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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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CodeLink™ Mouse Whole Genome Bioarray data from hematopoietic stem cells (HSCs) of miR-125a (+/+) wild-type mice and miR-125a (+/-) heterozygous mice with myeloproliferative disorder

ABSTRACT: miR-125a knockout mice develop myeloproliferave disorder (MPD). To investigate the molecular mechanisms of MPD induced by the loss of miR-125a, gene expression profiling on hematopoietic stem cells of miR-125a (+/+) and (+/-) MPD mice was performed using CodeLink Whole Genome DNA array analysis. Codelink Mouse Whole Genome Bioarrays were performed according to the manufacturer’s instruction on total RNA extracted from hematopoietic stem cells of miR-125a (+/+) wild-type mice and miR-125a (+/-) heterozygous mice with MPD. One replicate per array.

ORGANISM(S): Mus musculus

SUBMITTER: Naoya Tatsumi

PROVIDER: E-GEOD-65648 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Deficiency in WT1-targeting microRNA-125a leads to myeloid malignancies and urogenital abnormalities.

Tatsumi N N Hojo N N Yamada O O Ogawa M M Katsura Y Y Kawata S S Morii E E Sakamoto H H Inaba R R Tsuda A A Fukuda I I Moriguchi N N Hasuwa H H Okabe M M Fujiki F F Nishida S S Nakajima H H Tsuboi A A Oka Y Y Hosen N N Sugiyama H H Oji Y Y

Oncogene 20150511 8

The Wilms' tumor gene WT1 is overexpressed in leukemia and solid tumors and has an oncogenic role in leukemogenesis and tumorigenesis. However, precise regulatory mechanisms of WT1 overexpression remain undetermined. In the present study, microRNA-125a (miR-125a) was identified as a miRNA that suppressed WT1 expression via binding to the WT1-3'UTR. MiR-125a knockout mice overexpressed WT1, developed myeloproliferative disorder (MPD) characterized by expansion of myeloid cells in bone marrow (BM) ...[more]

PMID: 25961914

Similar Datasets

CodeLink Mouse Whole Genome Bioarray data from hematopoietic stem cells (HSCs) of miR-125a (+/+) wild-type and miR-125a knockout mice with myeloproliferative disorder (MPD)

Project description:miR-125a knockout mice develop myeloproliferative disorder (MPD). To investigate the molecular mechanisms of MPD induced by the loss of miR-125a, gene expression profiling on hematopoietic stem cells of miR-125a (+/+), (+/-) MPD, and (-/-) MPD mice was performed by using CodeLinkTM Whole Genome DNA array analysis. CodeLink Mouse Whole Genome Bioarrays were performed according to the manufacturerâs instruction on total RNA extracted from hematopoietic stem cells of miR-125a (+/+) wild-type mouse, miR-125a (+/-) heterozygous mouse with MPD, and miR-125a (-/-) homozygous mouse with MPD. One replicate per array.

2015-12-31 | E-GEOD-69621 | biostudies-arrayexpress

CodeLink™ Mouse Whole Genome Bioarray data from hematopoietic stem cells (HSCs) of miR-125a (+/+) wild-type mice and miR-125a (+/-) heterozygous mice with myeloproliferative disorder

Project description:miR-125a knockout mice develop myeloproliferave disorder (MPD). To investigate the molecular mechanisms of MPD induced by the loss of miR-125a, gene expression profiling on hematopoietic stem cells of miR-125a (+/+) and (+/-) MPD mice was performed using CodeLink Whole Genome DNA array analysis.

2015-06-30 | GSE65648 | GEO

Expression profiles of HSPCs overexpressing microRNA cluster 99b/let-7e/125a, miR-125a, miR-155 and empty vector.

