RFX4 antibody - middle region (ARP33224_T100)
- Known as:
- RFX4 (anti-) - middle region (ARP33224_T100)
- Catalog number:
- arp33224_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RFX4 antibody - middle region (ARP33224_T100)
Related genes to: RFX4 antibody - middle region (ARP33224_T100)
- Gene:
- RFX4 NIH gene
- Name:
- regulatory factor X4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 12q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-11
- Date modifiied:
- 2016-10-05
Related products to: RFX4 antibody - middle region (ARP33224_T100)
Related articles to: RFX4 antibody - middle region (ARP33224_T100)
- Despite the recent identification of RFX4 as a neurodevelopmental disorder risk gene, its role in cortical development remained unclear. Here, we identified both shared and lineage-specific RFX4 requirements for human cortical development using new human stem cell models of deficiency and pathogenic mutation. We found that RFX4 restrains neurogenesis by acting cooperatively with NOTCH signaling, specifically repressing pro-neuronal and synaptic gene expression in neural progenitors. We also determined that genome-wide binding of RFX3, another neurodevelopmental disorder risk gene, depends upon RFX4 to regulate synaptic gene expression. Furthermore, we identified lineage-specific functions for RFX4 in regulating proliferation during cortical inhibitory neuron development. Ultimately, we demonstrated that RFX4 deficiency persistently dysregulates neuronal gene expression through neuronal differentiation and disrupts cortical neuron stratification in organoid models. These consequences were absent in neurons generated by direct differentiation, confirming that neuronal phenotypes resulted from unconstrained neurogenesis. Finally, we modeled pathogenic missense mutation of the RFX4 DNA-binding domain. While this mutation strongly reduced DNA binding, it dysregulated synaptic gene expression distinctly from our deficiency models, supporting pathogenic mechanisms distinct from haploinsufficiency. Together, this work identified both shared and lineage-specific requirements for RFX4 during cortical development, building a necessary foundation for elucidating the etiology of RFX4-associated disorders. - Source: PubMed
Publication date: 2026/02/17
Determan Julianna JChapman GarethCrump Sydney RBatool FaizaMalik SofiaGujral TaranBuchser WilliamValentine CalebElia SerenaSentmanat MonicaCui XiaoxiaJetter HaleyKroll Kristen L - Sporadic early-onset Alzheimer's disease (sEOAD) represents a substantial but less-studied subtype of Alzheimer's disease (AD). Here, we generated a single-nucleus multiome atlas derived from the postmortem prefrontal cortex, entorhinal cortex, and hippocampus of nine individuals with or without sEOAD. Comprehensive analyses were conducted to delineate cell type-specific transcriptomic changes and linked candidate cisregulatory elements (cCREs) across brain regions. We prioritized eight conservative transcription factors in glial cells in multiple brain regions, including RFX4 in astrocytes and IKZF1 in microglia, which are implicated in regulating sEOAD-associated genes. Moreover, we identified the top 25 altered intercellular signaling between glial cells and neurons, highlighting their regulatory potential on gene expression in receiver cells. We reported 33 cCREs linked to sEOAD-associated genes overlapped with late-onset AD risk loci, and found that, in addition, sEOAD cCREs are enriched for neuropsychiatric disorder risk variants. This atlas helps dissect transcriptional and chromatin dynamics in sEOAD, providing a key resource for AD research. - Source: PubMed
Publication date: 2025/12/17
Liu AndiCitu CituEnduru NiteshChen XianTung Chia-HaoSinha TirthankarSepulveda Sofia EManuel Astrid MGorski DamianFernandes Brisa SYu MeifangSchulz Paul ESimon Lukas MSoto ClaudioZhao Zhongming - Glioblastoma is a highly aggressive and devastating brain malignancy with dismal prognosis and extremely limited therapeutic options. Identification of prognostic biomarkers and therapeutic targets from multi-omics data is critical for improving patient outcomes. In this study, we investigated the clinical significance of cellular heterogeneity and super-enhancer-driven regulatory networks, which are critically implicated in glioblastoma progression and treatment resistance. We first performed scRNA-seq to dissect tumour microenvironment heterogeneity, identifying 16 distinct cell clusters, including astrocytes, macrophages, and CD8+ T cells. CellChat analysis revealed key intercellular signalling pathways, with astrocytes and macrophages acting as central communication hubs. To integrate bulk RNA