YBX1 antibody - middle region (ARP34396_P050)
- Known as:
- YBX1 (anti-) - middle region (ARP34396_P050)
- Catalog number:
- arp34396_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- YBX1 antibody - middle region (ARP34396_P050)
Related genes to: YBX1 antibody - middle region (ARP34396_P050)
- Gene:
- YBX1 NIH gene
- Name:
- Y-box binding protein 1
- Previous symbol:
- NSEP1
- Synonyms:
- YB-1, YB1, DBPB, NSEP-1, MDR-NF1, BP-8, CSDB, CSDA2
- Chromosome:
- 1p34.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-10-20
- Date modifiied:
- 2016-10-05
Related products to: YBX1 antibody - middle region (ARP34396_P050)
Related articles to: YBX1 antibody - middle region (ARP34396_P050)
- - Source: PubMed
Publication date: 2026/04/24
Ma GuoluFeng JianyuZeng JianyingLiao RongxinZhong XiaojunLv ZhuoChen Fengsheng - Non-small cell lung cancer (NSCLC) is the most common type of lung cancer and a major contributor to cancer-related deaths globally. The mechanisms of NSCLC metastasis, largely driven by epithelial-mesenchymal transition (EMT), remain incompletely understood. The Cancer Genome Atlas - Lung Adenocarcinoma (TCGA-LUAD) dataset analysis revealed that suppression of tumorigenicity 7 (ST7) may play a role in preventing the EMT process and metastasis in NSCLC. In this study, we revealed that ST7 suppressed the expression of Matrix metalloproteinase 14 (MMP14) by binding Y-box binding protein 1 (YBX1) and blocking its nuclear translocation. Consequently, ST7 silencing enhanced both EMT and metastatic progression in NSCLC experimental models, including A549 and H1299 cell lines in vitro and a tail-vein lung metastasis model in BALB/c nude mice in vivo. Collectively, our results revealed a novel ST7/YBX1/MMP14 signaling axis that might be targeted in NSCLC metastasis. - Source: PubMed
Publication date: 2026/04/21
Qin YangChen YahanCao QianZhang BinWan Yulei - - Source: PubMed
Publication date: 2026/04/22
Chen LingWan ZimingGao XuejingChen ChaoGan Hua - Drug resistance has emerged as a significant factor contributing to the dismal prognosis of patients with hepatocellular carcinoma (HCC). Since tyrosine kinase Inhibitors (TKIs) are the standard first-line therapy for advanced HCC, however, its effectiveness is significantly hindered by the development of drug resistance, the mechanisms of which are still not fully understood. This study aims to investigate the potential role of the transcription factor YBX1 in mediating drug resistance and to validate it as a potential therapeutic target in HCC. We identified increased YBX1 levels in human HCC patient cohorts and found that it is associated with tumor aggressiveness, metastasis, and poor survival, and is a key transcription factor contributing to drug resistance. Our results show that YBX1 overexpression confers sorafenib resistance in HCC. Elevating YBX1 levels in HCC cell lines increased cell survival, viability, and sorafenib IC50 values, as well as tumorigenic features and drug resistance markers. Conversely, siRNA-mediated knockdown of YBX1 reduced these effects. Sorafenib-resistant cells exhibited increased YBX1 and resistance markers. Inhibiting YBX1 significantly decreased the viability of resistant cells. In vivo studies demonstrated that inhibiting YBX1 with the small-molecule SU056 reduces tumor size. Thus, YBX1 is a promising target for extending drug resistance in HCC. - Source: PubMed
Publication date: 2026/04/07
Tripathi ManishNagati VeerababuKwabiah DennisAnaya Yamile AbuchardPazzi AnaShaham SaliqueHussain MohammadBracho RicardoDoxtater KyleLopez SamanthaLeslie Sophia - Oxaliplatin resistance is a key challenge in gastric cancer therapy. This study explored how bufalin, an active component of Chansu, reverses this resistance. We found that bufalin targets the transcription factor YBX1, which is upregulated in resistant cells. YBX1 activates STC1 expression, leading to PI3K/Akt pathway activation, increased HK2 levels, and enhanced glycolysis-all contributing to resistance. Bufalin inhibits this YBX1/STC1/glycolysis axis. Using in vitro assays (proliferation, apoptosis, glycolysis measurement) and in vivo models, we demonstrated that bufalin suppresses glycolysis and restores oxaliplatin sensitivity. Mechanistic studies (RNA-seq, ChIP, SPR, etc.) confirmed the direct YBX1-bufalin interaction. Our work reveals YBX1/STC1-mediated glycolysis as a novel resistance mechanism and identifies bufalin as a promising therapeutic agent to overcome it. - Source: PubMed
Publication date: 2026/04/15
Li XiaotongLi QiuyingNi ZhenhuaXiao ZengyouYang ZeanZuo QingsongLi WeiWang XiongbiaoChen TengWang Jie