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)
- Insufficient T-cell infiltration is a major barrier to the efficacy of immune checkpoint inhibitors (ICIs) in lung adenocarcinoma (LUAD). We aimed to investigate how the tumor-intrinsic mC methyltransferase NSUN2 shapes the immune landscape of LUAD. - Source: PubMed
Publication date: 2026/09/07
Meng WangyangLu TongDu MingyuanDai XinHan YichaoLi YingyiXu HaiminYang BiaolongWang ZeyuDu HaileiLiao KemanLiu XinnanSun YidanYang CuiDong DongYan YanGuo WeiLi BinLi Hecheng - Y-box binding protein 1 (YBX1) has been implicated across an unusually broad range of malignancies and processes: immune remodeling, epithelial plasticity, metabolic rewiring, epitranscriptomic reading, and resistance to chemotherapy, targeted agents, and checkpoint blockade. A linear one-gene/one-pathway oncogene model does not readily accommodate this breadth. We argue that the apparent diffuseness reflects a context-dependent regulatory node rather than experimental noise, and develop the hypothesis that YBX1 acts as an , a regulator whose transcript outputs are set by cellular state rather than by a fixed binding program, which acts in both the transcriptional and post-transcriptional compartments, and which sits inside feedback loops linking downstream metabolic states back to its own activity. We organize the literature into three coupled layers: a state code, in which post-translational modifications, ubiquitin balance, localization, and phase separation determine which YBX1 is active (Layer 1); an RNA program, in which m5C reading and non-coding-RNA scaffolds are associated with a restricted survival transcriptome (Layer 2); and the immune, metabolic, and plasticity phenotypes these outputs generate (Layer 3). Evidence further suggests that tumor-specific dependency is carried by the configuration of the YBX1/YBX2/YBX3 family rather than by any single member. We specify what would falsify the framework: if state-resolved readouts do not predict downstream circuit activity better than total YBX1 abundance, the hub reduces to a promiscuous, abundant RNA-binding protein whose correlations are epiphenomenal. We give explicit weight to evidence resisting an oncogenic reading: circuits in which restraining YBX1 is tumor-suppressive, non-coding-RNA and family-level interactions running in opposite directions, and effectors regulated divergently between tumors, treating these as boundary conditions rather than exceptions. This reframing shifts the actionable question from whether YBX1 is high to which YBX1-dependent circuit a tumor uses; its value remains contingent on prospective, state- and circuit-level validation. - Source: PubMed
Publication date: 2026/08/21
XiaoTian ZhangYiTong WangChongchong Feng - Varicocele (VC) represents a primary etiology of male infertility, yet the epigenetic landscapes and molecular triggers driving VC-associated spermatogenic failure remain largely enigmatic. Herein, it is demonstrated that Sertoli cell ferroptosis is a critical pathological feature of VC, and its pharmacological inhibition effectively rescues VC-induced reproductive impairment . Through small RNA sequencing of clinical testicular tissues, piRNA-46403 is identified as a significantly upregulated mediator in VC patients with asthenospermia. Functionally, piRNA-46403 is shown to orchestrate Sertoli cell ferroptosis, whereas its silencing attenuates spermatogonial apoptosis and restores spermatogenic function. Mechanistically, piRNA-46403 acts as a molecular decoy that binds to the RNA-binding protein YBX1. This interaction disrupts the binding of YBX1 to m5C-modified USP18 mRNA, thereby reducing USP18 mRNA stability and triggering ferroptosis. These findings elucidate a novel piRNA-46403/YBX1/m5C-modified USP18 regulatory axis in the male reproductive system and position piRNA-46403 as a promising therapeutic target for mitigating VC-mediated infertility. - Source: PubMed
Publication date: 2026/08/12
Fang XiaoSong LiLiu DongXin ZhixiangPang WenjuanTong QiangHuang JingWang AnbangYin LeiHuang HejingJiang AiminRen Shancheng - RNA-binding proteins (RBPs) are central players in post-transcriptional gene regulation (PTGR), and their mode of action often depends on subcellular localization. Conventional crosslinking and immunoprecipitation (CLIP) methods map the RNA targets of RBPs with nucleotide resolution but lack spatial specificity, making it impossible to distinguish how one RBP can contribute to biological processes across distinct compartments simultaneously. Here, we present RBProximity-CLIP, an extension of Proximity-CLIP that integrates APEX2-mediated proximity labeling with UV crosslinking of 4-thiouridine-labeled RNAs, followed by sequential biotin- and RBP-specific immunoprecipitations, to capture RBP-RNA complexes with both spatial and protein specificity. RBProximity-CLIP generates nucleotide-resolution maps of RBP-RNA interactions and enables proteomic characterization of complete ribonucleoprotein (RNP) compositions. Using Y-box binding protein 1 (YBX1) as a model RBP, we provide a detailed protocol for RBProximity-CLIP. - Source: PubMed
Nowak IwonaHuynh Hang TKaur MahekdeepKorchev OrliMoskovicz VeronicaLobo VivianFong MichelleSarshad Aishe ABenhalevy Daniel - Impaired osteogenic differentiation of periodontal ligament stem cells (PDLSCs) is a key factor in the failure of alveolar bone repair. Ferroptosis, a form of regulated cell death, has been implicated in osteogenic dysfunction. Wilms' tumor 1-associated protein (WTAP) regulates RNA fate through m6A modification; however, whether WTAP modulates ferroptosis in PDLSCs remains unknown. This study aims to investigate the role of WTAP in LPS-induced ferroptosis in PDLSCs. LPS-treated hPDLSCs were used as cell models. Osteogenic differentiation and inflammation of hPDLSCs, ferroptosis biomarkers, and the expression circular RNA CDK8 (circCDK8), microRNA let-7a-5p (let-7a-5p), transferrin receptor (TFRC), and Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4) were measured. m6A enrichment on circCDK8 and its binding to Insulin-like Growth Factor 2 mRNA Binding Protein 3 (IGF2BP3) were analyzed. Interactions among circCDK8, let-7a-5p, and TFRC, as well as Y-box Binding Protein 1 (YBX1) recruitment to circCDK8 and ACSL4, were confirmed. Following LPS induction, the expression of WTAP, circCDK8, TFRC, and ACSL4 was upregulated in hPDLSCs, while let-7a-5p expression was downregulated. WTAP knockdown enhanced osteogenic differentiation, reduced inflammation, and decreased ferroptosis in hPDLSCs. Mechanistically, WTAP-mediated m6A modification stabilized circCDK8 through IGF2BP3 binding. CircCDK8 then promoted ferroptosis via two parallel routes: competitively sponging let-7a-5p to upregulate TFRC, and recruiting YBX1 to stimulate ACSL4 expression. Overexpression of circCDK8 or knockdown of let-7a-5p inhibited osteogenic differentiation and promoted ferroptosis. These findings reveal that WTAP drives ferroptosis in PDLSCs through m6A-dependent stabilization of circCDK8, which activates the let-7a-5p/TFRC and YBX1/ACSL4 axes, offering mechanistic insights for alveolar bone repair. - Source: PubMed
Publication date: 2026/09/01
Yang XuShi Peikun