sequencing data, we applied the Scissor algorithm to identify survival-associated cell states. By combining single-cell and bulk transcriptomic data, we uncovered 642 survival-related genes, including QKI and RBM47, which robustly predicted patient survival and immunotherapy response. Furthermore, WGCNA analysis identified seven co-expression modules and super enhancer-regulated networks orchestrated by transcription factors (RFX2, RFX4) and hub genes (NEAT1, CFLAR). These networks stratified patients into high- and low-risk groups with significant survival differences. Collectively, our findings elucidate the intricate interplay between cellular heterogeneity and super enhancer-driven gene regulation in glioblastoma, providing a translational framework for targeting oncogenic hubs and modulating microenvironment interactions. - Source: PubMed
Xu ZijunXi BohanHuang JiamingZhang LiqiangCui SifuWang XianweiChen DongLi Shupeng - Glioblastoma (GBM) is the most common primary brain cancer. It causes death mainly by local invasion via several routes, including infiltration of white matter tracts and penetration of perivascular spaces. However, the pathways that mediate these invasion routes are only partly known. Here, we conduct an integrative study to identify cell states and central drivers of route-specific invasion in GBM. Combining single-cell profiling and spatial protein detection in patient-derived xenograft models and clinical tumor samples, we demonstrate a close association between the differentiation state of GBM cells and their choice of invasion route. Computational modeling identifies ANXA1 as a driver of perivascular involvement in GBM cells with mesenchymal differentiation and the transcription factors RFX4 and HOPX as orchestrators of growth and differentiation in diffusely invading GBM cells. Ablation of these targets in tumor cells alters their invasion route, redistributes the cell states, and extends survival in xenografted mice. Our results define a close association between GBM cell differentiation states and invasion routes, identify functional biomarkers of route-specific invasion, and point toward targeted modulation of specific invasive cell states as a therapeutic strategy in GBM. - Source: PubMed
Publication date: 2025/07/19
Doroszko MilenaStockgard RebeckaUppman IremHeinold JosephineVoukelatou FaidraMangukiya Hitesh BhagavanbhaiMillner Thomas OSkeppås MadeleineBallester Bravo MarElgendy RamyBerglund MariaElfineh LudmilaKrona CeciliaKundu SoumiKoltowska KatarzynaMarino SilviaLarsson IdaNelander Sven - Opsins are G-protein-coupled receptors often expressed in neuronal photoreceptor cells and used for light detection in most animals, including cnidarians like corals, jellyfish, and anemones. Opsins may also be expressed in non-neuronal cell types, where they may confer light sensitivity. For example, opsins might be involved in pre-neural phototaxis of larval box jellyfish. However, the overall extent of non-neuronal expression of opsins is not well understood, despite the potential for identifying additional light or opsin-mediated organismal functions. To investigate the prevalence of non-neuronal opsin expression in a cnidarian, we analyzed published data from Hydra vulgaris, a freshwater hydroid that responds to light despite lacking distinct photosensory structures such as eyes. We quantified opsin expression across Hydra cell types and states of cell differentiation using published single-cell RNA sequencing (scRNA-seq) data and assay for transposase-accessible chromatin sequencing data. We identified 45 opsin transcripts in Hydra expressed in neuronal and non-neuronal cell types, as well as across inferred states of cell differentiation. We found a wider diversity of opsin gene transcripts in neuronal cell types, predominantly in fully differentiated cells. In contrast, we detected fewer opsin transcripts in non-neuronal cell types, and they were expressed from stem cell to progenitor cell to fully differentiated cell state-all within the same inferred cell type. These opsin transcripts appear to be expressed at higher levels in ectodermal epithelial cells near the head organizer of Hydra (a key developmental patterning region) and share transcription factor binding motifs with development genes such as Six, Otx, Ptx, Rfx4, and Hxa. Overall, we outline an array of opsin gene transcripts, their expression, and open chromatin patterns across cell type diversity in Hydra, and highlight potential co-regulatory relationships that may pave the way for future work on unconventional roles for opsin genes in Hydra. - Source: PubMed
Stoilova Marina IPicciani NatashaMacias-Muñoz AideOakley Todd H