Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA269974 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:mTORC1 regulates microRNA biogenesis in mouse bone marrow hematopoietic stem and progenitor cells
| PRJNA269959 | 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
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Project description:This study addresses how ER stress impacts hematopoietic regeneration in the bone marrow microenvironment. We evaluated how endothelial PERK-DLL4 axis regulates early HSC and B progenitor regeneration by using single-cell analysis of regenerating bone marrow cells collected from mice with endothelial-specific deletion of Perk (EP), Dll4 (ED), or combined (DKO). Through bone marrow transplantation and single cell analysis, we revealed that perturbation of PERK or DLL4 resulted in opposite changes in B and granulomonocytic progenitor recovery. Further, PERK-DLL4 axis orchestrates the regenerative network by regulating endothelial DLL4 signaling to NOTCH3 on MSCs, lymphoid commitment of hematopoietic stem cells, IL7 expression in MSCs, and coordinated interferon response. These findings establish that ER stress regulates a regenerative pre-B niche through PERK-regulated endothelial DLL4 signaling to NOTCH3 on MSCs.
2026-08-13 | GSE308168 | GEO