publication_authors:Vasar E Results

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Organism

Mus musculus (205)

Homo sapiens (25)

Technology

Microarray (205)

Platform

Affymetrix Mouse Genome 430 2.0 Array (mouse4302) (205)

Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2) (25)

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GSE15293

Gene expression profiling of temporal lobes of wfs1 deficient mice

Mus musculus
34 Downloadable Samples

Description

Aim of present study was to describe the changes induced deletion of the Wfs1 gene in the temporal lobe of mice. Mutant mice were backcrossed to two different genomic backgrounds in order to exclude confounding foreign genomic background influence. Samples from temporal lobes were analyzed by using Affymetrix Genechips, expression profiles were functionally annotated by using GSEA and Ingenuity Pathway Analysis. We found that Wfs1 mutant mice are significantly smaller (20.9 1.6 g) than their wild-type counterparts (31.0 0.6g, p < 0.0001). Interestingly, genechip analysis identified growth hormone transcripts up-regulated and functional analysis found appropriate pathways activated. Moreover, we found significant increase in the level of IGF1 in the plasma of wfs1 mutant mice. Taken together, wfs1 mutation induces growth retardation whereas the growth hormone pathway is activated. Further studies are needed to describe biochemical and molecular details of the growth hormone axis in the wfs1 mutant mice.

Publication Title

Wfs1 gene deletion causes growth retardation in mice and interferes with the growth hormone pathway.

Alternate Accession IDs

E-GEOD-15293

Sample Metadata Fields

Specimen part

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GSE27322

de novo DNA Methylation Balances Hematopoietic Stem Cell Self-Renewal and Differentiation

Mus musculus
6 Downloadable Samples

Description

Cytosine methylation is an epigenetic mark usually associated with gene repression. Despite a requirement for de novo DNA methylation for differentiation of embryonic stem cells, its role in somatic stem cells is unknown. Using conditional ablation, we show that loss of either, or both, Dnmt3a or Dnmt3b, progressively impedes hematopoietic stem cell (HSC) differentiation during serial in vivo passage. Concomitantly, HSC self-renewal is immensely augmented in absence of either Dnmt3, particularly Dnmt3a. Dnmt3-KO HSCs show upregulation of HSC multipotency genes and downregulation of early differentiation factors, and the differentiated progeny of Dnmt3-KO HSCs exhibit hypomethylation and incomplete repression of HSC-specific genes. HSCs lacking Dnmt3a manifest hyper-methylation of CpG islands and hypo-methylation of genes which are highly correlated with human hematologic malignancies. These data establish that aberrant DNA methylation has direct pathologic consequences for somatic stem cell development, leading to inefficient differentiation and maintenance of a self-renewal program.

Publication Title

Dnmt3a is essential for hematopoietic stem cell differentiation.

Alternate Accession IDs

E-GEOD-27322

Sample Metadata Fields

Sex, Specimen part

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GSE27816

Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation

Mus musculus
14 Downloadable Samples

Description

Recurrent somatic mutations in TET2 and in other genes that regulate the epigenetic state have been identified in patients with myeloid malignancies and in other cancers. However, the in vivo effects of Tet2 loss have not been delineated. We report here that Tet2 loss leads to increased stem-cell self-renewal and to progressive stem cell expansion. Consistent with human mutational data, Tet2 loss leads to myeloproliferation in vivo, notable for splenomegaly and monocytic proliferation. In addition, haploinsufficiency for Tet2 confers increased self-renewal and myeloproliferation, suggesting that the monoallelic TET2 mutations found in most TET2-mutant leukemia patients contribute to myeloid transformation. This work demonstrates that absent or reduced Tet2 function leads to enhanced stem cell function in vivo and to myeloid transformation.

Publication Title

Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation.

Alternate Accession IDs

E-GEOD-27816

Sample Metadata Fields

Specimen part

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GSE17886

Gene expression data of BBB and BCB two-cell embryos

Mus musculus
14 Downloadable Samples

Description

We constructed one-cell stage embryos by maternal pronuclear (mPN) transfer having B6 ooplasm, B6 paternal PN (pPN), and either B6 or C3H mPN (BBB and BCB, respectively). We collected embryos of each type that were either treated (BBB+a, BCB+a) or untreated with -amanitin (BBB, BCB) at the two-cell stage for microarray analysis.

Publication Title

Early transcription from the maternal genome controlling blastomere integrity in mouse two-cell-stage embryos.

