POU3F1 antibody - N-terminal region (ARP33061_T100)
- Known as:
- POU3F1 (anti-) - N-terminal region (ARP33061_T100)
- Catalog number:
- arp33061_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- POU3F1 antibody - N-terminal region (ARP33061_T100)
Related genes to: POU3F1 antibody - N-terminal region (ARP33061_T100)
- Gene:
- POU3F1 NIH gene
- Name:
- POU class 3 homeobox 1
- Previous symbol:
- OTF6
- Synonyms:
- OCT6, SCIP
- Chromosome:
- 1p34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-06-03
- Date modifiied:
- 2015-08-25
Related products to: POU3F1 antibody - N-terminal region (ARP33061_T100)
Related articles to: POU3F1 antibody - N-terminal region (ARP33061_T100)
- Uncovering the mechanisms that generate the immense diversity of neuronal cell types remains a fundamental goal of developmental biology. Different "cardinal classes" of spinal neurons that share a common molecular identity are produced from spatially segregated progenitor domains. Within many classes, a stereotyped sequence of neuronal subtypes of related function is generated over time, raising the question of the mechanisms that control this process. Here, we show that the successive expression of mouse transcription factors Onecut2, Pou2f2, and Pou3f1 correlates with the emergence of sequentially generated subpopulations within several cardinal classes. We demonstrate that loss of Pou2f2 impairs the development of two early-born motor neuron columns and respecifies anterolateral system projection neurons into a later-born subset. Similarly, we show that Pou3f1 expression is required for the normal development of later-born subsets of motor neurons and anterolateral system projection neurons. Together, our observations provide functional evidence that horologic diversification of spinal circuits is driven by a conserved sequence of transcription factors. - Source: PubMed
Publication date: 2026/03/18
Segarra Laia CaudetSangster KevinSagner JuliaKania ArturSagner Andreas - Acute myeloid leukemia (AML)'s treatment and remission remains unsatisfactory. A prognostic risk-scoring model containing seven signature genes (POU3F1, RPGR, PTP4A3, SOCS1, FAM83G, GREB1 and COL2A1), was developed by LASSO-Cox regression analysis. In the training set, the test group, area under the curve values of 1, 3, and 5 years were 0.876, 0.877, 0.937, and 0.974, 0.878, 0.976 respectively, which indicates a good predictive efficacy. In the two external GEO (GSE71014 and GSE6891) datasets, area under the curve values of 1, 3, 5 years were 0.847, 0.857, 0.822, and 0.830, 0.863, 0.891 respectively. Our seven signature genes containing risk-scoring model performed excellently in evaluating the OS of AML patients. - Source: PubMed
Publication date: 2025/12/26
Liu BinZhang JianWang JingWang QianLiu XiaomanSun Hui - Ras-GTPase-activating protein SH3 domain-binding protein 1 (G3BP1) mediates stress granules (SGs) via phase separation. However, there is limited understanding of the allosteric mechanism and the identification of regulatory molecules. Here, we identify icariin (ICA), a small-molecule inducer that promotes G3BP1-driven biomolecular condensate formation, which effectively restructures SGs architecture. Moreover, we demonstrate that ICA interacts with the N-terminal nuclear transport factor 2-like (NTF2L) domain of G3BP1, inducing a conformational switch from "closed-to-open" that facilitates G3BP1 oligomerization and phase separation. Crucially, G3BP1 condensates recruit N-methyladenosine (mA) reader insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) through topology-selective scaffolding, establishing epitranscriptomic hubs that resolve proteotoxic stress via mA-dependent AMP-activated protein kinase (AMPK)-mitogen-activated protein kinase (MAPK)-glutathione peroxidase 4 (GPX4) signaling pathways. Strikingly, this chemical intervention shows translational potential, as ICA reduces cerebral infarct volume in ischemia models via G3BP1-dependent SGs remodeling. Additionally, single-nucleus transcriptomics identify Fezf2, Pou3f1, and Kcnn2 neuronal subpopulations as mechanistically aligned responders. Furthermore, ischemic stroke patients reveal G3BP1-IGF2BP1-mA axis within peripheral blood mononuclear cells. Taken together, this study redefines SGs as dynamically druggable epitranscriptomic processors for precision neuroprotection. In particular, a framework for leveraging biomolecular condensate topology in the development of next-generation neurological therapeutics is offered. - Source: PubMed
