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accession-icon SRP053096
Identification of the miRNA targetome in hippocampal neurons using RIP-seq
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

We established a neuron-specific Argonaute2:GFP-RNA immunoprecipitation followed by high throughput sequencing (AGO2-RIP-seq) to analyse the regulatory role of miRNAs in mouse hippocampal neurons. Using this technique, we identified more than two thousand miRNA target genes in hippocampal neurons, regulating essential neuronal features such as axon guidance and transcription. Furthermore, we found that stable inhibition of the highly expressed miR-124 in hippocampal neurons led to significant changes in the AGO2 binding of target mRNAs, resulting in subsequent upregulation of numerous miRNA target genes. Our data suggest that target redundancies are common among microRNA families. Together, these findings greatly enhance our understanding of the mechanisms and dynamics through which miRNAs regulate their target genes in neurons. Overall design: Analysis of the miRNA targetome in hippocampal neurons after inhibition of 2 different miRNAs. AAV5 injections into the hippocampus of adult C57BL/6 mice producing either of the following under a synapsin promoter: GFP only (Samples beginning with ''GFP124…'' or ''GFP125…''), GFP-miR124sp (Samples beginning with ''miR124…''), GFP-miR125sp (Samples beginning with ''miR125…''), GFP-AGO2-miR292sponge (samples ending with ''…292''), GFP-AGO2-miR124sponge (samples ending with ''…124''), GFP-AGO2-miR125sponge (samples ending with ''…125''). All other samples were sham-injected.

Publication Title

Identification of the miRNA targetome in hippocampal neurons using RIP-seq.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE15623
Expression data from mNSc after 48 hour of treatment with CD95L-T4
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

In neural stem cells, stimulation of the death receptor CD95 does not trigger apoptosis but resulted in increased stem cell survival and neuronal specification via activation of the Src /PI3K /AKT/mTOR signalling pathway. To further characterize CD95-dependent neural stem cell survival and differentiation we used conventional gene expression profiling combined with translation state array analysis. Mouse neural stem cells grown in neurosphere cultures were stimulated with a trimerized CD95L construct (CD95L-T4) and total as well as polysomal bound RNA was isolated 48 hours after stimulation and analysed by microarrays. CD95L-T4 treatment induced a global increase in ribosome-bound mRNA and protein translation as well as changes on genes involved in neurogenesis, protein synthesis and transcription factors.

Publication Title

The death receptor CD95 activates adult neural stem cells for working memory formation and brain repair.

Sample Metadata Fields

Sex, Treatment

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accession-icon GSE42257
Murine bone marrow gene expression profiling
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Mice have been treated with NOX-A12. Whole BM cells have been harvested, RNA isolated, and gene expression profiling was performed on cDNA using Mouse Genome 430 2.0 array. Untreated mice have been used as control.

Publication Title

SDF-1 inhibition targets the bone marrow niche for cancer therapy.

Sample Metadata Fields

Treatment

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accession-icon GSE16655
Developmental stage-specific interplay between GATA1 and IGF signaling in fetal hematopoiesis and leukemogenesis
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 43 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Developmental stage-specific interplay of GATA1 and IGF signaling in fetal megakaryopoiesis and leukemogenesis.

Sample Metadata Fields

Specimen part, Disease, Cell line, Treatment

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accession-icon GSE16677
Gene expression profiling of Down Syndrome (DS)-AMKL and non-DS AMKL samples
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The goal of this study is to define a gene expression signature unique to DS-AMKL (acute megakaryoblastic leukemia or FAB M7 leukemia).

Publication Title

Developmental stage-specific interplay of GATA1 and IGF signaling in fetal megakaryopoiesis and leukemogenesis.

Sample Metadata Fields

Specimen part, Disease, Cell line

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accession-icon SRP090905
p53 activity results in DNA replication fork processivity
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

p53 induces cell death upon DNA damage, but this may not confer all of its tumor suppressor activity. We report that p53 activation enhances the processivity of DNA replication, as monitored by multi-label fiber assays, whereas removal of p53 reduces fork progression. This was observed in tumor-derived U2OS cells, but also in murine embryonic fibroblasts with heterozygous or homozygous p53 deletion, and in freshly isolated thymocytes from mice with differential p53 status. Mdm2, a p53-inducible gene product, similarly supported DNA replication even in p53-deficient cells, suggesting that sustained Mdm2-expression is at least one of the mechanisms allowing p53 to prevent replicative stress. Thus, p53 helps to protect the genome during S phase, by preventing the occurrence of stalled or collapsed replication forks. These results expand p53’s tumor-suppressive functions, adding to the ex-post model (elimination of damaged cells) an ex-ante activity, i.e. the prevention of DNA damage during replication. Overall design: Expression profiling by high throughput sequencing

Publication Title

p53 Activity Results in DNA Replication Fork Processivity.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE16676
Rescue of murine Gata1s mutant M7 leukemic cells by full-length Gata1
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In this project, we studied a mouse model of human Down Syndrome (DS) megakaryocytic leukemia involving mutations in the GATA1 transcription factor (called GATA1s mutation). The model was generated through retroviral insertional mutagenesis in Gata1s mutant fetal liver progenitors. In this study, we analyzed the dependency of these leukemic cells on the Gata1s mutant protein.

Publication Title

Developmental stage-specific interplay of GATA1 and IGF signaling in fetal megakaryopoiesis and leukemogenesis.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE16679
Plag1 overexpression cooperates with Evi1 overexpression and Gata1s mutation in leading to M7 leukemia
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The goal of this study is to develop a Plag1 signature and determine how its overexpression contributes to leukemogenesis.

Publication Title

Developmental stage-specific interplay of GATA1 and IGF signaling in fetal megakaryopoiesis and leukemogenesis.

Sample Metadata Fields

Cell line

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accession-icon GSE16684
Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors depends on IGF signaling
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The goal of this study is to derive a mouse model of human Down Syndrome (DS) megakaryocytic leukemia involving mutations in the hematopoietic transcription factor, GATA1 (called GATA1s mutation). We achieved this through transduction of Gata1s mutant fetal progenitors by MSCV-based retrovirus expressing a GFP marker, followed by in vitro selection (for immortalized cell lines), and then in vivo selection (for transformed cell lines) through transplantation.

Publication Title

Developmental stage-specific interplay of GATA1 and IGF signaling in fetal megakaryopoiesis and leukemogenesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE16682
Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The goal of this study is to derive a mouse model of human Down Syndrome (DS) megakaryocytic leukemia involving mutations in the hematopoietic transcription factor, GATA1 (called GATA1s mutation). We achieved this through transduction of Gata1s mutant fetal progenitors by MSCV-based retrovirus expressing a GFP marker, followed by in vitro selection (for immortalized cell lines), and then in vivo selection (for transformed cell lines) through transplantation.

Publication Title

Developmental stage-specific interplay of GATA1 and IGF signaling in fetal megakaryopoiesis and leukemogenesis.

Sample Metadata Fields

Specimen part

View Samples
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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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