Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1142940 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30082936_1.fastq.gz | Fastqsanger.gz | |||
| SRR30082936_2.fastq.gz | Fastqsanger.gz | |||
| SRR30082937_1.fastq.gz | Fastqsanger.gz | |||
| SRR30082937_2.fastq.gz | Fastqsanger.gz | |||
| SRR30082938_1.fastq.gz | Fastqsanger.gz |
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Project description:Oncogenic NRAS mutations are frequently identified in human myeloid leukemias. In mice, expression of endogenous oncogenic Nras (NrasG12D/+) in hematopoietic cells leads to expansion of myeloid progenitors, increased long-term reconstitution of bone marrow cells, and a chronic myeloproliferative neoplasm (MPN). However, acute expression of NrasG12D/+ in a pure C57BL/6 background does not induce hyperactivated GM-CSF signaling or increased proliferation in myeloid progenitors. It is thus unclear how NrasG12D/+ signaling promotes leukemogenesis. Here we show that hematopoietic stem cells (HSCs) expressing NrasG12D/+ serve as MPN initiating cells. They undergo moderate hyperproliferation with increased self-renewal. The aberrant NrasG12D/+ HSC function is associated with hyperactivation of ERK1/2 in HSCs. Conversely, downregulation of MEK/ERK by pharmacological and genetic approaches attenuates the cycling of NrasG12D/+ HSCs and prevents the expansion of NrasG12D/+ HSCs and myeloid progenitors. Our data delineate critical mechanisms of oncogenic Nras signaling in HSC function and leukemogenesis. three NrasG12D/G12D HSCs samples, three NrasG12D/+ HSCs samples, two Nras+/+ HSCs control samples.
2013-05-29 | E-GEOD-46948 | biostudies-arrayexpress
Project description:Global Expression profiling of non-committed lineage negative hematopoietic progenitors was performed on bone marrow aspirates from wild type control and mutant mice. Lineage negative (lin-) bone marrow progenitors were isolated from wild type or mutant Npm1cA/+, NrasG12D, Npm1cA/+;NrasG12D using MACS Microbeads (Miltenyl Biotec).
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Project description:Global Expression profiling of mutant mouse multipotent progenitors was performed. In order to mitigate the impact of the studied driver mutations on cell surface phenotypes, we performed transcriptome analysis on a homogeneous population of purified lineage negative, Sca-1/Kit positive multipotent progenitor cells (MPPs, cell surface profile: Lin-/CD34+/Flt3+/CD48+/CD150-). Aprroximately 1000 multipotent progenitors were isolated from wild type or mutant Npm1cA/+, NrasG12D, Npm1cA/+;NrasG12D, Flt3ITD/+ and Npm1cA/+;Flt3ITD/+ murine bone marrow cells. Total RNA extracted and mRNA amplified using
2017-07-30 | E-MTAB-5358 | biostudies-arrayexpress
Project description:Global Gene Expression of hematopoietic stem cells expressing endogenous NrasG12D/G12D, NrasG12D/+, Nras+/+
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Project description:Oncogenic NRAS mutations are frequently identified in human myeloid leukemias. In mice, expression of endogenous oncogenic Nras (NrasG12D/+) in hematopoietic cells leads to expansion of myeloid progenitors, increased long-term reconstitution of bone marrow cells, and a chronic myeloproliferative neoplasm (MPN). However, acute expression of NrasG12D/+ in a pure C57BL/6 background does not induce hyperactivated GM-CSF signaling or increased proliferation in myeloid progenitors. It is thus unclear how NrasG12D/+ signaling promotes leukemogenesis. Here we show that hematopoietic stem cells (HSCs) expressing NrasG12D/+ serve as MPN initiating cells. They undergo moderate hyperproliferation with increased self-renewal. The aberrant NrasG12D/+ HSC function is associated with hyperactivation of ERK1/2 in HSCs. Conversely, downregulation of MEK/ERK by pharmacological and genetic approaches attenuates the cycling of NrasG12D/+ HSCs and prevents the expansion of NrasG12D/+ HSCs and myeloid progenitors. Our data delineate critical mechanisms of oncogenic Nras signaling in HSC function and leukemogenesis.
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Project description:SYNCRIP depletion results in HSCs losing their self renewal abilities. Single cell sequencing was conducted in SYNCRIP WT and KO bone marrow LK (lineage -, cKit+) cells to decipher the effect of Syncrip deletion on cellular identities along the hematopoietic hierarchy, and to gain an in-depth assessment of the transcriptomic changes in different cell types upon SYNCRIP loss.
