Ontology highlight
ABSTRACT:
PROVIDER: PRJNA239582 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1178490_1.fastq.gz | Fastqsanger.gz | |||
| SRR1178490_2.fastq.gz | Fastqsanger.gz | |||
| SRR1178491_1.fastq.gz | Fastqsanger.gz | |||
| SRR1178491_2.fastq.gz | Fastqsanger.gz | |||
| SRR1178492_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:TG-interacting factor1 (Tgif1) maintains the identity of mouse ES cells by counterbalancing the expression of core pluripotency factors.
| PRJNA239580 | ENA
Project description:TG-interacting factor1 (Tgif1) is well-known as a transcriptional repressor in transforming growth factor beta (TGFβ) signaling pathway. Target mapping of ES cell core factors in mouse embryonic stem (ES) cells revealed that Tgif1 is occupied by Oct4 and Nanog. Moreover, recent interactome study of mouse gene regulatory regions showed a preferential regulation of Tgif1 by mouse ES cell specific enhancers. However, the detailed role and mode of actions of Tgif1 in stem cell maintenance and development remains elusive. We show that Tgif1 is indispensable for self-renewal and pluripotency of mouse embryonic stem (ES) cells. Aberrant expression of Tgif1 promotes differentiation of ES cells even in the presence of LIF in part by deregulation of pluripotency factors. Intriguingly, we find that Tgif1 level is a critical factor to determine specific lineage commitment in a dosage-dependent manner. We further show that Tgif1 interacts with ES cell core factors and co-localizes at their binding sites, which eventually restricts expression of ES cell core factors including Oct4, Sox2, and Nanog. Taken together, we provide new insights into the roles of Tgif1 in maintenance as well as differentiation of ES cells.
2015-09-26 | GSE55404 | GEO
Project description:TG-interacting factor1 (Tgif1) is well-known as a transcriptional repressor in transforming growth factor beta (TGFβ) signaling pathway. Target mapping of ES core factors in mouse embryonic stem (ES) cells revealed that Tgif1 is occupied by Oct4 and Nanog. Moreover, recent interactome study of mouse gene regulatory regions showed a preferential regulation of Tgif1 by mouse ES cell specific enhancers. However, the detailed role and mode of actions of Tgif1 in stem cell maintenance and development remains elusive. We show that Tgif1 is indispensable for self-renewal and pluripotency of mouse embryonic stem (ES) cells. Aberrant expression of Tgif1 promotes differentiation of ES cells even in the presence of LIF in part by deregulation of pluripotency factors. Intriguingly, we find that Tgif1 level is a critical factor to determine specific lineage commitment in a dosage-dependent manner. We further show that Tgif1 interacts with ES cell core factors and co-localizes at their binding sites, which eventually restricts expression of ES cell core factors including Oct4, Sox2, and Nanog. Taken together, we provide new insights into the roles of Tgif1 in maintenance as well as differentiation of ES cells.
2015-09-26 | GSE55401 | GEO
Project description:TG-interacting factor1 (Tgif1) maintains the identity of mouse ES cells by counterbalancing the expression of ES cell core factors
| PRJNA239579 | ENA
Project description:Core circuits of transcription factors stabilize stem and progenitor cells by suppressing genes required for differentiation. We do not know how such core circuits are reorganized during cell fate transitions to allow differentiation and lineage choice to proceed. Here, we asked how the pluripotency circuit, a core transcriptional circuit that maintains mouse embryonic stem (ES) cells in a pluripotent state, is dismantled as ES cells differentiate and choose between the neural ectodermal and mesendodermal progenitor cell fates. When ES cells are recultured from pluripotency maintaining conditions to the basal media N2B27, the expression of the pluripotency circuit genes begins to change. At 48 hours post N2B27 addition, the ES cells are competent to respond to differentiation signals. Here, our microarray analysis compares the gene expression profile of ES cells vs. the gene expression profile of cells that have been treated with N2B27 for 48 hours, reaching the competent state. 2 x mouse ES cells in pluripotency maintaining conditions. 3 x mouse ES cells after 48 hr of N2B27 culture
2011-05-03 | E-GEOD-29005 | biostudies-arrayexpress
Project description:Core circuits of transcription factors stabilize stem and progenitor cells by suppressing genes required for differentiation. We do not know how such core circuits are reorganized during cell fate transitions to allow differentiation and lineage choice to proceed. Here, we asked how the pluripotency circuit, a core transcriptional circuit that maintains mouse embryonic stem (ES) cells in a pluripotent state, is dismantled as ES cells differentiate and choose between the neural ectodermal and mesendodermal progenitor cell fates. When ES cells are recultured from pluripotency maintaining conditions to the basal media N2B27, the expression of the pluripotency circuit genes begins to change. At 48 hours post N2B27 addition, the ES cells are competent to respond to differentiation signals. Here, our microarray analysis compares the gene expression profile of ES cells vs. the gene expression profile of cells that have been treated with N2B27 for 48 hours, reaching the competent state.
