysis, highlighting the prognostic value of tissue-specific epigenetic aging measures. These findings demonstrate that BTECs not only improve age prediction in breast tissue but also capture biologically meaningful alterations in tumor epigenetic aging with potential clinical implications. - Source: PubMed
Publication date: 2026/09/11
Garma Leonardo DPernas SoniaFullana BartomeuVethencourt AndreaVicente Baz DavidGarcía Manrique TeresaGarcía Campelo RosarioReboredo CristinaTerrasa JosefaPerello AntoniaColomer RamónJiménez DesiréeVera García Ruthde la Cruz Sánchez SusanaBermejo BegoñaTapia MartaGonzález Santiago SantiagoQuintela-Fandino Miguel - Cadmium (Cd) is a widespread environmental contaminant that has a detrimental impact on male reproductive toxicity (MRT) due to oxidative stress, endocrine imbalance, inflammation and cell death processes. Despite the known potential of melatonin (MLT) to ameliorate the adverse effects of Cd on MRT, the exact molecular mechanisms of such multistep action are still obscure. In this work, an integrated computational approach based on network pharmacology, protein-protein interaction (PPI) network analysis, molecular docking, MM-GBSA binding energy calculation, molecular dynamics (MD) simulation, and functional annotation was used for understanding of the molecular basis of MLT-mediated protection. Forty shared targets were found between MLT-related genes and MRT-related genes caused by cadmium exposure. Ten hub genes (PTGS2, ESR1, MAPK8, EGFR, AR, NR3C1, PGR, CCND1, MMP9, and NFKB1) were selected based on network topology analysis. Functional annotation revealed that these targets are mostly involved in steroid hormone signaling, reproductive system development, transcription regulation, inflammatory signaling, and cancer pathways. Molecular docking identified that MAPK8 and PGR are the two best-binding proteins of MLT with docking scores of -7.783 and -6.830kcal/mol, respectively and MM-GBSA binding energies of -66.10 and -63.63kcal/mol, respectively. Further MD simulations over 300ns proved to be successful in achieving a stable ligand-protein complex, maintaining structural stability, and stable binding during the course of the simulations. Taken together, these results indicate that MLT might operate via modulation of the oxidative stress-related, endocrine-related, and inflammation-related pathways simultaneously instead of operating through one specific target. - Source: PubMed
Publication date: 2026/09/10
Wanjari Uddesh RameshMukherjee Anirban GoutamJayaraman ManikandanPrabhu DhamodharanJeyaraman JeyakanthanMataghare Bhairav Chandroday - Electronic nicotine delivery systems (ENDS) may contain or generate low levels of tobacco-specific nitrosamines (TSNAs), including N-nitrosoanatabine (NAT) and N-nitrosoanabasine (NAB), under certain thermal conditions. Given the uncertain long-term carcinogenic effects of ENDS, this study explored potential molecular associations between TSNA-related exposure signatures and LCNEC using an integrative computational framework. - Source: PubMed
Publication date: 2026/09/08
Xiong ZheYin LiuzheYu JiahuiLiu ZhichengWu WeiYang Gang - To quantitatively compare the expression levels of cyclin D1, epidermal growth factor receptor, Kiel-67 antigen and tumour suppressor protein P53 between gallbladder flat dysplasia and reactive epithelial changes. - Source: PubMed
Solmaz Ozgen ArslanEmiroglu MuminBozan Mehmet Bugra