POU3F2 antibody - C-terminal region (P100858_P050)
- Known as:
- POU3F2 (anti-) - C-terminal region (P100858_P050)
- Catalog number:
- p100858_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- POU3F2 antibody - C-terminal region (P100858_P050)
Related genes to: POU3F2 antibody - C-terminal region (P100858_P050)
- Gene:
- POU3F2 NIH gene
- Name:
- POU class 3 homeobox 2
- Previous symbol:
- OTF7
- Synonyms:
- POUF3, BRN2, OCT7
- Chromosome:
- 6q16.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-06-03
- Date modifiied:
- 2016-10-05
Related products to: POU3F2 antibody - C-terminal region (P100858_P050)
Related articles to: POU3F2 antibody - C-terminal region (P100858_P050)
- Heterotypic cell-cell interactions are critical to governing cellular physiology, disease progression, and responses to the environment and pharmacologic interventions. For example, neurons and astrocytes engage in intricate interactions that are essential for brain development and function. However, the transformation of these extracellular signals into epigenomic regulation that governs cell function is poorly understood. Here, we report that weeks of co-culture between human induced pluripotent stem cell (hiPSC)-derived neurons and mouse cortical astrocytes extensively reprograms gene expression and the chromatin accessibility landscape in neurons, affecting thousands of genes and putative gene regulatory elements (REs), including many transcription factors (TFs). These genes are enriched for functions implicated in neuronal differentiation and maturation, and tend to be impacted in schizophrenia, and autosomal dominant Alzheimer's disease. Through complementary CRISPR interference and activation screens, we recapitulated hundreds of astrocyte-induced transcriptional and chromatin remodeling events in mono-cultured neurons at both promoters and distal regulatory elements (REs) of TF genes. We discovered functional REs for ~50 astrocyte-responsive TF genes, providing a map of gene regulatory network control. Astrocyte-responsive TF genes fall into groups that exert independent or counter-balancing transcriptional effects, highlighting the complex coordination of the neuronal response to astrocytes. Functional effects of specific TFs, including POU3F2 and TFAP2E, on neurite morphology and neuronal electrophysiology are consistent with transcriptional effects, demonstrating the capacity of direct epigenetic control to mimic heterotypic cellular signals. This work illuminates the regulation of neurodevelopment- and disease-relevant gene modules by neuron-astrocyte interactions, and provides a blueprint for applying modern functional genomics to uncover the links between cell microenvironment and epigenomic programming. - Source: PubMed
Publication date: 2026/03/07
Li BoxunHagy Kevin TSafi AlexiasBeer Michael ABarrera AlejandroGeraghty SaraRai RuhiPederson Alyssa NReisman Samuel JLove Michael ISullivan Patrick FEroglu CaglaCrawford Gregory EGersbach Charles A - Reprogramming of spinal astrocytes into motor neurons holds great promise for spinal cord injury in regeneration medicine. Here we identified a set of four transcription factors-achaete-scute complex homolog-like 1, myelin transcription factor 1 like, POU class 3 homeobox 2, and ISL LIM homeobox 1-collectively referred to as the 4 F cocktail. The 4 F cocktail reprograms rat and human reactive astrocytes into motoneuron-like cells. The reprogrammed cells display neuronal morphology and stain positive for microtubule-associated protein 2 (MAP2), a neuronal-specific marker, and choline acetyltransferase, which is a known motor neuron-specific marker. Early in the process of astrocytic reprogramming mediated by the 4 F cocktail, quantitative real-time reverse transcription polymerase chain reaction revealed that the expression of the astrocytic gene glial fibrillary acidic protein was inhibited. Additionally, the expression of the neural progenitor cell markers SRY-box transcription factor 2 and neural cell adhesion molecule 1 was upregulated within 5 days, while the motor neuron progenitor marker oligodendrocyte transcription factor 2 was activated within 7 days. Furthermore, the expression of the neural genes Map2, synapsin I, tubulin β-3, and neurofilament heavy, as well as the motor neural genes ISL LIM homeobox 1, motor neuron and pancreas homeobox 1, LIM homeobox 1, LIM homeobox 3, and NK6 homeobox 1, and survival of motor neuron 1 increased in the reprogrammed cells after induction with the 4 F cocktail. More importantly, 4 F cocktail-reprogrammed motoneuron-like cells can release acetylcholine and exhibited vulnerability to glutamate-induced excitotoxicity. Our findings demonstrate that the 4 F cocktail first reprograms spinal astrocytes into a neural progenitor-like and motor neuron progenitor-like intermediate plastic state, which then gives rise to motoneuron-like cells. - Source: PubMed
Publication date: 2026/02/26
Yang RiyunShen JianhongJin PengjieYao QiChen SiyingWu TianqiChang SuyanPan JingyingChen YingChen Gang - Voltage-gated calcium channels (VGCCs) are essential for neuronal excitability and synapse transmission as well as gene transcription regulation controlling cellular differentiation and survival. Recently, genetic variants in the CACNA1D gene, which encodes the α-subunit of voltage-gated Ca1.3 L-type Ca-channels, were linked to neurodevelopmental disorders, but their pathophysiological role on neuronal activity and development in a human background remains unknown. Here, we report the first functional characterization of a patient-derived iPSC-based disease model of the CACNA1D L271H variant. We observed that Ca1.3 is the dominantly expressed L-type calcium channel isoform in neural progenitor cells (NPCs). NPCs expressing the L271H variant exhibit increased spontaneous calcium transients compared to the WT controls. Differentiated L271H-variant midbrain neurons show a more depolarized resting membrane potential and reduced excitability. Cortical organoids generated from the L271H-iPSCs contain fewer and smaller ventricular-like structures indicating impaired cellular organization. We identify spatial distortion of radial glial cell distribution and accelerated neuronal differentiation in patient-derived organoids as judged by premature intermediate progenitor cell and neuron emergence. Unbiased transcriptomic analysis revealed numerous dysregulated genes that according to gene ontology analysis were associated with "transcriptional regulation", "CNS development", and "neurogenesis" including PTN, POU3F2, CNTN4 and AUTS2. These findings imply that disease-causing Ca1.3 variants alter ion homeostasis, result in aberrant neuronal function and distort human neurodevelopment, contributing to the complex disease phenotype observed in patients with high-risk CACNA1D variants. - Source: PubMed
Publication date: 2026/01/09
Tisch MarcelGeisler Stefanie MGabassi ElisaSchlemmer QuirinLechner MiriamUlz Julia-AnnaSuarez-Cubero MartaDe Gaetano LauraSpathopoulou AngelikiStriessnig JörgOrtner Nadine JGünther KatharinaTuluc PetronelEdenhofer Frank - Despite advancements in diagnostic techniques and therapeutic strategies, the prognosis for Lung adenocarcinoma (LUAD) patients remains poor. Cell proliferation and cycle dysregulation drive cancer via uncontrolled cell growth. These genes also modulate tumor immune microenvironment (TIME), yet the precise mechanisms in LUAD remain largely unknown. - Source: PubMed
Publication date: 2025/12/31
Lin ChenjingZhang ManSun PanHe YulinTian YiLi WenwenPu ShengyanLuo JizhuangWang Kai - Breast cancer (BCa) is a common malignant tumor in women, and the prognostic value of NAD+ metabolism-related genes (NMRGs) in BCa remains to be clarified. - Source: PubMed
Publication date: 2025/12/09
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