Mouse polyclonal to MED8, Host Mouse
- Known as:
- Mouse pab MED8, Host Mouse
- Catalog number:
- YF-PA26806
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse polyclonal MED8 Host
Related genes to: Mouse polyclonal to MED8, Host Mouse
- Gene:
- MED8 NIH gene
- Name:
- mediator complex subunit 8
- Previous symbol:
- -
- Synonyms:
- MGC17544, MGC19641, ARC32
- Chromosome:
- 1p34.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-09
- Date modifiied:
- 2016-10-05
Related products to: Mouse polyclonal to MED8, Host Mouse
Related articles to: Mouse polyclonal to MED8, Host Mouse
- PDGFRA genetic alterations are a well-established oncogenic driver in gliomas. However, targeted monotherapy against PDGFRA such as avapritinib has achieved limited clinical efficacy, and the mechanism underlying avapritinib resistance remains poorly understood. - Source: PubMed
Publication date: 2026/05/19
Xie HanXiong ZhangHuang RuixiangDong YongfeiWang YunlongChen TaoZhong ChunlongJiang YuanTian DashengBian Erbao - Disulfidptosis, a recently identified form of cell death, plays a crucial role in cancer progression, specifically by altering intracellular disulfide bonds within the actin cytoskeleton. Our research centres on developing a prognostic model based on disulfidptosis-related long noncoding RNAs (DRLRs) to differentiate high-grade (G3-G4) from low-grade (G1-G2) Hepatocellular Carcinoma (HCC). Utilizing transcriptomic data from The Cancer Genome Atlas (TCGA), we employed univariate Cox regression analysis, Least Absolute Shrinkage and Selection Operator(LASSO) regression, and multivariate Cox regression to ultimately identify nine key drlncRNAs (AL442125.2, AC018529.2, AL031985.3, AC119150.1, LINC02256, AC026979.4, POLH-AS1, MED8-AS1, and AC026356.1). These were subsequently used to construct a prognostic risk signature model. This 9-DRLR model demonstrated robust discriminative capacity, achieving Area Under the Curve(AUCs) of 0.845, 0.841, and 0.885 for 1-, 3-, and 5-year overall survival prediction in G3-G4 HCC patients, respectively. The model provides strong prognostic stratification of HCC patients by grade and correlates with biological processes linked to tumour aggressiveness and immune evasion, as shown by Gene Ontology (GO) and gene set enrichment analyses (GSEA). High-risk groups exhibited markers of immune dysfunction, elevated tumour mutation burden (TMB), and increased sensitivity to targeted therapies including 5-Fluorouracil and Dasatinib. AL031985.3 emerged as a key lncRNA within this model, with its significant overexpression in HCC tissues versus adjacent controls (p < 0.001) validated through quantitative Real-Time PCR (qRT-PCR). Functional analyses revealed AL031985.3 as a critical oncogenic driver, where its knockdown significantly suppressed colony formation (p < 0.01) and reduced invasive capacity (p < 0.01) in vitro. These findings were corroborated in vivo, with orthotopic implantation and experimental pulmonary metastasis models demonstrating attenuated tumour growth and modulated epithelial-mesenchymal transition markers following AL031985.3 silencing. Our findings underscore the prognostic value of the DRLR signature and establish AL031985.3 as a potential therapeutic target for advanced HCC. - Source: PubMed
Publication date: 2026/03/30
Yang LingLi FeiYu HailinGu XuefengYou Wei - Mediator complex subunits have recently been reported to be associated with tumor progression, the tumor immune microenvironment, and therapeutic responses. However, limited research about oncology has been conducted on Mediator complex subunit 8 (MED8). The functional role and molecular mechanism of MED8 in bladder cancer (BLCA) require further systematic bioinformatic analysis and experimental validation. Analysis of The Cancer Genome Atlas pan-cancer cohort and multiple bladder cancer datasets revealed MED8 upregulation in various tumors. More importantly, MED8 expression was correlated with poor prognosis in bladder cancer patients. In vitro proliferation and migration assays demonstrated