GTF2B antibody - N-terminal region (P100990_T100)
- Known as:
- GTF2B (anti-) - N-terminal region (P100990_T100)
- Catalog number:
- p100990_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GTF2B antibody - N-terminal region (P100990_T100)
Related genes to: GTF2B antibody - N-terminal region (P100990_T100)
- Gene:
- GTF2B NIH gene
- Name:
- general transcription factor IIB
- Previous symbol:
- -
- Synonyms:
- TFIIB
- Chromosome:
- 1p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-08-16
- Date modifiied:
- 2016-10-05
Related products to: GTF2B antibody - N-terminal region (P100990_T100)
Related articles to: GTF2B antibody - N-terminal region (P100990_T100)
- The RAW264.7/THP1 cells have been extensively employed as macrophage models in inflammation research. However, comprehensive comparisons of their expression profiles remain largely unexplored. In this study, we conducted a systematic bioinformatics analysis to characterize the whole-cell proteome, phosphoproteome, acetylome, and ubiquitinome profiles of lipopolysaccharide-stimulated RAW264.7/THP1 cells. Through comparative temporal analysis of differentially regulated proteins (classified as rapid, persistent, or slow dysregulation patterns), we identified IGF2, COPZ1, and GTF2B, exhibiting persistent downregulation in both cell models. Additionally, we observed that nearly all dysregulated proteins within each modification type exhibited significant enrichment in the other two modification types, forming a highly interconnected protein-protein interaction network. Notably, VIMENTIN demonstrated significant downregulation across three modification types (phosphorylation at Ser56/214, acetylation at Lys235, and ubiquitination at Lys139), with coordinated downregulation observed in both cell lines. It was also shown that VIMENTIN mutation at Ser56, Lys235, and Lys139 dramatically reduces the expression of CDK1, which may help the inflammation response by averting mitotic catastrophe and changing the macrophage cell cycle. These findings provide valuable molecular insights into species-specific macrophage responses and establish an important reference data set for discovering novel inflammatory proteins and investigating macrophage-associated diseases using these experimental models. Notably, our work delineates vimentin-centered regulatory networks that may offer novel diagnostic biomarkers and therapeutic targets for inflammatory diseases. - Source: PubMed
Publication date: 2026/06/18
Yuan GangZhi LiangeWang JieyanWang JinhongZhu BingwenHan XinaiLiu JiachengCai LiminJie HongyuYan Zhengzheng - This study aimed to investigate the expression and prognostic significance of genes associated with copper-induced cell death in glioblastoma multiforme (GBM). Using a suite of bioinformatics tools and databases, the researchers analyzed gene expression, survival rates, and immune infiltration in GBM. Complementary in vitro experiments were performed to evaluate the effects of LIPT1 inhibition on GBM cell behavior in the context of copper-induced cell death. The team further explored upstream mechanisms leading to LIPT1 overexpression in GBM, specifically focusing on transcription factors and the role of ubiquitination degradation. The findings indicated a significant upregulation of LIPT1 in GBM, correlating with increased sensitivity to copper-induced cell death. Inhibition of LIPT1 was observed to exacerbate malignant behaviors in GBM cells post-copper exposure. Subsequent analysis pinpointed three transcription factors—CBX3, E2F6, and GTF2B—as regulators of LIPT1. Notably, GTF2B was also found to be co-expressed with LIPT1 and positively associated with recurrence-free survival in patients. ChIP-seq data analysis revealed significant GTF2B binding peaks near the LIPT1 promoter. Further exploration using UbiBrowser 2.0 identified E3 ubiquitin ligases that potentially target GTF2B, with RBX1 emerging as a viable anti-cancer target in GBM. Data from the UALCAN database showed a notable decrease in RBX1 protein expression in GBM tissues. Moreover, several ubiquitination modification sites were detected on the GTF2B protein. In conclusion, the study proposes a novel scientific hypothesis: RBX1 inhibits LIPT1 transcription by promoting the ubiquitin-mediated degradation of GTF2B, thereby suppressing copper-induced cell death in GBM cells. These findings offer new insights into the molecular mechanisms governing copper death sensitivity in GBM and identify potential therapeutic targets for further exploration. - Source: PubMed
Publication date: 2026/01/31
Zeng JianpingLiu JingHua ShushanLiu ShuaiTong ShoufangZhang JieMungur RajneeshChen ShangshiFeng JiugengDing Cong - The growing epidemiological burden of multimorbidity among older adults underscores an urgent need to develop interventions that can address multiple age-related diseases (ARDs) at once. Yet, the biological mechanisms driving their co-occurrence remain poorly understood. In this study, we conducted a multivariate genome-wide association analysis to dissect the shared genetic architecture of five common ARDs: heart attack, high cholesterol, hypertension, stroke, and type 2 diabetes. We defined this shared genetic component as the multivariate age-related disease factor (mvARD) and identified 263 independent variants across 180 genomic loci associated with mvARD. These variants were significantly enriched for associations with extreme human longevity, lending empirical support for the geroscience hypothesis in humans. Integrative gene prioritization using transcriptome-wide association studies, colocalization analysis, and Mendelian randomization identified four high-confidence genes in blood-DCAF16, PHF13, MGA, and GTF2B-with putative causal roles on mvARD. Using two-sample Mendelian randomization, we also found several modifiable lifestyle factors, including body mass index and dietary intake, that causally influenced the risk for multiple ARDs. Together, our findings revealed a shared genetic basis for common ARDs that overlapped with the biology of human aging and pointed to potential molecular and behavioral targets for delaying disease onset and promoting healthy aging. - Source: PubMed
Publication date: 2025/12/17
Dinh Phuong-AnhHan HyeRimKim SeungsooGuo QinghuaZhang Zhengdong DVijg JanSuh Yousin - - Source: PubMed
Publication date: 2025/06/27
Wang YaojunLi Qiang - The monkeypox virus (MPXV) is currently spreading rapidly around the world, but the mechanisms by which it interacts with lupus nephritis (LN) are unknown. The aim of this study was to investigate the role and mechanism of lupus nephritis combined with monkeypox virus infection. The data comes from GEO and GeneCards.Through Limma and Weighted Gene Co-expression Network Analysis (WGCNA) analysis, differential expression genes (DEGs) and module genes were identified, and KEGG and GO enrichment analysis was carried out.In addition, a protein-protein interaction (PPI) network was constructed and LASSO regression was used to screen genes related to senescence. The diagnostic effectiveness was evaluated using a Nomogram and the receiver operating characteristic (ROC) curve and verified using GSE99967.Immune infiltration and gene set enrichment analysis (GSEA) Were also included in the study.In the end, miRNet was used to construct a miRNA-mRNA-TF network and screen targeted drugs through DGIdb. 5707 DEGs were identified in the lupus nephritis and 737 in the monkeypox data. WGCNA and Lasso regression analyses screened for three important targets (STAT1, ORC2, and GTF2B) .Predictive modeling and ROC of STAT1, ORC2 and GTF2B by Nomogram showed good diagnostic value .Immune infiltration analysis showed immune cell disorders and related pathway activation.The miRNA-mRNA-TF network covers 516 miRNAs and 15 transcription factors, and enrichment analysis shows that it plays an important role in senescence and inflammation.Potential Target Drugs Screened Include Guttiferone K And Silicon Phthalocyanine 4. This study identifies STAT1, ORC2, and GTF2B as key factors in cellular senescence and immune dysregulation associated with lupus nephritis and monkeypox infection, suggesting they may serve as important predictive targets. - Source: PubMed
Publication date: 2025/04/19
Wang YaojunLi Qiang