2011-05-03 | GSE29005 | GEO
Project description:Abstract: The Promyelocytic Leukemia protein (PML) and its associated nuclear bodies have re-cently emerged as essential factors for maintaining the characteristics of embryonic stem (ES) cells. However, the full repertoire of PML driven gene regulatory events in ES cells is not resolved. In this report we have studied the role of PML in shaping the proteomic and SUMO proteomic landscape in ES cells. Our analysis of the PML KD proteome revealed a suppression of proteins related with self-renewal and an up-regulation of proteins vital for translation and proteasome functions, reflecting a cellular transition from pluripotency to differentiation. Major targets of PML-directed sumoylation include pluripotency factors, chromatin organizers and cell cycle regulators. We demonstrate that PML promotes the sumoylation of SALL1 and CDCA8, two proteins that are highly expressed in undifferentiated ES cells. SALL1 sumoylation increases the activation of the Wnt pathway, contributing to its ability to inhibit ES cell differentiation. Similarly, CDCA8 sumoylation enhances its capacity to promote cell proliferation. Our results demonstrate that PML maintains ES cell functions by modulating the abundance or sumoylation of key regulators involved in pluripotency and cell cycle progression.
2025-05-23 | PXD057990 | Pride
Project description:Abstract: The Promyelocytic Leukemia protein (PML) and its associated nuclear bodies have re-cently emerged as essential factors for maintaining the characteristics of embryonic stem (ES) cells. However, the full repertoire of PML driven gene regulatory events in ES cells is not resolved. In this report we have studied the role of PML in shaping the proteomic and SUMO proteomic landscape in ES cells. Our analysis of the PML KD proteome revealed a suppression of proteins related with self-renewal and an up-regulation of proteins vital for translation and proteasome functions, reflecting a cellular transition from pluripotency to differentiation. Major targets of PML-directed sumoylation include pluripotency factors, chromatin organizers and cell cycle regulators. We demonstrate that PML promotes the sumoylation of SALL1 and CDCA8, two proteins that are highly expressed in undifferentiated ES cells. SALL1 sumoylation increases the activation of the Wnt pathway, contributing to its ability to inhibit ES cell differentiation. Similarly, CDCA8 sumoylation enhances its capacity to promote cell proliferation. Our results demonstrate that PML maintains ES cell functions by modulating the abundance or sumoylation of key regulators involved in pluripotency and cell cycle progression.
2025-05-07 | PXD058024 | Pride
Project description:Eric Hesse 9 Jan 2019, 17:34 (15 hours ago) to me, Hartmut Lieber Marcel, unten ist das abstract kopiert, reicht das? Lg, Eric Abstract Osteoporosis is caused by increased bone resorption and decreased bone formation. Intermittent administration of a fragment of Parathyroid hormone (PTH) activates osteoblast-mediated bone formation and is used in patients with severe osteoporosis. However, the mechanisms by which PTH elicits its anabolic effect are not fully elucidated. Here we show that the absence of the homeodomain protein TG-interacting factor 1 (Tgif1) impairs osteoblast differentiation and activity, leading to a reduced bone formation. Deletion of Tgif1 in osteoblasts and osteocytes decreases bone resorption due to an increased secretion of Semaphorin 3E (Sema3E), an osteoclast-inhibiting factor. Tgif1 is a PTH target gene and PTH treatment failed to increase bone formation and bone mass in Tgif1-deficient mice. Thus, our study identifies Tgif1 as a novel regulator of bone remodeling and an essential component of the PTH anabolic action. These insights contribute to a better understanding of bone metabolism and the anabolic function of PTH.
2019-01-29 | PXD012303 | Pride
Project description:Orphan nuclear receptor Esrrb is vital in maintaining ES cells and like Oct4, Sox2 and Nanog is essential for self-renewal and pluripotency. Esrrb functions in somatic cells via LBD/AF-2-dependent coactivator recruitment to target genes. Here we show that in ES cells coactivator recruitment is similarly required and identify Ncoa3 as the Esrrb coactivator needed for activation of its target genes. Ncoa3 is essential for self-renewal and the induction of pluripotency in reprogramming, and genome-wide analysis of Ncoa3 binding reveals extensive overlap with Esrrb and pluripotency factors along with marks of active genes. Mechanistically, we show Ncoa3 is specifically required to bridge RNApol2 to Esrrb. We thus identify a new member of the ES pluripotency network and describe Esrrb and Ncoa3 as key factors linking core pluripotency factors to the general transcription machinery.
2012-10-02 | GSE37262 | GEO