Ask about this productRelated genes to: POU2F1 Blocking Peptide
- 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 Blocking Peptide
Related articles to: POU2F1 Blocking Peptide
- 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 - To elucidate the paracrine regulatory mechanism of dermal papilla cells (DPCs) on melanocyte (MC) melanogenesis, we focused on exosomal miR-199a-3p as a key mediator. DPCs, MCs, and DPC-Exos were identified by immunofluorescence, Western blot (WB), nanoparticle tracking analysis (NTA), and transmission electron microscopy (TEM). Functional assays showed DPC-Exos were internalized by MCs, enhanced proliferation, decreased apoptosis, and elevated melanin production. miRNA sequencing identified miR-199a-3p as the key exosomal cargo, which was localized to hair follicle bulbs by fluorescence in situ hybridization (FISH). Transwell co-culture and Cy3-tracing revealed intercellular transfer. Dual-luciferase assays confirmed miR-199a-3p directly targets the 3'UTR of POU2F1. Additionally, exosomal miR-199a-3p promoted the growth of ex vivo hair follicles and significantly regulated the expression of melanogenesis-related genes in hair follicles. Gain-of-function experiments demonstrated that DPC-Exos transfected with miR-199a-3p mimics suppressed POU2F1, effectively reversing its anti-melanogenic activity. This study elucidates an exosome-mediated DPC-MC regulatory axis centered on miR-199a-3p/POU2F1, providing novel therapeutic targets for pigmentation disorders and advancing animal coat color modulation strategies. - Source: PubMed
Yang AnqiLu TingtingWang SenZhang JingCao ChengpengFang YinuoZhao BohaoWu XinshengChen Yang - - Source: PubMed
Publication date: 2026/04/07
Zhang Zi-HuiYuan Fei-FeiYang LianZhang WeiLi ShuangHuang Yu-Qin - This study elucidated the mechanistic role of the Suppressor of Cytokine Signaling 5 (SOCS5) in diabetic retinopathy (DR), focusing on DNA damage and cellular senescence pathways. Utilizing both in vitro (high glucose (HG)-induced human retinal microvascular endothelial cells (HRMECs)) and in vivo (streptozotocin-induced DR mouse models) approaches, we demonstrated that SOCS5 was significantly upregulated in DR. SOCS5 knockdown mitigated retinal tissue damage, vascular leakage, and apoptosis in DR mice while reducing DNA damage and cellular senescence in HG-stimulated HRMECs. Mechanistically, SOCS5 promoted DR progression by regulating the expression of Cyclin-Dependent Kinase Inhibitor 1 A (CDKN1A), a key mediator of cell cycle arrest and senescence. Furthermore, we identified POU Class 2 Homeobox 1 (POU2F1) as an upstream transcriptional activator of SOCS5, forming a novel POU2F1-SOCS5-CDKN1A axis that drove DR pathogenesis. Inhibition of POU2F1 and SOCS5 ameliorated DR-related pathology in mice, suggesting a novel therapeutic strategy. These findings reveal a previously unrecognized signaling pathway in DR and highlight SOCS5 as a promising target for intervention. - Source: PubMed
Publication date: 2026/04/01
Yang DiLu SiduoLiu HongmeiZhou YouZhong Hua