YBX2 (C-term) antibody Ab host: Rabbit
- Known as:
- YBX2 (C-terminus) (anti-) Antibody production species: Rabbit
- Catalog number:
- 'AP31229PU-N
- Product Quantity:
- 50 Вµg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- YBX2 (C-term) antibody host: Rabbit
Related genes to: YBX2 (C-term) antibody Ab host: Rabbit
- Gene:
- PPP1R18 NIH gene
- Name:
- protein phosphatase 1 regulatory subunit 18
- Previous symbol:
- KIAA1949
- Synonyms:
- phostensin
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-02
- Date modifiied:
- 2016-10-05
- 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 (C-term) antibody Ab host: Rabbit
Related articles to: YBX2 (C-term) antibody Ab host: Rabbit
- 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 - Growing oocytes accumulate maternal mRNA to support subsequent meiotic maturation and maternal-to-zygotic transition. However, the regulatory mechanisms governing the fate of these maternal mRNAs remain largely unknown. Here, we identified heterogeneous nuclear ribonucleoprotein M (hnRNPM) as a critical regulator of pre-mRNA alternative splicing during mouse oocyte development. Genetic ablation of hnRNPM leads to severe cytoplasmic defects, meiotic arrest, and complete female infertility. Using SCAN-seq, we uncovered novel transcript isoforms and systematically characterized hnRNPM-regulated alternative splicing events. Furthermore, LACE-seq revealed hnRNPM-binding sites at single-nucleotide resolution in oocytes, linking its RNA-binding activity to splicing fidelity. Additionally, hnRNPM interacts with BCAS2, a known splicing factor critical for oocyte development, and modulates its binding to pre-mRNA loci to precisely control the alternative splicing. Overall, our study not only uncover an essential role of hnRNPM in mammalian oocyte development and female fertility but also unveils a critical regulatory network governing alternative splicing during oocyte development. - Source: PubMed
Publication date: 2026/02/12
Zhou ShuminLiu DalinGan ShimingYu ZiqiSu RuibaoZhou HaoZhang JiaqiXu HaoranZhao YifanZhang HuaDeng ZuoqiWu XuanLuo ChunhaiLiu YunlongYuan ShuiqiaoFan Heng-YuSun Fei - Y-box-binding protein 2 (YBX2) is a germ cell-specific protein that plays important roles in mRNA stability, transcription, and translation. However, the effects of YBX2 on porcine embryos development remain unclear. To investigate the function of YBX2 in early porcine embryonic development, YBX2 knockdown (KD) was performed via siRNA microinjection at the single-cell stage. The expression level of YBX2 gene was measured by quantitative real-time polymerase chain reaction (qRT-PCR). The effect of YBX2 on mitochondrial function and zygotic genome activation were detected by qRT-PCR, western blot, immunofluorescence staining. The results showed that YBX2 is essential for early embryonic development. YBX2 KD decreased the blastocyst rate, mitochondrial activity, and the expression levels of NRF1, NRF2, and SIRT1, thereby reducing mitochondrial biogenesis. In addition, YBX2 KD led to an increase in maternal mRNA levels and a decrease in zygotic genome activation mRNA levels. However, maternal protein levels were reduced, indicating that YBX2 can affect the maternal-to-zygotic transition. Meanwhile, H3K9ac levels decreased and H3K9me3 levels increased following YBX2 KD, suggesting that YBX2 regulates gene transcription. YBX2 affected embryonic development by regulating mitochondrial biogenesis and ZGA expression. - Source: PubMed
Publication date: 2025/11/30
Jiang Wen-JieLee Song-HeeSong Hyeon-JiCui Xiang-Shun