Murine hamatopoietic stem cell (HSC): wild type and Skp2 knockout
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE23064 | GEO | 2015/04/02
SECONDARY ACCESSION(S): PRJNA129889
REPOSITORIES: GEO
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Project description:Transcriptional profiling of mouse HSC comparing wild type (WT) and Skp2 knockout Collected bone marrow (BM) cells from WT and Skp2 knockout mice, stained with HSC surface markers for FACS. Collected HSC and extracted total RNA then sent out for microarray analysis.
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Project description:Investigation of whole genome gene expression level changes in WASH knockout LT-HSCs, compared to the WASH WT strain. To find the reason that causes LT-HSC abnormal.
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Project description:rs04-04_skp2_cul4 - comparison_col0vsskp2 - Antisense and mutants of the SKP2 and CUL4 genes are compared to the Wt in order to identify the genes controlled by those SCF proteins. - Comparison Col0 versus skp2
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Project description:rs04-04_skp2_cul4 - comparison_col0vsskp2 - Antisense and mutants of the SKP2 and CUL4 genes are compared to the Wt in order to identify the genes controlled by those SCF proteins. - Comparison Col0 versus skp2 2 dye-swap - wt vs mutant comparison
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Project description:The SKP2 was knockdown by siRNAs in MDA-MB231 cells and RNA-Seq was used to define the transcriptome response to SKP2
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Project description:Tight regulation of hematopoietic stem cell (HSC) homeostasis is essential for life-long hematopoiesis, for preventing blood cancers and for averting bone marrow failure. The underlying mechanisms are incompletely understood. Here, we identify production of inositol-tetrakisphosphate (IP4) by inositoltrisphosphate 3-kinase B (ItpkB) as essential for HSC quiescence and function. Young ItpkB-/- mice accumulated phenotypic HSC and showed extramedullary hematopoiesis. ItpkB-/- HSC were less quiescent and proliferated more than wildtype controls. They downregulated quiescence and stemness associated mRNAs, but upregulated activation, oxidative metabolism, protein synthesis and lineage associated transcripts. Although they showed no significant homing defects, ItpkB-/- HSC had a severely reduced competitive long-term repopulating potential. Aging ItpkB-/- mice lost hematopoietic stem and progenitor cells and died with severe anemia. Wildtype HSC normally repopulated ItpkB-/- hosts, incidating a HSC-intrinsic ItpkB requirement. ItpkB-/- HSC had reduced cobblestone-area forming cell activity in vitro and showed increased stem-cell-factor activation of the phosphoinositide 3-kinase (PI3K) effector Akt, reversed by exogenous provision of the known PI3K/Akt antagonist IP4. They also showed transcriptome changes consistent with hyperactive Akt/mTOR signaling. Thus, we propose that ItpkB ensures HSC quiescence by limiting cytokine-induced PI3K signaling in HSC. For each of 3 replicate ItpkB-/- or wt samples, we enriched Lin- cells from BM of 4 pooled age-matched mice with Rapidspheres (Stemcell Technologies), FACS-sorted ?10,000 LSK CD34-CD150+CD48-Flk2- LT-HSC into lysis buffer and prepared RNA with RNeasy Micro kits (Quiagen). RNA sequencing was done using an Illumina HISeq Analyzer 2000, Casava v1.8.2 genome analyzer pipeline, TopHat v1.4.1/Bowtie2 genome alignment and Partek v6.6 mRNA annotation software. Statistical analyses were done with edgeR (Bioconductor package), excluding genes with false discovery rates >0.15, fold-change magnitudes ?1.4 and log2(counts per million) ?4 to avoid undefined values and the poorly defined log fold-changes for low counts close to 0. Unsupervised clustering of 441 significantly changed genes was done with dChip using rank correlation and a centroid linkage method. Scatter plots were generated in Spotfire. GSEA was performed with gene set permutation, using gene sets from MSigDB (www.broadinstitute.org/gsea/msigdb/index.jsp) or manually curated from, excluding genes without HUGO approved symbols
2015-03-31 | E-GEOD-56613 | biostudies-arrayexpress
Project description:This project aims to identify the SKP2 interaction proteins.
2023-01-05 | PXD039225 | Pride
Project description:Tight regulation of hematopoietic stem cell (HSC) homeostasis is essential for life-long hematopoiesis, for preventing blood cancers and for averting bone marrow failure. The underlying mechanisms are incompletely understood. Here, we identify production of inositol-tetrakisphosphate (IP4) by inositoltrisphosphate 3-kinase B (ItpkB) as essential for HSC quiescence and function. Young ItpkB-/- mice accumulated phenotypic HSC and showed extramedullary hematopoiesis. ItpkB-/- HSC were less quiescent and proliferated more than wildtype controls. They downregulated quiescence and stemness associated mRNAs, but upregulated activation, oxidative metabolism, protein synthesis and lineage associated transcripts. Although they showed no significant homing defects, ItpkB-/- HSC had a severely reduced competitive long-term repopulating potential. Aging ItpkB-/- mice lost hematopoietic stem and progenitor cells and died with severe anemia. Wildtype HSC normally repopulated ItpkB-/- hosts, incidating a HSC-intrinsic ItpkB requirement. ItpkB-/- HSC had reduced cobblestone-area forming cell activity in vitro and showed increased stem-cell-factor activation of the phosphoinositide 3-kinase (PI3K) effector Akt, reversed by exogenous provision of the known PI3K/Akt antagonist IP4. They also showed transcriptome changes consistent with hyperactive Akt/mTOR signaling. Thus, we propose that ItpkB ensures HSC quiescence by limiting cytokine-induced PI3K signaling in HSC.
2015-03-31 | GSE56613 | GEO