2023-03-01 | GSE202421 | GEO
Project description:Purpose: Multi-omics characterization of the consequences of deleting the SWI/SNF subunit Dpf2 in the transcriptome (RNAseq), accessibility of the genome (ATACseq) and binding of SWI/SNF subunits (CUT&RUN) in hematopoietic stem/progenitor cells, resting and polarized bone-marrow derived macrophages and resting and activated CD4+ T cells obtained from Dpf2f/f and Dpf2D/D mice. Methods: Lin- cKit+ cells were sorted from bone marrow of 28-days old Dpf2f/f and Dpf2D/D mice. Bone-marrow derived macrophages were obtained from 28-days old Dpf2f/f and Dpf2D/D mice and polarized with IFNg and LPS, or IL-4 for 24hours. CD4+ splenic T helper cells were obtained from 28-days old Dpf2f/f and Dpf2D/D mice and activated by treatment with PMA and Ionomycin. Methods: For ATACseq, Lin- cKit+ cells were processed following the OMIM-ATAC-seq protocol (Corces MR et al., Nature Methods 2017). Libraries were sequenced on a NextSeq (75bp, paired end reads) to obtain more than 40 million reads/sample. Results: For ATACseq, we obtained more than 40 million reads per sample. ATAC-Seq chromatin accessible regions were determined using ENCODE pipeline standards (https://github.com/ENCODE-DCC/atac-seq-pipeline; git commit 2b693ab). Conclusions: The absence of Dpf2 in LK cells results in downregulation of anti-oxidative and anti-inflammatory gene expression programs in bone marrow LK cells, bone-marrow derived macrophages and CD4+ T cells.
2023-06-06 | GSE192776 | GEO
Project description:Purpose: Multi-omics characterization of the consequences of deleting the SWI/SNF subunit Dpf2 in the transcriptome (RNAseq), accessibility of the genome (ATACseq) and binding of SWI/SNF subunits (CUT&RUN) in hematopoietic stem/progenitor cells, resting and polarized bone-marrow derived macrophages and resting and activated CD4+ T cells obtained from Dpf2f/f and Dpf2D/D mice. Methods: Lin- cKit+ cells were sorted from bone marrow of 28-days old Dpf2f/f and Dpf2D/D mice. Bone-marrow derived macrophages were obtained from 28-days old Dpf2f/f and Dpf2D/D mice and polarized with IFNg and LPS, or IL-4 for 24hours. CD4+ splenic T helper cells were obtained from 28-days old Dpf2f/f and Dpf2D/D mice and activated by treatment with PMA and Ionomycin. Methods: For CUT&RUN experiments, Lin- cKit+ cells were obtained from bone marrow of 28-days old Dpf2f/f and Dpf2D/D mice. Cells were crosslinked (1 min, 1% formaldehyde), quenched (125mM Glycine) and washed in buffers following the CUTANA ChIC/CUT&RUN kit according to the manufacturer’s CUT&RUN cross-linking protocol (EpiCypher, 14-1048). Results: For CUT&RUN experiments, 5 million (paired-end, 75bp) reads were obtained per sample. Pair-end fastq files were processed with the ENCODE Transcription Factor and Histone ChIP-Seq processing pipeline (https://github.com/ENCODE-DCC/chip-seq-pipeline2). Reads were trimmed using cutadapt v2.5. and aligned to the mm10 genome using Bowtie2 v2.3.4.3. SAMtools v1.9 were used to convert the output file to BAM format. Duplicates were removed using Picard Tools v2.20.7. Peak calling was performed with MACS2 v2.2.4. Conclusions: The absence of Dpf2 in LK cells results in downregulation of anti-oxidative and anti-inflammatory gene expression programs in bone marrow LK cells, bone-marrow derived macrophages and CD4+ T cells.
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Project description:Investigation of the transcriptional profile of AML in response to DHODH inhibition by AG636. I1DN model was generated by co-transduction of foetal liver derived HSPCs with constructs encoding IDH1R132H, DNMT3AR882H and NrasG12D. Cells were transplanted into Ptprca recipients. Mice bearing I1DN tumors were treated with AG636 for one day. Leukemic stem cells (cKit high; CD11b low) from bone marrow and spleen were isolated and RNA sequencing performed.
2022-04-26 | GSE181663 | GEO