Mouse pre-microRNA Expression Construct mir-214
- Known as:
- Mouse pre-microRNA Expression Construct mir-214
- Catalog number:
- mmir-214-pa-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sbi systeme bioscience
- Gene target:
- Mouse pre-microRNA Expression Construct mir-214
Ask about this productRelated genes to: Mouse pre-microRNA Expression Construct mir-214
- Gene:
- MIR214 NIH gene
- Name:
- microRNA 214
- Previous symbol:
- MIRN214
- Synonyms:
- hsa-mir-214
- Chromosome:
- 1q24.3
- Locus Type:
- RNA, micro
- Date approved:
- 2004-04-23
- Date modifiied:
- 2019-01-18
Related products to: Mouse pre-microRNA Expression Construct mir-214
Related articles to: Mouse pre-microRNA Expression Construct mir-214
- - Source: PubMed
Publication date: 2026/07/28
- Vascular endothelial injury is a critical driver of renal dysfunction and glomerulosclerosis in chronic kidney disease (CKD). While endothelial damage-induced inflammation contributes to sclerosis, the underlying mechanisms remain unclear. Although miR-214 has been implicated in renal fibrosis, its role in vascular endothelial cells during glomerulosclerosis is undefined. - Source: PubMed
Publication date: 2026/05/30
Tan LingxiaoFan XinwenZhang XiaoluLi ShanshanYang BingyuZhang YueHuang SongmingJia ZhanjunGong WeiZhang AihuaLi Shuzhen - Liver and cardiac fibrosis are critical drivers of chronic organ dysfunction, characterised by fibroblast activation, excessive extracellular matrix deposition, and inflammation. While these fibrotic processes are initiated by distinct triggers and monitored by organ-specific biomarkers, emerging evidence reveals both shared and unique regulatory networks, particularly involving non-coding RNAs (ncRNAs). This review focuses on the roles of microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), such as miR-21, miR-22, miR-29, miR-34a, miR-122, miR-133a, miR-210, miR-214, H19, MALAT1, MEG3, NEAT1, and circHIPK3, in modulating key fibrotic pathways including TGF-β/SMAD signalling, oxidative stress, and extracellular matrix remodelling in both hepatic and cardiac tissues. Some ncRNAs exhibit convergent regulatory functions across both organs, while others demonstrate divergent or context-dependent effects within and between tissues. Furthermore, circulating ncRNAs, potentially transferred via extracellular vesicles (EVs), hold potential as minimally invasive biomarkers for early detection of combined cardio-hepatic fibrosis, as exemplified in conditions like Fontan circulation, though extensive validation in large, prospective cohorts is essential. This article summarises established clinical biomarkers, discusses the ncRNA-mediated mechanisms operating in liver and heart fibrosis, distinguishing shared, divergent, and mixed evidence, and explores their translational potential in diagnostics and experimental therapeutics. Finally, it addresses remaining challenges and outlines future directions, emphasising multi-omic integration, longitudinal ncRNA profiling, and mechanistic validation to advance precision management of fibrotic diseases. - Source: PubMed
Publication date: 2026/06/17
Boichenko VeronikaFrolova SvetlanaVoellenkle ChristineZaccagnini GermanaFerrero PaoloBassareo Pier PaoloLuciani Giovanni BattistaGorelik JuliaMartelli Fabio - Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are clinically heterogeneous, making prediction of metastatic behavior challenging. This study examined Cell Adhesion Molecule 1 (CADM1) and the differentially expressed in adenocarcinoma of the lung-1 expression in 75 resected GEP-NETs and evaluated their associations with clinicopathological features, tumor grade, and established adhesion- or prognosis-related markers, including E-cadherin (ECAD), CD56, progesterone receptor (PgR), and cytokeratin 19 (CK19). CADM1 promoter methylation was assessed using methylation-specific PCR, and the miR-214 and miR-375 expressions were analyzed by quantitative real-time PCR. The expression of CADM1 was significantly lower in tumors with lymph node and/or distant metastasis (p = 0.01), and a low CADM1 expression was independently associated with metastatic disease (p = 0.0004; OR = 4.63). Additionally, low PgR (p = 0.014; OR = 4.13) and a high CK19 (p = 0.0002; OR = 4.83) expression, as reported previously, were linked to poor outcomes. In contrast, neither ECAD nor CD56 showed any notable associations with aggressive features in a univariable assessment. No significant relationship was observed between CADM1 promoter methylation and the CADM1 expression. These findings suggest that a reduced CADM1 expression may be associated with lymph node and distant metastasis in GEP-NETs and could be a potential prognostic marker. - Source: PubMed
Miyabe KenUmakoshi MichinobuKudo-Asabe YukitsuguKoyama KeiIshinari TakahiroTakahashi AyanaTsukita HikaruIto YukinobuYoshida MakotoTakahashi MasatoSugiyama TatsuoSageshima MasatoNanjo HiroshiMurakami YoshinoriGoto Akiteru - Although bone marrow mesenchymal stem cells (BMSCs) are an important resource for tissue engineering and have been shown capable of differentiating into uterine smooth muscle cells (USMCs) to aid uterine regeneration, the precise conditions and mechanisms that control this process require further investigation. This study employed a Transwell co-culture system of rat BMSCs and USMCs to investigate both the differentiation of BMSCs into USMCs and the involvement of protein acetylation and microRNA (miR)-214 in this transition. Our results showed that co-cultured BMSCs exhibited upregulated expression of smooth muscle markers (Calponin, alpha-smooth muscle actin, and smooth muscle myosin heavy chain), enhanced contractility, and decreased CD44 levels. Furthermore, we observed increased protein acetylation and a time-dependent upregulation of miR-214 during differentiation. Enhancement of either protein acetylation or miR-214 expression promoted BMSCs differentiation toward a USMC lineage, with miR-214 overexpression also elevating overall protein acetylation levels. These findings demonstrate that BMSCs can be directed to differentiate into USMC-like cells under defined conditions, a process likely mediated by miR-214 through promotion of protein acetylation, thereby providing mechanistic insights and experimental support for stem cell-based therapies in uterine regeneration. - Source: PubMed
Publication date: 2026/05/25
Chen ZhengYongLiao YuanYang JingZeng XiaoLing