Alternate Accession IDs

E-GEOD-17886

Sample Metadata Fields

Treatment

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GSE54206

Growth factor independence 1b (Gfi1b) is required for erythroid cell maturation and regulates embryonic globin expression

Mus musculus
6 Downloadable Samples

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Growth factor independence 1b (gfi1b) is important for the maturation of erythroid cells and the regulation of embryonic globin expression.

Alternate Accession IDs

E-GEOD-54206

Sample Metadata Fields

Specimen part

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GSE26621

Metastasis and Survival of Breast Cancer Stem Cells Mediated by Cytoskeleton Remodeling and PI3K/mTOR Signaling transcription factors

Mus musculus
6 Downloadable Samples

Description

Cancer metastasis is a fetal problem that claims life of over 90% of cancer patients. It is hypothesized that cancer stem cells (CSCs) mediate cancer metastasis and such cells are often resistant to chemotherapy. Studying BRCA1 associated cancers, we found that CSCs form fillopodia and protrusions enriching for active forms of ezrin/radixin/moesin proteins and they have a much higher potential to metastasize than non-CSCs. Microarray analysis indicated that many pathways related to cell adhesion, extracellular matrix and cytoskeleton were differentially regulated in CSCs. Although inhibition of cytoskeleton remodeling by cisplatin treatment retarded CSC motility and cancer metastasis, drug resistant cancers eventually emerge containing markedly increased number of CSCs. This event is at least partially attributed to the activation of PI3K/mTOR signaling, and can be significantly inhibited by the treatment of rapamycin. These results provide strong evidence that cytoskeletal rearrangement and PI3K/mTOR signaling play a distinct role in mediating CSC mobility and viability, and blocking of both pathways in CSCs synergistically inhibits primary and metastatic cancer growth in BRCA1 associated tumors.

Publication Title

Synergistic therapeutic effect of cisplatin and phosphatidylinositol 3-kinase (PI3K) inhibitors in cancer growth and metastasis of Brca1 mutant tumors.

Alternate Accession IDs

E-GEOD-26621

Sample Metadata Fields

Specimen part

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GSE31561

Transcriptional analysis of organ-specific toxicity induced by a panPPAR agonist in mice: Identification of organ-specific toxicity biomarkers

Mus musculus
36 Downloadable Samples

Description

In this study, we aim to identify candidate biomarkers which may be useful as surrogate indicators of toxicity for pre-clinical development of panPPAR-agonist drug candidates. Gene expression microarray, histopathology and clinical chemistry data were generated from liver, heart, kidney and skeletal muscles of three groups of mice administered with three different dosages of an experimental pan-peroxisome proliferator-activated receptor (pan-PPAR) agonist, PPM-201, for 14 days. The histopathology and clinical chemistry data were compared with the gene expression analysis and candidate biomarker genes were identified.

Publication Title

Simultaneous non-negative matrix factorization for multiple large scale gene expression datasets in toxicology.

Alternate Accession IDs

E-GEOD-31561

Sample Metadata Fields

Specimen part, Treatment

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GSE17297

Mndal, a new interferon-inducible family member, suppresses cell growth and may modify plasmacytoma susceptibility

Mus musculus
30 Downloadable Samples

Description

Mndal, a new interferon-inducible family member, is highly polymorphic, suppresses cell growth and may modify plasmacytoma susceptibility.

Publication Title

Mndal, a new interferon-inducible family member, is highly polymorphic, suppresses cell growth, and may modify plasmacytoma susceptibility.

Alternate Accession IDs

E-GEOD-17297

Sample Metadata Fields

Specimen part, Time

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GSE19693

STAR RNA-binding protein, Quaking, suppresses cancer via regulation of microRNA

Mus musculus, Homo sapiens
25 Downloadable Samples

Description

MicroRNAs have emerged as major genetic elements in the genesis and suppression of cancer. Here, multi-dimensional cancer genome analysis and validation has defined a novel Glioblastoma Multiforme (GBM) tumor suppressor pathway and mechanism of action centered on Quaking (QK), a member of the STAR family of RNA-binding proteins. Combined functional, biochemical and computational studies establish that p53 directly regulates QK gene expression, QK protein binds and stabilizes miR-20a of the cancer-relevant miR-17-92 cluster, and miR-20a in turn functions to regulate TGFR2 and the TGF signaling network. Linkage of these pathway components is supported by their genome and expression status across GBM specimens and by their gain- and loss-of-function interactions in in vitro and in vivo complementation studies. This p53-QK-miR-20a axis expands our understanding of the p53 tumor suppression network in cancer and reveals a novel tumor suppression mechanism involving regulation of specific cancer-relevant microRNAs.