Ask about this productRelated genes to: POU2F1 antibody
- Gene:
- POU2F1 NIH gene
- Name:
- POU class 2 homeobox 1
- Previous symbol:
- OTF1
- Synonyms:
- OCT1
- Chromosome:
- 1q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-03-09
- Date modifiied:
- 2016-04-25
Related products to: POU2F1 antibody
Related articles to: POU2F1 antibody
- Colorectal cancer (CRC) remains one of the leading causes of cancer-related mortality worldwide, yet the underlying mechanisms driving its progression are not fully elucidated. Long non-coding RNAs (lncRNAs) have recently emerged as key regulatory molecules in tumor biology. In this study, we identified ABHD11-AS1 as a tumor-suppressive lncRNA that is significantly downregulated in CRC tissues, its low expression is correlated with poor patient prognosis. Functional assays demonstrated that ABHD11-AS1 inhibits CRC cell proliferation, migration, and invasion, and enhances sensitivity to oxaliplatin. Mechanistically, ABHD11-AS1 directly binds to EIF4E and disrupts its phase separation, thereby suppressing the translation of USP18, a deubiquitinating enzyme that stabilises the oncogenic protein POU2F1. Reduced USP18 expression leads to increased ubiquitination and proteasomal degradation of POU2F1, ultimately inhibiting malignant progression and enhancing chemotherapy sensitivity. Collectively, our findings uncover a previously unrecognised mechanism by which ABHD11-AS1 modulates EIF4E-mediated phase separation to regulate protein homeostasis, highlighting its potential as a therapeutic target in CRC. - Source: PubMed
Publication date: 2026/04/23
Li ShizhenJiang XianjieOyang LindaXia LongzhengTan ShimingRen ZongyaoPeng QiuLin JinguanLiao QianjinZhou Yujuan - Exploring the targeted regulatory effect of isorhynchophylline on lipopolysaccharide (LPS)-induced acute lung injury (ALI) by constructing a drug delivery system of GEF-modified exosomes derived from M2 macrophages (M2-Exos) loaded with isorhynchophylline (GEF-M2-Exos-IRN; GMI). - Source: PubMed
Publication date: 2026/05/14
Zou Jin-RuYang DanZhang Chuan-MingZhang LuZhang Hao-NanSong MiaoMa Jun-BingYang ZhengQiu Min - Epstein-Barr virus (EBV) latent infection is causally linked to several epithelial cancers, including endemic forms of undifferentiated nasopharyngeal carcinoma (NPC), and to a subtype of gastric cancer (GC). EBNA1 is the virus-encoded sequence-specific DNA-binding protein required for episome maintenance but also contributes to host-cell survival through multiple mechanisms, including binding to the host chromosome. We previously developed small-molecule inhibitors of EBNA1 DNA-binding that block host cell cycle progression and growth of EBV+ cell lines and tumor models . However, the underlying molecular mechanisms of EBNA1 function and inhibition have not been completely elucidated. In this study, we employ VK1727 to inhibit EBNA1 DNA-binding to viral and cellular genomes in three EBV+ epithelial tumor-derived cell models (patient-derived xenograft C15, C666-1, and SNU719). We integrate EBNA1 ChIP-seq and transcriptomic RNA-seq analyses to identify the cell cycle-dependent kinase CDC7 and a stem cell transcription factor POU2F1 as direct functional targets of EBNA1 in each of these epithelial cancer models. EBNA1 binding to the CDC7 promoter and POU2F1 intron promotes RNA Pol II-pS5 to initiate transcription of these two genes. We show that CDC7 inhibitor simurosertib phenocopies VK1727, while Bcl-2 inhibitor venetoclax shows a synergistic effect with VK1727 for inhibition of EBV+ epithelial cancer cell proliferation and survival. Our study reveals new functional gene targets and pathways of VK1727 in EBV+ epithelial cancers that provide new biomarkers and combinatorial strategies to treat EBV-driven cancers. - Source: PubMed
Publication date: 2026/05/14
He SongtaoTerhuja NisenoSoldan Samantha SChen ChristopherCassel JoelYin XiangfanLiu QinChung Sun SookCastro-Muñoz Leonardo JosuéYoon LeenaWang JieSalvino Joseph MGewurz Benjamin ETempera ItaloMessick Troy ELieberman Paul M - Osteoarthritis (OA), the most prevalent form of arthritis globally, is characterized by debilitating pain driven by inflammatory and degenerative processes in chondrocytes. Here, we demonstrate that arctigenin (ATG), a bioactive lignan from Arctium lappa, alleviates OA pain by suppressing chondrocyte pyroptosis through the POU Class 2 Homeobox 1 (POU2F1)/growth factor receptor Bound Protein 10 (GRB10) signaling axis. In a monosodium iodoacetate (MIA)-induced OA rat model, ATG administration reduced pain hypersensitivity, lowered pro-inflammatory cytokines, and elevated anti-inflammatory interleukin-10 (IL-10), while diminishing expression of pyroptosis effectors including cleaved caspase-1, Gasdermin-D-N (GSDMD-N), and NOD-like receptor thermal protein domain associated protein 3 (NLRP3). In vitro studies in C28/I2 chondrocytes revealed that ATG dose-dependently attenuated inflammation and pyroptosis markers. Mechanistically, ATG upregulated POU2F1, a transcription factor that directly binds and activates the GRB10 promoter, as confirmed by enrichment and binding assays. Silencing POU2F1 or GRB10 reversed ATG's inhibitory effects on pyroptosis. In vivo validation further showed that ATG's pain-relieving effects in OA rats depend on this axis to curb chondrocyte pyroptosis. Collectively, these findings highlight ATG's potential as a novel analgesic agent for OA by targeting pyroptotic pathways, offering insights into inflammation-driven pain mechanisms. - Source: PubMed
Zhai Tian-JunFeng WeiZhu Cheng-ChengChen Ye-PingZhang Hui - To investigate the specific role of long non-coding RNA (lncRNA) XIST in recurrent spontaneous abortion (RSA). - Source: PubMed
Publication date: 2026/03/25
Qian YanpingChen ZhuoNiu HongpingXing LiweiWang YiwenJiang Lijuan