Ask about this productRelated genes to: BOP1 Blocking Peptide
- Gene:
- BOP1 NIH gene
- Name:
- BOP1 ribosomal biogenesis factor
- Previous symbol:
- -
- Synonyms:
- KIAA0124
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-28
- Date modifiied:
- 2018-11-02
Related products to: BOP1 Blocking Peptide
Related articles to: BOP1 Blocking Peptide
- N6-methyladenosine (m6A) is a crucial messenger RNA (mRNA) modification that plays a significant role in tumor development and metastasis. Ginsenoside Rk1 possesses notable anticancer activity; however, its effects on m6A modification have not yet been elucidated. - Source: PubMed
Publication date: 2026/06/29
Wu HuanyanLiu YuanZhu ChenhuiDuan ZhiguangQu LinlinFu Rongzhan - This study investigates the complex role of tumor-associated macrophages (TAMs) in the aggressive head and neck squamous cell carcinoma (HNSCC) microenvironment. Contrary to the typical protumorigenic role, functional coculture assays revealed that TAMs significantly suppressed HNSCC cell migration and invasion without affecting proliferation or apoptosis, an effect accompanied by the inhibition of epithelial-mesenchymal transition (EMT). Transcriptomic profiling identified block of proliferation 1 (BOP1) as a key gene downregulated following TAM coculture. Subsequent loss-of-function studies confirmed that silencing BOP1 alone recapitulated the suppressive effects of TAMs on cancer cell motility. Analysis of multiple independent clinical cohorts demonstrated that high BOP1 expression is significantly correlated with advanced tumor stage and worse overall survival in HNSCC patients. Importantly, elevated BOP1 levels were also associated with a reduced abundance of CD8+ T cells within the tumor microenvironment. These findings collectively unveil a tumor-restraining role for TAMs through motility and EMT inhibition, and identify BOP1 as a critical oncogenic driver that promotes HNSCC progression and is linked to impaired antitumor immunity, highlighting its dual potential as a prognostic biomarker and therapeutic target. - Source: PubMed
Publication date: 2026/06/05
Mu XingyuZhao GuileHua YufeiWang GuanruBao MingzheGao NingLi Chunjie - The interferon response is a signalling pathway unique to vertebrates that links the innate and adaptive immune responses. Interferons signal through a cascade of factors including the JAK-STAT pathway to induce the transcription of hundreds of interferon-stimulated genes (ISGs). Although the main interferon signal transduction pathways and ISGs have been elucidated, translational regulation of ISG transcripts is not fully understood. Prior work demonstrated that ribosomal protein RPL28 negatively regulates a subset of ISGs; however, we find that this effect may be due to a reduction in overall ribosome abundance. Multi-omics analysis of RNA-seq and LC-MS/MS data reveal proteins, including several ISGs, that are translationally up-regulated in IFN-β-stimulated cells depleted of ribosome biogenesis factor . Analysis of codon usage demonstrates a significant reduction in codon optimality for proteins that are translationally up-regulated during knockdown and IFN-β stimulation. Using reporter constructs, we demonstrate that codon nonoptimal reporters are translated more than codon-optimized reporters in -depleted IFN-β cells. We propose that ribosome biogenesis may in part regulate the translational fine-tuning of integral ISG protein production to ensure optimal interferon responses, with potential effects extending beyond this pathway. - Source: PubMed
Hay Brenna NSmid RachelLouie NathanZhong HuanFlibotte StephaneJan EricFoster Leonard J - Metabolic reprogramming is closely linked to tumor proliferation, invasion, and immune escape. Despite its central role in amino acid metabolism, the regulatory mechanisms of asparagine metabolism in hepatocellular carcinoma (HCC) progression remain poorly characterized. Rather than focusing on canonical metabolic genes, prognostic markers were identified from co-expression modules associated with asparagine metabolism signatures. Using the TCGA database and asparagine metabolism-related gene sets, a prognostic risk-scoring model was developed through differential expression analysis, univariate Cox regression, and the LASSO algorithm and externally validated with the GEO dataset (GSE14620). Survival analysis, ROC curve evaluation, nomogram construction, scRNA-seq, GSEA, and drug sensitivity analysis were performed to systematically delineate the molecular mechanisms by which asparagine metabolism drives HCC progression. A three-gene signature comprising BOP1, SAC3D1, and PDE2A effectively stratified patients into high- and low-risk groups. High-risk patients exhibited markedly poorer overall survival, enrichment in tumor proliferation-associated pathways, increased tumor purity, reduced immune cell infiltration, and a substantially higher TP53 mutation rate (38% vs. 13%). In contrast, the low-risk group showed enrichment in pathways linked to hepatoblastoma suppression and liver function, alongside improved predicted response to immunotherapy. Single-cell analysis identified NK cells and endothelial cells as central mediators of asparagine metabolism-driven HCC progression, with BOP1, SAC3D1, and PDE2A displaying dynamic expression patterns during differentiation. Furthermore, the high-risk group was predicted to be more sensitive to chemotherapeutics such as cyclophosphamide and 5-fluorouracil. These findings highlight a potential interplay between nitrogen metabolism and asparagine metabolism in HCC and suggest mechanisms by which these pathways may influence NK cell and endothelial cell function to promote disease progression. This study establishes a novel prognostic model and identifies potential chemotherapeutic vulnerabilities in high-risk patients, warranting further experimental and clinical validation. - Source: PubMed
Publication date: 2026/05/15
Feng JiantingWei KaihuaLi NanaLi YinshiDu FeiLv MengjiaoMa LifeiWang SuwenNiu ShuliangFeng Liang - Chinese Simmental cattle serve as an important dual-purpose breed in sustainable livestock systems. Despite their economic value, the genetic architecture underlying milk-production traits in this breed under temperate conditions remains poorly characterized. In this study, we estimated genetic parameters and identified associated genomic loci for 9 milk-production traits in a Chinese Simmental population. Our dataset consisted of 17,556 test-day records from 1,788 cows (parities 1 to 3), including whole-genome sequencing data for 781 individuals. Using a random regression test-day model with Legendre polynomials, we estimated variance components, heritabilities, breeding values (EBVs), and genetic correlations between different DIM. Heritability estimates ranged from 0.09 (fat-to-protein ratio) to 0.52 (protein percentage), with intermediate values for fat percentage (0.28), lactose percentage (0.35), and total milk solids (0.35). Within-lactation genetic correlations varied by trait, ranging from -0.88 to 0.99, with the strongest correlations between adjacent DIM, which weakened as intervals widened. Genome-wide association analysis (using the mixed linear model in SLEMM version 0.90.1) and Bayesian fine-mapping analysis identified significant SNPs near known candidate genes (BOP1, MROH1, NEGR1). These analyses also revealed putative novel associations with CACNB4, MTHFD2L, and SGMS1. Overall, the results enhance our understanding of the genetic regulation of milk production and provide practical targets for genomic selection to improve dairy performance in dual-purpose breeding programs. - Source: PubMed
Publication date: 2025/12/18
Dong ChunxiaoMa PeipeiTang YongjieHan HaoqiChen SiqianYang JiaziSun ZhigangWang WeiYu YingLi Shengli