YBX2 antibody
- Known as:
- YBX2 (anti-)
- Catalog number:
- orb32233
- Product Quantity:
- 5 ug(Trial size)
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- YBX2 antibody
Related genes to: YBX2 antibody
- Gene:
- YBX2 NIH gene
- Name:
- Y-box binding protein 2
- Previous symbol:
- -
- Synonyms:
- MSY2, CSDA3, Contrin
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-08-11
- Date modifiied:
- 2015-11-19
Related products to: YBX2 antibody
Related articles to: YBX2 antibody
- 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 - Zinc deficiency is associated with impaired male fertility and with reduced DNA and histone methylation in oocytes, but the temporal relationship between acute dietary zinc deficiency and sperm function is unclear. To fill in these gaps, the effects of acute dietary zinc deficiency on sperm function were tested. Five-week-old F1 (DBA × C57BL/6) male and female mice were fed a control diet (29 mg Zn/kg) or zinc-deficient diet (< 1 mg Zn/kg) for 6 days (n = 11/group), a duration selected to model acute zinc depletion based on previous studies demonstrating rapid reproductive defects within a similar timeframe (Tian and Diaz 2012). Sperm number and motility were evaluated by computer-assisted sperm analysis in all animals (n = 11), and testicular histology and DDX4 and YBX2 (MSY2) immunostaining and global m6A levels in testes and liver were measured in a subset of males (n = 6) and in ovaries and liver in females (n = 6) by an ELISA-based assay. Zinc deficiency did not alter body weight but significantly reduced total sperm number recovered from the cauda epididymis and impaired total and progressive motility, straight-line velocity, and hyperactivation. Testes from zinc-deficient males showed reduced thickness of germinal epithelium and increased basement membrane thickness, disorganized seminiferous tubules, and fewer DDX4-positive germ cells, while YBX2-positive cells were largely preserved. Despite these structural and functional defects, zinc deficiency did not significantly change global m6A levels in testes or ovaries, although hepatic m6A methylation was increased in females. These findings demonstrate that a short-term zinc-deficient diet rapidly compromises sperm production, motility, and testicular morphology without measurably altering global gonadal mRNA methylation. - Source: PubMed
Ibadin Ngozi ODiaz Francisco J - Backfat thickness is an economically important trait in pig production, yet the functional regulatory variants underlying it remain poorly characterized. Here, we performed a genome-wide association study (GWAS) for backfat thickness at 100 kg (BF100) in a large Landrace population (n = 5923) using 13.46 million imputed SNPs. We identified two significant quantitative trait loci (QTLs) on SSC2 (1.21-3.69 Mb; explaining 2.3% of phenotypic variance) and SSC12 (51.70-52.88 Mb; explaining 0.8% of phenotypic variance). While nonsynonymous SNPs were limited (16 variants), we prioritized functional non-coding variants by integrating high-resolution Hi-C interaction maps, epigenomic marks, and previously published enhancer and promoter annotation results from public backfat datasets. This multi-omics strategy revealed that the SSC2 QTL functions as an active three-dimensional regulatory hub, with over 20 enhancer-promoter loops physically engaging the promoters of IGF2, CTSD, TSPAN32, and TSSC4. Similarly, the SSC12 QTL formed more than 10 long-range interactions with the promoters of ASGR1, YBX2, GPS2, MDPU1, and TP53. Focusing on SSC2, we prioritized two tightly linked SNPs (2-1280617 and 2-1280654) located within a putative enhancer, representing two major haplotypes. Dual-luciferase reporter assays in PK15 and 3T3-L1 cells confirmed that the GG haplotype drives significantly higher transcriptional activity than the AT haplotype (p < 0.001). Consistently, pigs carrying the GG haplotype exhibited significantly lower backfat thickness. By integrating multi-omics and functional assays, this study not only decodes the regulatory architecture of two backfat QTLs but also provides new molecular markers for genetic improvement in Landrace breeding. - Source: PubMed
Feng XigangZhou XiuqiLiang HaoLi JingjinYu MeiZhao ShuhongLi XinyunLi Xiaoping - RNA 5-methylcytosine (m5C) modification plays a critical role in multiple diseases; however, its function in hyperuricaemic nephropathy (HN) remains unclear. Here, we show that renal m5C levels are markedly decreased and the m5C methyltransferase NOP2/Sun RNA methyltransferase 5 (NSUN5) is downregulated in HN mice. Conditional knock-in (cKI) mice and mouse tubular epithelial cells overexpressing NSUN5 exhibit resistance to uric acid (UA), thereby alleviating kidney injury, inflammation, and fibrosis in HN. Bisulphite sequencing coupled with RNA sequencing identifies stearoyl-CoA desaturase-1 (SCD1) as a direct NSUN5 target and reveals the involvement of NSUN5 in ferroptosis regulation. Mechanistically, NSUN5 installs m5C on SCD1 mRNA. The m5C reader YBX2 binds to the modified transcript, prolonging the half-life of SCD1 mRNA and enhancing its stability, thereby suppressing ferroptosis. Elevated SCD1 also inhibits NF-κB p65 phosphorylation and nuclear translocation, dampens inflammatory responses and promotes ABCG2-dependent UA excretion. Recombinant NSUN5 further ameliorates renal injury in HN. Our findings revealed a novel NSUN5-mediated mechanism and highlight a potential therapeutic target for HN. - Source: PubMed
Publication date: 2026/04/21
Song Xiu-XiuSuo Xiao-GuoYu YueZhang KuoLi Chen-AoWang JieXu Hui-XiaNiu Si-YuLv Dong-XueHe Zi-HaoLi Feng-HeMeng Xiao-MingJin Juan - Formaldehyde is a colorless, strong-smelling chemical widely used in industrial and household products, including building materials and furniture manufacturing. Chronic exposure, even at low doses, has been associated with respiratory disease, neurotoxicity, immune dysregulation, and cancer. Although growing epidemiological evidence suggests a link between formaldehyde exposure and increased leukemia risk, the underlying molecular mechanisms remain poorly defined due to its high reactivity and limited biological traceability. In this study, we show that low-dose formaldehyde exposure (3 ppm) upregulates key oncogenic regulators-including RUNX1, ETV6, OCT4, and ISX-in B-ALL cell lines. Transcriptomic profiling combined with functional assays reveals that formaldehyde activates a RUNX1-ISX signaling axis, which in turn drives the expression of downstream oncogenic transcription factors (YBX2, HES2, FOXH1, MYCL, FOS, and PBX4). This activation reshapes transcriptional programs across major cancer-associated pathways, including metabolic signaling and hematopoietic cell-lineage regulation, ultimately promoting malignant activity and tumor formation in a xenograft model. Importantly, pharmacologic inhibition of the RUNX1-ISX axis significantly attenuated formaldehyde-induced oncogenic effects and reduced tumor growth. Analysis of human samples using immunofluorescence and Pearson correlation further confirmed a strong co-expression relationship between RUNX1 and ISX. Collectively, these findings identify the RUNX1-ISX axis as a critical mediator of formaldehyde-induced oncogenesis in B-ALL and highlight it as a promising therapeutic target for mitigating environmental leukemogenic risk. - Source: PubMed
Publication date: 2026/03/20
Lin Pei-ChinWang Li-TingYe Li-HengTseng Pin-YingHuang Pei-HsienHsu Wan-YiLiao Yu-MeiChiou Shyh-ShinHsu Shih-Hsien