that MED8 knockdown suppressed bladder cancer cell proliferation and motility. Conversely, MED8 overexpression promoted cellular proliferation and migration. Meanwhile, the influence of MED8 on the growth of BLCA was validated in vivo. Integrated multi-omics sequencing (RNA-seq combined with Astral-DIA proteomics) identified Stearoyl-CoA desaturase (SCD) as a potential downstream effector of MED8. Finally, rescue experiments confirmed that MED8 regulates bladder cancer cell proliferation and migration through SCD. In conclusion, this study is the first to reveal the oncogenic function and overexpression of MED8 in bladder cancer and its tumor-promoting effects are mediated through SCD regulation. These findings provide novel insights into the molecular mechanisms of bladder cancer progression and establish a theoretical foundation for targeting MED8 as a therapeutic strategy. - Source: PubMed
Publication date: 2026/02/03
Zhang HaiyuLiu YuhanHuang WeishengLi YanfengYao XiangyangChen XuanLiu YueMei QiaolinYang XiaokangWang JiajunLiao XinhuiMei Hongbing - The SEC13 is a multifaceted gene implicated in mTORC1 signaling regulation and the maintenance of genomic stability. Its function in cancer is complex, displaying potential oncogenic as well as potential tumor-suppressive roles across different malignancies. Therefore, this study aimed to investigate SEC13 expression, prognostic value, and its relationship with immune checkpoints across different cancer types. - Source: PubMed
Publication date: 2026/02/02
Gu YanlinYu YangLiu KaimingJin LiyanJiang Guoqin - The Mediator (MED) complex is an essential regulator of RNA polymerase II transcription. There is increasing evidence that pathogenic variants in several MED subunits are the cause of neurodegenerative and neurodevelopmental phenotypes, collectively referred to as "MEDopathies". This review aims to summarize current knowledge on the genetic basis, clinical manifestations, and neuroradiological features of MED-related disorders. We undertook a narrative synthesis of the literature focusing on the MED subunits most commonly associated with neurological disorders, including MED1, MED8, MED11, MED12/MED12L, MED13/MED13L, MED14, MED17, MED20, MED23, MED25, MED27, and CDK8. Sources included peer-reviewed genetic, clinical, and imaging studies, supplemented by relevant case reports and cohort analyses. In addition, representative facial phenotypes associated with selected MED variants () were visualized for educational purposes using artificial intelligence-based image generation derived from standardized clinical descriptors. : All MEDopathies show converging clinical patterns: global developmental delay/intellectual disability, hypotonia, epilepsy, speech disorders, and behavioral comorbidity. Non-neurological involvement, such as craniofacial or cardiac anomalies, is subunit-specific. Neuroradiological features include callosal abnormalities (agenesis, thinning, dysmorphia), delayed or hypomyelination, progressive cerebral and cerebellar atrophy, basal ganglia signaling changes, pontine hypoplasia, and, in deficiency, a "hot cross bun" sign. Gene-specific constellations emphasize catastrophic infantile progression (), X-linked syndromes with callosal defects (), language-dominant phenotypes (), and syndromic intellectual disability with systemic features (). : The growing spectrum of MEDopathies argues for their recognition as a unified nosological group with overlapping clinical and radiological signatures. Characteristic MRI constellations may serve as diagnostic clues and guide targeted molecular testing. Future directions include longitudinal imaging to describe disease progression and the integration of genomic data with curated clinical radiological datasets to refine genotype-phenotype correlations. - Source: PubMed
Publication date: 2025/12/02
Fazio AlessandroLeonardi RobertaAliotta LorenzoLo Bianco ManuelaAnastasio GennaroMessina GiuseppeSpatola CorradoFoti Pietro ValerioPalmucci StefanoBasile AntonioRuggieri MartinoDavid Emanuele