Project description:Hematopoietic stem/progenitor cell (HSPC) traits differ between genetically distinct mouse strains. For example, DBA/2 mice have a higher HSPC frequency compared to C57BL/6 mice. We performed a genetic screen for microRNAs that are differentially expressed between LSK, LS−K+, erythroid and myeloid cells isolated from C57BL/6 and DBA/2 mice. This analysis identified 131 microRNAs that were differentially expressed between cell types and 15 that were differentially expressed between mouse strains. Of special interest was an evolutionary conserved miR-cluster located on chromosome 17 consisting of miR-99b, let-7e and miR-125a. All cluster members were most highly expressed in LSKs and down-regulated upon differentiation. In addition, these microRNAs were higher expressed in DBA/2 cells compared to C57BL/6 cells, and thus correlated with HSPC frequency. To functionally characterize these microRNAs, we overexpressed the entire miR-cluster 99b/let-7e/125a and miR-125a alone in BM cells from C57BL/6 mice. Overexpression of the miR-cluster or miR-125a dramatically increased day-35 CAFC activity and caused severe hematopoietic phenotypes upon transplantation. We showed that a single member of the miR-cluster, namely miR-125a, is responsible for the majority of the observed miR-cluster overexpression effects. Finally, we performed genome-wide gene expression arrays and identified candidate target genes through which miR-125a may modulate HSPC fate. These data consist of total mRNA obtained from 7-day cultured post 5-FU BM cells positively transduced with empty vector, miR-cluster 99b/let-7e/125a, miR-125a or miR-155 retroviral vector. Dataset (A) and dataset (B) were analyzed individualy. In each dataset, all samples were analyzed in independent biological triplicates.

2011-12-15 | E-GEOD-33689 | biostudies-arrayexpress

CodeLink Mouse Whole Genome Bioarray data from hematopoietic stem cells (HSCs) of miR-125a (+/+) wild-type and miR-125a knockout mice with myeloproliferative disorder (MPD)

2015-12-31 | GSE69621 | GEO

Genetic Screen Identifies MicroRNA Cluster 99b/let-7e/125a as a Regulator of Primitive Hematopoietic Cells

Project description:This SuperSeries is composed of the following subset Series: GSE33689: Expression profiles of HSPCs overexpressing microRNA cluster 99b/let-7e/125a, miR-125a, miR-155 and empty vector. GSE33690: MicroRNA profiles of four developmentally related hematopoietic cell types isolated from the BM of B6 and D2 mice. Refer to individual Series

2011-12-15 | E-GEOD-33691 | biostudies-arrayexpress

miR-125a Confers Multi-Lineage Long-Term Repopulating Stem Cell Activity to Murine and Human Hematopoietic Progenitors

Project description:Umbilical cord blood (CB) is a non-invasive, convenient and broadly used source of hematopoietic stem cells (HSCs) for allogeneic stem cell transplantation. However, limiting numbers of HSCs remain a major constraint for its clinical application. One feasible option would be to expand HSCs to improve therapeutic outcome, however available protocols and the molecular mechanisms governing the self-renewal of HSC are unclear. Here we show that ectopic expression of a single miRNA, miR-125a, in purified murine and human multipotent progenitors (MPP) resulted in increased self-renewal and robust long-term multi-lineage repopulation in transplanted recipient mice. Using quantitative proteomics and Western blot analysis, we identified a restricted set of miR-125a targets which revealed the involvement of the MAP kinase signaling pathway in conferring long-term repopulating capacity to multipotent progenitors in human and mice. Our findings offer the innovative potential to use MPP with enhanced self-renewal activity to augment limited sources of HSC to improve clinical protocols.

2017-01-11 | PXD003931 | Pride

RIP-chip

Project description:Mutant genotype miR-125a precurrsor was found in recurrent pregnancy loss patients. We use RIP-chip assay to detect the disturbed mRNA profiling in RISC of HEK293T cells after wildtype or mutant genotype miR-125a expression vector transfection.

2015-12-01 | E-MTAB-2394 | biostudies-arrayexpress

Whole Transcriptome Microarray of Primary Human Monocytes Transfected With MiR-125a

Project description:Conducted to obtain information of the regulatory impact of miR-125a in human primary monocytes.

2022-10-28 | E-MTAB-11824 | biostudies-arrayexpress

Expression profiles of HSPCs overexpressing microRNA cluster 99b/let-7e/125a, miR-125a, miR-155 and empty vector.

2011-12-15 | GSE33689 | GEO

Expression data on Treg cells isolated from wildtype mice and miR-125a deficient mice

Project description:We found miR-125a was a key regulator that stabilizes the commitment and immunoregulatory capacity of Treg cells.To gain insights into the general functional features of miR-125a-deficient Treg cells, we performed a genome-wide gene array analysis on Treg population isolated from the spleens of 6 to 8-week-old miR-125a-deficient and WT mice

2015-05-08 | GSE66608 | GEO

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