POU6F2 antibody - N-terminal region (ARP31534_P050)
- Known as:
- POU6F2 (anti-) - N-terminal region (ARP31534_P050)
- Catalog number:
- arp31534_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- POU6F2 antibody - N-terminal region (ARP31534_P050)
Related genes to: POU6F2 antibody - N-terminal region (ARP31534_P050)
- Gene:
- POU6F2 NIH gene
- Name:
- POU class 6 homeobox 2
- Previous symbol:
- -
- Synonyms:
- RPF-1
- Chromosome:
- 7p14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-29
- Date modifiied:
- 2014-11-18
Related products to: POU6F2 antibody - N-terminal region (ARP31534_P050)
Related articles to: POU6F2 antibody - N-terminal region (ARP31534_P050)
- Cancer stem cells (CSC) and the immunosuppressive microenvironments are key drivers of breast cancer (BC) progression and drug resistance. However, the molecular mechanisms by which One Cut Homeobox 2 (ONECUT2) governs CSC and the tumor immune microenvironment (TIME) remain largely unknown. Given the critical knowledge gap, we sought to investigate ONECUT2's regulatory impact on CSC properties and TIME profiles using BC cell lines, animal models, and clinical specimens. Here, we demonstrated that inhibition of ONECUT2, a core transcription factor, potently drives CSC characteristics and reprograms the TIME to favor macrophage polarization to the M2-type, a tumor-promoting state. Mechanistically, ONECUT2 inhibition transcriptionally activated POU6F2, which subsequently triggered beta-catenin, thereby enhancing CSC properties and chemoresistance in BC. With respect to modulating the immune microenvironment, suppression of ONECUT2 governs macrophage polarization toward the immunosuppressive M2 phenotype. CCL28 is identified as a transcriptional target of ONECUT2 required for M2-type macrophage polarization, and CCR10 as a key receptor involved in this immune modulation. These findings highlight the critical involvement of ONECUT2 in modulating BC stemness via targeting the POU6F2-beta-catenin axis and managing macrophage polarization to M2 phenotype through the CCL28-CCR10 pathway. Our study suggests that ONECUT2 modulates cancer stemness and the TIME, and that targeting its downstream POU6F2-beta-catenin axis and CCL28-CCR10 pathway may provide an effective approach for BC treatment. - Source: PubMed
Publication date: 2026/06/02
Shen MengJin HaixiaHuang ZiqiDong NanLiu GenZeng YuMeng YuanLiu YumengYang LiliRen Xiubao - Retinal ganglion cells (RGCs) are the principal conduits responsible for propagating visual stimuli from the retina to visual centers in the brain. The loss of RGCs leads to visual deficits following trauma or in diseases such as glaucoma. Mouse models are consistently used to investigate root causes for RGC loss. This study quantifies the total number of RGCs and selected RGC subtypes across six strains of inbred mice used in ophthalmic research. - Source: PubMed
Publication date: 2026/02/20
Lin Su-TingLin FangyuWang JiaxingGeisert Eldon E - The contribution of retinal ganglion cells (RGCs) subtypes to visually guided behavior continues to be an active area of research. We identify POU6F2-expressing RGCs essential for binocular predatory behavior. The POU6F2 RGCs are ON-OFF direction-selective RGCs that are vulnerable to glaucomatous injury. In knockout ( ) mice, there is a 12% loss of RGCs, and these cells are the POU6F2-expressing RGCs. Functionally, mice exhibited profound deficits in contrast sensitivity. In this study we found a deficit in the ability of mice to perform a binocularly driven cricked predation test. Wildtype mice detect and capture the cricket rapidly; while, both mice and mice with one optic nerve crushed, required significant longer times to complete the task. After optic nerve crush no further impairment in performance is seen in the knockout mouse. These data demonstrate that the POU6F2-positive RGCs are essential for this binocularly driven behavior. - Source: PubMed
Publication date: 2026/03/18
Lin FangyuLin Su-TingGeisert Eldon E - Genomic imprinting, a mechanism resulting in parent-of-origin expression of genes through epigenetic regulation, intersects with a broad range of biological fields, including evolution, molecular genetics and epigenetics, and determinism of complex traits. Although next generation sequencing technologies nowadays enable imprinted genes to be detected in a genome-wide manner, a wide spectrum of this phenomena is evaluated only in humans and rodents. - Source: PubMed
Publication date: 2026/03/09
Perret MathildeIannuccelli NathalieLeroux SophieFève KatiaDehais PatriceJacomet EvaHubert Jean-NoëlIampietro CaroleVandecasteele CélineMaman-Haddad SarahFaraut ThomasLiaubet LaurenceBonnet AgnèsDonnadieu CécileRiquet JulietteDemars Julie - Type 1 diabetes mellitus (T1DM) is a metabolic disease leading threat to human health around the world. Here we aimed to explore new biomarkers and potential therapeutic targets in T1DM through adopting integrated bioinformatics tools. The gene expression Omnibus (GEO) database was used to obtain next generation sequencing data (GSE270484) of T1DM and normal control samples. Furthermore, differentially expressed genes (DEGs) were screened using the DESeq2 package in R bioconductor package. Gene Ontology (GO) and pathway enrichment analyses were performed by g:Profiler. The protein-protein interaction (PPI) network was plotted with IID PPI database and visualized using Cytoscape. Module analysis of the PPI network was done using PEWCC. Then, microRNAs (miRNAs) and transcription factors (TFs) in T1DM were screened out from the miRNet and NetworkAnalyst database. Then, the miRNA-hub gene regulatory network and TF-hub gene regulatory network were constructed by Cytoscape software. Moreover, a drug-hub gene interaction network of the hub genes was constructed and predicted the drug molecule against hub genes. The receiver operating characteristic (ROC) curves were generated to predict diagnostic value of hub genes. Finally we performed molecular docking, ADMET profiling and molecular dynamics simulation studies of marine derived chemical constituents using Schrodinger Suite 2025-1. A total of 958 DEGs were screened: 479 up regulated genes and 479 down regulated genes. DEG were mainly enriched in the terms of developmental process, membrane, cation binding, response to stimulus, cell periphery, ion binding, neuronal system and metabolism. Based on the data of protein-protein interaction (PPI), the top 10 hub genes (5 up regulated and 5 down regulated) were ranked, including FN1, GSN, ADRB2, CEP128, FLNA, CD74, EFEMP2, POU6F2, P4HA2 and BCL6. The miRNA-hub gene regulatory network and TF-hub gene regulatory network showed that hsa-mir-657, hsa-miR-1266-5p, NOTCH1 and GTF3C2 might play an important role in the pathogenesis of T1DM. The drug-hub gene interaction network showed that Clenbuterol, Diethylstilbestrol, Selegiline and Isoflurophate predicted therapeutic drugs for the T1DM. Molecular docking and molecular dynamics simulation study revealed that CMNPD5805 and CMNPD30286 as potential inhibitors of FN1 (pdb id: 3M7P) a key biomarker in pathogenesis of T1DM. These findings promote the understanding of the molecular mechanism and clinically related molecular targets for T1DM. - Source: PubMed
Publication date: 2026/01/14
Vastrad BasavarajPattanashetti ShivalingSadashivanavar VeereshPai K S RVastrad Chanabasayya