Publication date: 2025/11/20
Li LingGuo Yong-DongZhang Xiao-WenDu Zhi-YongWang Yu-QiYang ZhuoLuo Qian-WeiZhuo Fang-FangWei Tian-TianLiu Zheng-PingHan BoYu WeiZhang Pei-PeiZhou WeiLu Zhi-YuanTu Peng-FeiZheng Chun-HongZeng Ke-Wu - Type 2 diabetes mellitus (T2DM) is a chronic and debilitating condition characterized by both insufficient production of insulin and insulin resistance, leading to poor blood sugar control. India ranks second globally in diabetes prevalence, with approximately 77 million individuals currently affected by the disease. Although extensive research has been conducted, the molecular mechanisms of T2DM remain inadequately understood, which continues to pose challenges in the development of effective therapeutic strategies. In this study, we analyzed the GSE25724 microarray dataset and identified 2048 differentially expressed genes (DEGs) associated with T2DM. Among these, key hub genes include and , which were identified through Cytoscape as central regulators, implicating inflammatory and immune pathways in T2DM progression. Using NetworkAnalyst, identified key transcription factors ( and ) and microRNA (hsa-miR-16-5p, hsa-miR-26b-5p, hsa-miR-93-5p, hsa-miR-192-5p, and hsa-miR-155-5p) that regulates important genes involved in T2DM, highlighting the complex gene regulation behind the disease. Genes such as , and from key signalling pathways, as well as , and identified through gene-disease association databases, have strong links to type 2 diabetes. These genes are believed to play potential roles in the development and progression of T2DM by participating in biological pathways relevant to the disease. Among the hub genes, , and exhibited strong diagnostic accuracy for T2DM, with each achieving ROC curve and AUC values greater than 0.90. This indicates exceptional sensitivity and specificity in distinguishing T2DM from non-diabetic controls. Overall, our findings shed light on the molecular mechanism of T2DM and identify novel biomarkers and therapeutic targets that may support future precision medicine strategies to enhance diagnosis and treatment outcomes. - Source: PubMed
Publication date: 2025/08/08
Yadav MadhuAkhter Yusuf - Schwann cells (SCs) are required for supporting axons, forming myelin, and facilitating repair through remyelination after injury in the peripheral nervous system (PNS). Processes of differentiation, myelination, and remyelination of SCs are tightly modulated by a complex network of transcription factors and coregulators, including Sox10, Oct6/Pou3f1, Krox20/Egr2, Nab1/2, YY1, COUP-TFII/NR2F2, YAP/TAZ-TEAD1, c-Jun, Sox2, Zeb2, and Etv1/Er81. These factors can regulate the expression of essential target genes such as Mpz and Mbp in SC myelination and repair. Genetic mutations or dysregulation within this network can lead to peripheral neuropathies such as Charcot-Marie-Tooth disease. However, the transcriptional regulatory network of differentiation, myelination, and remyelination of SCs has not been fully understood yet. Thus, this review briefly introduces processes of differentiation, myelination, and remyelination of SCs and explores the role and molecular mechanisms of each transcription factor and coregulator in differentiation and myelination of SCs and their remyelination following nerve injury. Clinical implications for peripheral neuropathies associated with specific gene mutations and variations of transcription factors and coregulators affecting SC biology are also discussed. - Source: PubMed
Han Sang-HeumCho Jun-GiPark Su-JeongShin Yoon KyungHong Young BinHan Jin-YeongPark Hwan TaePark Joo-In