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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- 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 - Primary hyperparathyroidism (PHPT), considered a rare disease almost a century ago, has shown a notable increase in incidence over the past five decades, driven largely by improved diagnostic screening and greater clinical awareness. Following the same trend, the incidence of parathyroid carcinoma (PC), a very rare but aggressive malignancy accounting for approximately 1% of PHPT cases, appears to be rising. This increase parallels the overall rise in PHPT detection, suggesting that enhanced surveillance contributes to identifying more PC cases. PC is mostly characterized by severe hypercalcaemia, due to tumoral parathyroid hormone (PTH) over-secretion and a high rate of local recurrence and metastasis, making early diagnosis and surgical treatment crucial. Recent advances in genetics and epigenetics have profoundly expanded our understanding of PC pathogenesis. Germline and somatic mutations in the tumour suppressor gene (encoding parafibromin) are implicated in up to 75% of familial and sporadic PC cases. Additional recurrent mutations in genes such as and , alterations in cell cycle regulators such as and , and disruptions in signalling pathways including PI3K/AKT/mTOR have been identified. Epigenetic modifications, including microRNA expression changes and promoter hypermethylation, also play a significant role in tumour development and progression. This mini review synthesizes epidemiological trends demonstrating an increasing incidence of PC following the rise of PHPT and highlights pivotal genetic and epigenetic findings contributing to tumourigenesis. Integrating new molecular insights with advances in clinical surveillance offers promise for improved diagnosis, prognostic stratification, and the development of future targeted therapies for parathyroid carcinoma. - Source: PubMed
Publication date: 2026/08/14
Betea DanielaPetrossians Patrick - JMJD2D is a histone demethylase implicated in cancer-associated gene regulation, but its role in non-small cell lung cancer (NSCLC) remains incompletely defined. We examined JMJD2D expression and functional effects in patient specimens and lung cancer models. JMJD2D expression was higher in 41 paired NSCLC tissues than in adjacent non-tumor tissues, was greater in stage III-IV than in stage I-II tumors, and was associated with worse overall survival. JMJD2D was also elevated in A549 and H1975 cells relative to HBE cells. shRNA-mediated JMJD2D knockdown reduced CCK-8 and colony-formation readouts and attenuated migration and invasion in both cell lines; it also reduced xenograft tumor growth and lowered MYC, CCND1, MMP2, and MMP9 mRNA and protein levels in tumors. In A549 cells, endogenous co-immunoprecipitation detected JMJD2D and β-catenin in the same complex. PRI-724 or Z-JIB-04 treatment conditions were associated with lower malignancy-associated readouts and lower levels of selected transcripts, without an apparent change in total β-catenin abundance. These findings associate JMJD2D with aggressive clinical and experimental phenotypes in lung cancer and support further investigation of its molecular role and therapeutic relevance. - Source: PubMed
Publication date: 2026/09/02
Lu QiuxiaTang YicongLi SidaChen XuFan MingMin XiangboWen XueLin XiaominLi Dongqing - Drug-target Mendelian randomisation (MR) studies investigate whether genetically proxied modulation of druggable proteins affects the risk of periodontitis, thereby identifying potential pharmacological targets. - Source: PubMed
Publication date: 2026/09/02
Nibali LuigiKang JingHaworth SimonPolizzi AlessandroIsola Gaetano - Stevioside, a natural glycoside with diverse bioactivities, holds therapeutic potential in liver diseases, but its role in cholestatic liver repair remains largely unexplored. This study investigates the regenerative efficacy and underlying mechanisms of stevioside in bile duct ligation (BDL)-induced cholestatic liver injury. A combined pre- and post-treatment regimen of stevioside (90 mg/kg) robustly mitigated hepatic damage, evidenced by reduced necrosis, suppressed inflammation, attenuated ductular reaction, and improved hepatic function. Notably, stevioside significantly stimulated hepatocyte proliferation, as indicated by increased liver-to-body weight ratios, upregulation of cell-cycle regulators (Ccnd1, Ccna2), and transcriptomic enrichment of proliferation-related pathways. Utilizing the genetic proliferation tracing system (ProTracer), we further demonstrated that stevioside preferentially promotes the regeneration of periportal (Zone 1) and midzonal (Zone 2) hepatocytes. Conversely, it constrained the expansion of biliary epithelial cells and immune cells, thereby collectively alleviating pathological ductular reaction and inflammatory infiltration. Mechanistically, stevioside activated YAP signaling in hepatocytes and remodeled bile acid metabolism, together creating a favorable microenvironment for liver regeneration. Furthermore, stevioside exhibited a favorable safety profile with no detectable hepatotoxicity, fibrosis, or tumorigenic risk under the experimental conditions. Our findings establish that stevioside repairs cholestatic injury by directly driving region-restricted hepatocyte proliferation via YAP signaling, highlighting its potential as a mechanistically innovative candidate for the treatment of cholestatic liver diseases. - Source: PubMed
Publication date: 2026/08/31
Jiang WeiFang Xu-YiSun Yi-MengXu Meng-YuanHan XinYan Shuo-JunLiu XuLiu Ya-YunZeng XianLai Wen-QiangHuang Jin-QuanZhou BinMeng Xiao-WeiZhao Yong-XuLi Yan