Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA396025 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We FACS-purified GFP+ LSK cells from mice transplanted with stably engrafted miR-99 KD and Scr HSCs and performed RNA-sequencing, demonstrating miR-99 KD results in significant depletion of hematopoietic stem cell gene expression signature and induces a differentiated progenitor gene expression signature.
2017-07-27 | GSE101903 | GEO
Project description:We FACS purified L-GMP cells (GFP+ tdTom+ c-Kit+ Sca-1+ CD16/32+ CD34+) from mice transplanted with post-transformed Scr or miR-99 KD MLL-AF9 bone marrow and performed RNA-sequencing, demonstrating miR-99 KD results in induction differentiation and enrichment for a normal GMP gene expression signature
2017-07-27 | GSE101957 | GEO
Project description:We FACS purified GFP+ cells 2 days post-transduction of LSK (Lin-Negative c-Kit+ Sca1+) cells with miR-99 KD and Scr lentiviral vectors and performed RNA-sequencing; this allowed us to identify potential miR-99 target genes for inclusion in the shRNA library
2017-07-27 | GSE101902 | GEO
Project description:RNA-sequencing of Scr or miR-99 KD L-GMPs from MLL-F9 AML secondary recipients
| PRJNA396027 | ENA
Project description:The ketogenic diet has been successful in promoting weight loss among patients that have struggled with weight gain. This is due to the cellular switch in metabolism that utilizes liver-derived ketone bodies for the primary energy source rather than glucose. Fatty acid transport protein 2 (FATP2) is highly expressed in liver, small intestine, and kidney where it functions in both the transport of exogenous long chain fatty acids (LCFA) and in the activation to CoA thioesters of very long chain fatty acids (VLCFA). We have completed a multi-omic study of FATP2-null (Fatp2-/-) mice maintained on a ketogenic diet (KD) or paired control diet (CD), with and without a 24-hour fast (KD-fasted and CD-fasted) to address the impact of deleting FATP2 under high-stress conditions. Control (wt/wt) and Fatp2-/- mice were maintained on their respective diets for 4-weeks. Afterwards, half the population was sacrificed while the remaining were fasted for 24-hours prior to sacrifice. We then performed paired-end RNA-sequencing on the whole liver tissue to investigate differential gene expression. The differentially expressed genes mapped to ontologies such as the metabolism of amino acids and derivatives, fatty acid metabolism, protein localization, and components of the immune system’s complement cascade, and were supported by the proteome and histological staining.
2020-06-10 | GSE152110 | GEO
Project description:RNA-sequencing of GFP+ cells 2 days post-transduction of LSK cells with Scr or miR-99 KD lentiviral vectors
| PRJNA396026 | ENA
Project description:MiR-142 is dynamically expressed and plays a regulatory role in hematopoiesis. Based on the simple observation that miR-142 levels are significantly lower in CD34+CD38- cells from blast crisis (BC) chronic myeloid leukemia (CML). CML patients compared with chronic phase (CP) CML patients (p=0.002), we hypothesized that miR-142 deficit plays a role in BC transformation. To test this hypothesis, we generated a miR-142 KO BCR-ABL (i.e., miR-142−/−BCR-ABL) mouse by crossing a miR-142−/− mouse with a miR-142+/+BCR-ABL mouse. While the miR-142+/+BCR-ABL mice developed and died of CP CML, the miR-142−/−BCR-ABL mice developed a BC-like phenotype in the absence of any other acquired gene mutations and died significantly sooner than miR-142+/+BCR-ABL CP controls (p=0.001). Leukemic stem cell (LSC)-enriched Lineage-Sca-1+c-Kit+ cells (LSKs) from diseased miR-142−/−BCR-ABL mice transplanted into congenic recipients, recapitulated the BC features thereby suggesting stable transformation of CP-LSCs into BC-LSCs in the miR-142 KO CML mouse. Single cell (sc) RNA-seq profiling showed that miR-142 deficit changed the cellular landscape of the miR-142−/−BCR-ABL LSKs compared with miR-142+/+BCR-ABL LSKs with expansion of myeloid-primed and loss of lymphoid-primed factions. Bulk RNA-seq analyses along with unbiased metabolomic profiling and functional metabolic assays demonstrated enhanced fatty acid β-oxidation (FAO) and oxidative phosphorylation (OxPhos) in miR-142−/−BCR-ABL LSKs vs miR-142+/+BCR-ABL LSKs. MiR-142 deficit enhanced FAO in miR-142−/−BCR-ABL LSKs by increasing the expression of CPT1A and CPT1B, that controls the cytosol-to-mitochondrial acyl-carnitine transport, a critical step in FAO. MiR-142 deficit also enhanced OxPhos in miR-142−/−BCR-ABL LSKs by increasing mitochondrial fusion and activity. As the homeostasis and activity of LSCs depend on higher levels of these oxidative metabolism processes, we then postulate that miR-142 deficit is a potentially druggable target for BC-LSCs. To this end, we developed a novel CpG-miR-142 mimic oligonucleotide (ODN; i.e., CpG-M-miR-142) that corrected the miR-142 deficit and alone or in combination with a tyrosine kinase inhibitor (TKI) significantly reduced LSC burden and prolonged survival of miR-142−/−BCR-ABL mice. The results from murine models were validated in BC CD34+CD38- primary blasts and patient-derived xenografts (PDXs). In conclusion, an acquired miR-142 deficit sufficed in transforming CP-LSCs into BC-LSCs, via enhancement of bioenergetic oxidative metabolism in absence of any additional gene mutations, and likely represent a novel therapeutic target in BC CML.
2023-01-13 | ST002446 | MetabolomicsWorkbench
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:RNA sequencing of Mus musculus thymic lymphomas
2019-06-06 | GSE85894 | GEO
Project description: Not available
| S-EPMC395764 | biostudies-literature