EOMES antibody - N-terminal region (ARP30096_P050)
- Known as:
- EOMES (anti-) - N-terminal region (ARP30096_P050)
- Catalog number:
- arp30096_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- EOMES antibody - N-terminal region (ARP30096_P050)
Related genes to: EOMES antibody - N-terminal region (ARP30096_P050)
- Gene:
- EOMES NIH gene
- Name:
- eomesodermin
- Previous symbol:
- -
- Synonyms:
- TBR2
- Chromosome:
- 3p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-15
- Date modifiied:
- 2014-11-19
Related products to: EOMES antibody - N-terminal region (ARP30096_P050)
Related articles to: EOMES antibody - N-terminal region (ARP30096_P050)
- A major technical challenge in single-cell transcriptomics is the absence of an integrative analytic pipeline that can simultaneously leverage gene regulatory network (GRN) architecture, AI-assisted gene panel discovery, and functional relevance analyses to generate coherent biological insights. Existing approaches often treat these components independently, focusing on clusters, marker genes, or predictive features without integrating them into a mechanistically grounded framework. Consequently, comprehensive screening that links regulatory association, gene signature screening, and functional interpretation within single-cell datasets remains limited, underscoring the need for an integrated strategy. - Source: PubMed
Publication date: 2026/04/06
Borra SantoshiYan DaWelner Robert SYue Zongliang - Innate lymphoid cells (ILCs) are distinct lineages defined by lineage-specifying transcription factors that drive their differentiation and effector programs. Despite being stable lineages, ILC plasticity has been reported. Plasticity is characterized by downregulation of the transcription factor that specifies the current ILC lineage, followed by upregulation of the transcription factor and surface markers that determine the phenotype of the ILC lineage it is acquiring. Even though NK cells rely on the lineage-specifying transcription factor Eomes, an unusual phenotype characterized by ILC1 marker expression was reported in the salivary glands and during Toxoplasma gondii infection. However, it remains unclear whether this reflects true ILC plasticity or simply phenotypic changes. Using a dual-reporter system that allows simultaneous detection of live expression and fate-labeling of Eomes, we observed downregulation of this lineage-specifying transcription factor in NK cells (Eomes cells) and upregulation of ILC1 markers in the salivary gland and multiple organs during Toxoplasma gondii infection, including organs that otherwise promote NK cell fate. While Eomes cells adopted an ILC1-like phenotype, they differentiated in the absence of Hobit, a pivotal transcription factor of ILC1s, distinguishing them from the ILC1 lineage. Therefore, our data demonstrate that NK cells can adopt an Eomes ILC1-like fate, even in the blood and secondary lymphoid organs, complementing previous findings on ILC2 and ILC3 plasticity towards the ILC1 lineage. - Source: PubMed
Publication date: 2026/04/09
Stokic-Trtica VladislavaSteffen JohannesGao XuemeiDüsedau HenningBoulekou SotiriaArnold Sebastian JTriantafyllopoulou AntigoniRomagnani ChiaraDiefenbach AndreasTanriver YakupDunay Ildiko RKlose Christoph S N - Epithelial cell adhesion molecule (EpCAM) is a tumor-associated antigen that marks pluripotent embryonic stem cells (ESCs). Regulation of Epcam expression yields a spatiotemporal patterning during embryogenesis that is thoroughly mimicked in a 3D model of spontaneous differentiation of embryoid bodies (EBs). Here, we present a role of EpCAM in exit from pluripotency of murine ESCs (mESCs) to establish cardiomyocytes in EBs. Comparative transcriptomic analysis of wildtype and Epcam-knockout mESCs at strategic time points of spontaneous differentiation uncovered molecular deficiencies of Epcam-knockout ESCs in "Wnt signaling" and "Heart development". Multi-level bioinformatic analyses revealed central lineage-defining transcription factors Eomes, Foxa2, and Gata6 as differentially expressed genes (DEGs) that are