Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA269959 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:mTORC1 regulates microRNA biogenesis in mouse bone marrow hematopoietic stem and progenitor cells
| PRJNA269974 | ENA
Project description:Mass spectrometry results from TurboID experiments using constructs expressing TurboID only, NPM1wt-Turbo ID (N- and C-terminal fusions) and NPMc-Turbo ID fusions (N- and C-terminal fusions) transduced in primary mouse hematopoietic stem/progenitor cells from lineage-depleted mouse bone marrow.
2022-03-09 | MSV000089028 | MassIVE
Project description:Hematopoietic stem cells give rise to all blood lineages, can fully re-populate the bone marrow, and easily outlive the host organism. To better understand how stem cells remain fit during aging, we analyzed the proteome of hematopoietic stem and progenitor cells.
2019-05-23 | MSV000083845 | MassIVE
Project description:mTOR senses nutrient and energy status to regulate cell survival and metabolism in response to environmental changes. Surprisingly, targeted mutation of Tsc1, a negative regulator of mTORC1, caused a broad reduction in miRNAs due to Drosha degradation. Conversely, targeted mutation of Raptor, an essential component of mTORC 1, increased miRNA biogenesis. mTOR activation increased expression of Mdm2, which is hereby identified as the necessary and sufficient ubiquitin E3 ligase for Drosha. Drosha was induced by nutrient and energy deprivation and conferred resistance to glucose deprivation. Using a high throughput screen of a miRNA library, we identified 4 miRNAs that were necessary and sufficient to protect cells against glucose deprivation-induced apoptosis. These miRNA was regulated by glucose through the mTORC1-MDM2- Drosha axis. Taken together, our data reveal an mTOR-Mdm2-Drosha pathway in mammalian cells that broadly regulates miRNA biogenesis as a response to alteration in cellular environment. Deletion of Raptor caused a global increase in both miRNA and pre-miRNA in mouse bone marrow hematopoietic stem and progenitor cells(HSPCs).
2014-12-11 | GSE64042 | GEO
Project description:Advances in sequencing-based genomic profiling present a new challenge of explaining how changes in DNA/RNA are translated into proteins linking genotypes to phenotypes. The developing erythroid cells require highly coordinated gene expression and metabolism, and serve as a unique model in dissecting regulatory events in development and disease. Here we compare the proteomic and transcriptomic changes in human hematopoietic stem/progenitor cells and lineage-committed erythroid progenitors, and uncover pathways related to mitochondrial biogenesis enhanced through post-transcriptional regulation. Two principal mitochondrial factors TFAM and PHB2 are tightly regulated at the protein level and indispensable for mitochondria and erythropoiesis. mTORC1 signaling is progressively enhanced to promote translation of mitochondrial proteins during erythroid specification. Genetic and pharmacological perturbation of mTORC1 or mitochondria impairs erythropoiesis. Our studies suggest a new mechanism for regulation of mitochondrial biogenesis through mTORC1-mediated protein translation, and may have direct relevance to the hematological defects associated with mitochondrial diseases and aging. Transcriptional profiling in human primary fetal and adult CD34+ hematopoietic stem/progenitor cells (HSPCs) erythroid progenitor cells (ProEs) by RNA-seq analysis.
2017-05-15 | E-GEOD-74053 | biostudies-arrayexpress
Project description:mTORC1 regulates microRNA biogenesis in mouse embryonic fibroblast cells
| PRJNA270086 | ENA
Project description:Single cell RNA sequencing of 37,501 cells representing four independently isolated hematopoietic stem and progenitor populations from mouse bone marrow
2023-03-03 | GSE168259 | GEO
Project description:We performed RNA sequencing analyses of adult mouse bone marrow endothelial cells. Especially, we investigated gene expression profiling of endothelial cells before and after lethal irradiation or hematopoietic cell depletion. We also analyzed mouse bone marrow endothelial cell subtypes, Apln+ and diaphyseal endothelial cells. Whole bone marrow cells, lineage negative hematopoietic stem and progenitor cells, Lin- Sca1+ cKit+ cells were used as controls for the differential gene expression analyses.
2019-11-14 | GSE115422 | GEO
Project description:mTORC1 regulates microRNA biogenesis in Hela cells
| PRJNA269975 | ENA
Project description:<p>We are studying the natural history, pathogenesis and treatment of patients with WHIM syndrome, an immunodeficiency disorder characterized by warts, hypogammaglobulinemia, recurrent infections and neutropenia usually due to autosomal dominant gain-of-function mutations in chemokine receptor <i>CXCR4</i>. We have identified a patient born with WHIM syndrome and the WHIM mutation <i>CXCR4<sup>R334X</sup></i> who has been disease-free for 20 years and who lacks <i>CXCR4<sup>R334X</sup></i> in myeloid cells, the cells that drive disease manifestations. She is a genetic and hematopoietic mosaic, since she still has the mutation in lymphoid cells and non-hematopoietic cells. Cytogenetics and microarray analysis revealed that the mechanism of loss of the mutation was deletion of the mutant allele from one copy of chromosome 2. Whole genome sequencing of patient neutrophil and skin fibroblast genomic DNA revealed that the mechanism of deletion was chromothripsis, a process of chromosome shattering resulting in deletions and rearrangements of the non-deleted chromosomal segments. In the patient, this process evidently occurred in a single hematopoietic stem cell (HSC), resulting in deletion of the disease allele <i>CXCR4<sup>R334X</sup></i> and one copy of 163 other genes on chromosome 2. This HSC evidently acquired a growth advantage and repopulated the HSC population and the myeloid lineage. Consistent with this, studies using gene targeted mice in competitive bone marrow transplantation experiments revealed that selective <i>Cxcr4</i> haploinsufficiency (inactivation of one copy of <i>Cxcr4</i> and not of any other genes) was sufficient to confer a strong engraftment advantage over bone marrow cells from wild type mice as well as bone marrow cells from a mouse model of WHIM syndrome. These results suggest that <i>CXCR4</i> knockdown may be a useful strategy to enhance bone marrow engraftment in the absence of toxic bone marrow conditioning regimens.</p>
| phs000856 | dbGaP