publication_authors:Elle IC Results

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Microarray (514)

Platform

Affymetrix Human Gene 1.1 ST Array (hugene11st) (285)

Affymetrix Mouse Genome 430 2.0 Array (mouse4302) (203)

Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2) (26)

Includes Publication

GSE10167

Microarray Analysis of Treacher Collins Syndrome

Mus musculus
6 Downloadable Samples

Description

The object of this study was to identify genes transcriptionally upregulated and downregulated in response to Tcof1 haploin-sufficiency during mouse embryogensis

Publication Title

Prevention of the neurocristopathy Treacher Collins syndrome through inhibition of p53 function.

Sample Metadata Fields

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GSE24451

Knockout of the Acyl CoA binding protein (ACBP) in mice - expression profile from the liver of 21 days old ACBP-/- and +/+ mice.

Mus musculus
5 Downloadable Samples

Description

The ACBP knockout were created by targeted disruption of the gene in mice. The expression profiling was performed on liver tissue from ACBP-/- (KO) and +/+ (WT) mice at the age of 21 days, which in our study is the time immediately before weaning. The mice used for this experiment were taken directly away from their mother. Thus, having free access to chow and breast milk until sacrificed at 8-11am

Publication Title

Disruption of the acyl-CoA-binding protein gene delays hepatic adaptation to metabolic changes at weaning.

Sample Metadata Fields

Specimen part

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GSE18446

BCR-ABL enhances differentiation of long-term repopulating hematopoietic stem cells

Mus musculus
6 Downloadable Samples

Description

The biology of chronic myeloid leukemia (CML)-stem cells is still incompletely understood. Therefore, we previously developed an inducible transgenic mouse model in which stem cell targeted induction of BCR-ABL expression leads to chronic phase CML-like disease. Here, we now demonstrate that the disease is transplantable using BCR-ABL positive LSK cells (lin-Sca-1+c-kit+). Interestingly, the phenotype is enhanced when unfractionated bone marrow (BM) cells are transplanted. However, neither progenitor cells (lin-Sca-1-c-kit+) nor mature granulocytes (CD11b+Gr-1+), or potential stem cell niche cells were able to transmit the disease or alter the phenotype. The phenotype was largely independent of BCR ABL priming prior to transplant. However, BCR-ABL abrogated the potential of LSK cells to induce full blown disease in secondary recipients. Subsequently, we found that BCR-ABL increased the fraction of multipotent progenitor cells (MPP) at the expense of long term HSC (LT-HSC) in the BM. Microarray analyses of LSK cells revealed that BCR-ABL alters the expression of genes involved in proliferation, survival, and hematopoietic development. Our results suggest that BCR-ABL induces differentiation of LT-HSC and decreases their self renewal capacity. Furthermore, reversion of BCR-ABL eradicates mature cells while leukemic stem cells persist, giving rise to relapsed CML upon re-induction of BCR-ABL.

Publication Title

BCR-ABL enhances differentiation of long-term repopulating hematopoietic stem cells.

Sample Metadata Fields

Specimen part

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GSE12466

Transcriptional signatures of Itk-deficient CD3+, CD4+ and CD8+ T-cells

Mus musculus
23 Downloadable Samples

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Transcriptional signatures of Itk-deficient CD3+, CD4+ and CD8+ T-cells.

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GSE22927

Hierarchical synergy of Pten, p53 and Rb pathways in high-grade astrocytoma induced in adult brain

Mus musculus, Homo sapiens
4 Downloadable Samples

Description

Mutations in the PTEN, TP53 and RB1 pathways are obligate events in the pathogenesis of human glioblastomas, the highest grade of astrocytoma. To investigate synergy between these tumor suppressors in mice, we induced various combinations of compound deletions conditionally in astrocytes and neural precursors in the mature brain. The resulting highly penetrant astrocytomas showed a spectrum of histopathological variation reminiscent of human tumors, and ranged from grade III to grade IV (glioblastoma). Secondary somatic mutations varied depending on the combination of initiating deletions and were relevant to human disease. Receptor tyrosine kinase amplifications were frequent in tumors initiated by combined conditional deletion of Pten and Tp53, but not when Rb, Pten and Tp53 were simultaneously deleted. Multiple mutations within PI3K and Rb pathways were acquired, however, Mapk activation was not consistently detected in astrocytomas. Gene expression profiling revealed striking similarities to previously described human astrocytoma subclasses. A subset of astrocytomas initiated outside of proliferative niches in the adult brain.