misregulated in Epcam-knockout mESCs. Gene expression association of Epcam with Eomes, Foxa2, and Gata6 was prominent at day three of spontaneous differentiation, representing primitive streak formation in EBs. Interrogation of public single-cell RNA sequencing (scRNAseq) datasets supported a co-expression of Epcam and Eomes at early stages of murine embryogenesis in epiblast, primitive streak, nascent mesoderm, extraembryonic ectoderm and endoderm. Newly generated scRNAseq of wildtype mESCs in spontaneous differentiation delineated the formation of epiblast, primitive streak, endo- and mesoderm cells, and cardiomyocytes. Expression and pseudotime analysis positioned Epcam expression slightly ahead of Eomes at the transition of early to late primitive streak, along with rising Wnt signaling. Accordingly, conditional re-expression of Epcam or Eomes but not of Foxa2 or Gata6 complemented differentiation defects of Epcam-knockouts and confirmed an involvement of Wnt signaling in the EpCAM-dependent activation of Eomes. Hence, defective exit of pluripotency in Epcam-deficient ESCs is linked to Eomes regulation via Wnt signaling. - Source: PubMed
Publication date: 2026/04/11
Gong NingyueGouda MaheshBalaz Ana MarijaSong JiahangKranz GiselaHess JuliaBaumeister PhilippUnger KristianKatalina VeraCanis MartinGires Olivier - CD4⁺ helper T (T) cells consist of multiple functional subsets defined by specific effector cytokines and transcription factors. Recently, single-cell transcriptomic analyses have revealed possible existence of additional populations. Here we identify a unique CD4⁺ T cell subset in mouse and human colitis characterized by high levels of granzyme K (Gzmk) expression, designated as TK cells. These cells exhibit unique transcriptional signatures, with minimal expression of classical T-defining factors but rather prominent Eomesodermin (Eomes) expression. Notably, TK cell differentiation is independent of T1, T2 and T17 lineages in colitis. EOMES is both necessary and sufficient for TK cell induction, by directly driving the expression of Gzmk and associated effector molecules. Genetic ablation of Eomes ameliorates intestinal immunopathology in a T cell-induced colitis model. The TK transcriptional program seems to be conserved across species and in diverse disease contexts. Our findings establish TK cells as a distinct T cell subtype, and the EOMES-TK axis may serve as a potential therapeutic target in inflammatory diseases. - Source: PubMed
Publication date: 2026/04/02
Xie TianDu YizhouWang QihanZhang HaoWei KunChi XinxinBai XueFu YujiePeng ZhilinZhu YichengLan QiuyanDong Chen - YAP1 signaling is essential for development but its specific roles in early embryogenesis remain poorly understood. To shed light on this, we analyze YAP1's role in regulating the pluripotency of the mammalian epiblast, using scRNAseq approaches. Conditional deletion of Yap1 in the mouse epiblast (Sox2-Cre) alters the expression of signaling genes, including Nodal, Wnt3, and Fgf8. Accordingly, Yap1 loss leads to enhanced differentiation of the epiblast toward primitive streak lineages, as evidenced by the upregulation of T/Brachyury and Eomes genes. A proximity labeling assay in human pluripotent stem cells, followed by biochemical assays and molecular modeling predictions, reveals that YAP1 cooperates with QSER1 protein to regulate lineage genes. Our analysis shows that YAP1:TEAD4 enhancers recruit QSER1 to prevent RNA Polymerase II recruitment. QSER1 depletion, similar to YAP1, increases NODAL gene expression and leads to hyperactive NODAL signaling during human embryonic stem cells differentiation. Overall, our findings define a role of YAP1 in the epiblast in vivo and uncover an interplay with QSER1 controlling the activity of developmental signaling pathways in pluripotent cells. - Source: PubMed
Publication date: 2026/03/26
Abraham ElizabethRoule ThomasDouglas AidanMegill EmilyPericak Olivia MHowe Jordan EChoya-Foces CarmenGarbincius Joanne FCohen Henry MRoig-Flórez PaulaZubillaga MikelAndrake Mark DKim SeonheeElrod John WAkizu NaiaraEstaras Conchi