Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA328011 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3745316_1.fastq.gz | Fastqsanger.gz | |||
| SRR3745316_2.fastq.gz | Fastqsanger.gz | |||
| SRR3745317.fastq.gz | Fastqsanger.gz | |||
| SRR3745318.fastq.gz | Fastqsanger.gz | |||
| SRR3745319.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
Project description:An inducible and reversible embryonic stem cell biobank reveals functional genomic pathways and disease targets
| PRJNA328006 | ENA
Project description:An inducible and reversible embryonic stem cell biobank reveals functional genomic pathways and disease targets [RNA-Seq]
| PRJNA327865 | ENA
Project description:An inducible and reversible embryonic stem cell biobank reveals functional genomic pathways and disease targets [iPCR]
| PRJNA328010 | ENA
Project description:An inducible and reversible embryonic stem cell biobank reveals functional genomic pathways and disease targets [iPCR/BC-PCR]
| PRJNA329111 | ENA
Project description:Developmental transcription factors act in networks, but how these networks achieve cell- and tissue specificity is still poorly understood. We here explored pre-B-cell leukemia homeobox 1 (PBX1) in adult neurogenesis combining genomic, transcriptomic, and proteomic approaches. ChIP-Seq analysis uncovered PBX1 binding to a wide range of different genes. Integration of PBX1 ChIP-seq with ATAC-seq data predicted interaction partners, which were subsequently validated by mass-spectrometry. Spatial transcriptomics revealed distinct temporal expression dynamics of Pbx1 and interacting factors. Among these were class I bHLH proteins TCF3, TCF4 and TCF12. RNA-seq upon Pbx1, Tcf3 and Tcf4 knockdown identified proliferation and differentiation associated genes as shared targets. Neuronal differentiation was reduced upon depletion of either factor, suggesting functional cooperation between PBX1 and TCF3/4. Notably, while physiological PBX1-TCF interactions have not yet been described, chromosomal translocation resulting in genomic TCF3::PBX1 fusion characterizes a subtype of acute lymphoblastic leukemia. Introducing Pbx1 into Nalm6 cells, a pre B-cell line expressing TCF3 but lacking PBX1, upregulated leukemogenic genes including BLK and NOTCH3, arguing that functional PBX1-TCF cooperation likely extends to hematopoietic contexts. Our study hence uncovers a PBX1-TCF module orchestrating the balance between progenitor cell proliferation and differentiation in adult neurogenesis with implications for leukemia etiology.
2024-09-16 | PXD048222 | Pride
Project description:The t(7;12) AML subtype in pediatric patients is associated with upregulation of homeodomain protein MNX1 as the initiating event for leukemogenesis. In this study, we investigated the downstream targets of MNX1 and their relationship to the histone modifications previously observed to be mediated by MNX1. Using a comprehensive approach combining TMT mass spectrometry, RNA-Seq, qPCR, ACT-seq, ATAC-seq, and ChIP-qPCR, we identified PBXIP1 along with its associated pioneer transcription factor PBX1 and PBX4 as downstream targets of MNX1. MNX1 binding to the Pbx1 promoter triggered its transcriptional activation, which was associated with an increase in the activating histone mark H3K4me3 and a decrease in the repressive mark H3K27me3 at the promoter site. Notably, despite the transient nature of MNX1’s promoter interaction, these histone marks persisted, suggesting a “hit-and-run” epigenetic remodeling mechanism. Enrichment of PBX motifs within MNX1-induced H3K4me1, H3K4me3, and ATAC-seq peaks underscores the pivotal role of the PBX family in MNX1-mediated chromatin dynamics. This was further confirmed by showing that MNX1-induced PBX1 expression could be downregulated using the Sinefungin inhibitor, a pan-methyltransferase inhibitor, that also prevent leukemia development. Our findings provide insights into how MNX1-driven epigenetic modifications are connected to its downstream targets and may offer new avenues for therapeutic intervention in t(7;12) AML.
2025-04-24 | PXD056378 | Pride
Project description:Aging is a universal biological phenomenon linked to many diseases, such as cancer or neurodegeneration. However, the molecular mechanisms underlying aging, or how lifestyle interventions such as cognitive stimulation can ameliorate this process, are yet to be clarified. Here, we performed a multi-omic profiling, including RNA-seq, ATAC-seq, ChIP-seq, EM-seq, SWATH-MS and single cell Multiome scRNA and scATAC-seq, in the dorsal hippocampus of young and old mouse subjects which were subject to cognitive stimulation using the paradigm of environmental enrichment. In this study we were able to describe the epigenomic landscape of aging and cognitive stimulation.
2023-09-29 | PXD045567 | Pride
Project description:Human cells identify invading pathogens and activate immune signaling pathways through a wide array of pattern recognition receptors, such as DNA sensors. The interferon-inducible protein 16 (IFI16) is a nuclear DNA sensor that recognizes double-stranded DNA from a number of viral sources, including genomes of nuclear-replicating viruses such as the prevalent human pathogen, herpes simplex virus 1 (HSV-1). Upon binding to the DNA genome of HSV-1, IFI16 both induces antiviral cytokine expression and suppresses virus gene expression. Here, we use a multi-omics approach of DNA sequencing techniques paired with targeted mass spectrometry to obtain an extensive view of the interaction between IFI16 and the HSV-1 genome, and how this binding affects the viral DNA structure and protein expression. Through ChIP-seq, we find that IFI16 binds to the HSV-1 genome in a sequence-independent manner while simultaneously exhibiting broad enrichment at two loci: UL30, the viral DNA polymerase gene, and US1-US7. ATAC-seq analysis reveals that these two regions are among the most accessible stretches of DNA on the genome, thereby facilitating IFI16 binding. Accessibility of the entire HSV-1 genome is elevated upon IFI16-KO, indicating that expression of IFI16 globally induces chromatinization of viral DNA, regardless of IFI16 enrichment. Deletion of IFI16 also results in a global increase in the expression of HSV-1 proteins, as measured by parallel reaction monitoring-mass spectrometry. Altogether, we demonstrate that IFI16 interacts with the HSV-1 genome in a sequence-independent manner, and this interaction coordinates epigenetic silencing of the viral genome, resulting in decreased protein expression and virus replication.
2022-04-27 | PXD031850 | panorama
Project description:Enhancers play key roles in gene regulation. However, comprehensive enhancer discovery is challenging because most enhancers, especially those affected in complex diseases, have weak effects on gene expression. Through gene regulatory network modeling, we identified that dynamic cell state transitions, a critical missing component in prevalent enhancer discovery strategies, can be utilized to improve the cells’ sensitivity to enhancer perturbation. Guided by the modeling results, we performed a mid-transition CRISPRi-based enhancer screen utilizing human embryonic stem cell definitive endoderm differentiation as a dynamic transition system. The screen discovered a comprehensive set of enhancers (4 to 9 per locus) for each of the core lineage-specifying transcription factors (TFs), including many enhancers with weak to moderate effects. Integrating the screening results with enhancer activity measurements (ATAC-seq, H3K27ac ChIP-seq) and three-dimensional enhancer-promoter interaction information (CTCF looping, Hi-C), we were able to develop a CTCF loop-constrained Interaction Activity (CIA) model that can better predict functional enhancers compared to models that rely on Hi-C-based enhancer-promoter contact frequency. Together, our dynamic network-guided enhancer screen and the CIA enhancer prediction model provide generalizable strategies for sensitive and more comprehensive enhancer discovery in both normal and pathological cell state transitions.
2023-06-17 | PXD043070 | Pride
Project description:We performed CRISPRi enhancer screens during differentiation of human embryonic stem cells (hESC) to definitive endoderm (DE) in genomic windows surrounding ten lineage-specifying core TFs. We also generated scRNA-seq, ATAC-seq, and TF ChIP-seq data and show that CTCF loops constrain the interactions between enhancers and their promoter targets.
2022-10-01 | GSE213394 | GEO