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accession-icon GSE29975
Expression data from FOG1+/- (or FOG1+/+) and FOG1 ki/ki mouse megakaryocyte (Meg)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
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Description

The transcription co-factor FOG1 interacts with the chromatin remodeling complex NuRD to mediate gene activation and gene repression during hematopoiesis. We have generated mice with a targeted mutation in the endogenous Fog1 locus that results in an N-ternimal mutation in FOG1 that disrupts the interaction with NuRD.

Publication Title

Pleiotropic platelet defects in mice with disrupted FOG1-NuRD interaction.

Sample Metadata Fields

Specimen part

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accession-icon GSE21041
Transcriptome analysis of miR-144/451-null bone marrow erythroid cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
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Description

microRNA miR-144/451 is highly expressed during erythropoiesis. We deleted the miR-144/451 gene locus in mice and compared the transcriptomes of miR-144/451-null bone marrow erythroid precursors to stage-matched wild-type control cells.

Publication Title

miR-451 protects against erythroid oxidant stress by repressing 14-3-3zeta.

Sample Metadata Fields

Specimen part

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accession-icon GSE14980
Consequences of GATA1 expression in Gata1- G1ME Murine Megakaryocyte/Erythrocyte Progenitor Cell Line
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
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Description

G1ME cells are GATA1-deficient murine bipotential megakaryocyte/erythrocyte progenitor cells derived from Gata1-negative murine ES cells. In order to assess the impact of GATA1 on gene regulation and cell differentiation, an expression construct was used to transiently produce high levels of GATA1. Cells transduced with this construct or a vector control were harvested at 18 and 42 hours, and gene expression was analyzed using Affymetrix MOE430 version 2 arrays.

Publication Title

Graded repression of PU.1/Sfpi1 gene transcription by GATA factors regulates hematopoietic cell fate.

Sample Metadata Fields

Cell line

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accession-icon GSE10904
Expression data from wildtype and alb/cre liver-conditional Pdss2 knockout mutant mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Utilizing M. musculus as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of liver-conditional knockout mice for Pdss2 compared with loxP controls.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE14416
ICSBP-mediated immune protection against BCR-ABL-induced leukemia requires the CCL6 and CCL9 chemokines
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Interferon is effective at inducing complete remissions in patients with Chronic Myelogenous Leukemia (CML), and evidence supports an immune mechanism. Here we show that the Type I Interferons (alpha and beta) regulate expression of the Interferon consensus sequence binding protein (ICSBP) in bcr-abl transformed cells and as shown previously for ICSBP, induce a vaccine-like immunoprotective effect in a murine model of bcr-abl induced leukemia. We identify the chemokines CCL6 and CCL9 as genes prominently induced by the Type I Interferons and ICSBP, and demonstrate that these immunomodulators are required for the immunoprotective effect of ICSBP expression. Insights into the role of these chemokines in the anti-leukemic response of interferons suggest new strategies for immunotherapy of CML.

Publication Title

ICSBP-mediated immune protection against BCR-ABL-induced leukemia requires the CCL6 and CCL9 chemokines.

Sample Metadata Fields

No sample metadata fields

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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 47 Downloadable Samples
  • Technology Badge Icon

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 GSE8715
Transcriptional Profiling of the Megabladder Mouse - A Unique Model of Bladder Dysmorphogenesis
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
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Description

Recent studies in our lab have identified a mutant mouse model of obstructive nephropathy designated mgb for megabladder. Homozygotic mgb mice (mgb-/-) develop lower urinary tract obstruction in utero due to a lack of bladder smooth muscle differentiation. This defect is the result of a random transgene insertion into chromosome 16 followed by a translocation of this fragment into chromosome 11. In an effort to identify potential gene targets affected in mgb mice, we performed transcriptional profiling on embryonic day 15 (E15) mgb-/- bladders using both a Chromosome 11/16 Custom GeneChip Array and the Affymetrix Mouse Genome 430 2.0 GeneChip. This analysis identified no definitive mis-expressed gene targets on chromosome 11. In contrast, mgb-/- mice significantly over-expressed a cluster of gene products located on the translocated fragment of chromosome 16 including urotensin II-related peptide (Urp), which was shown to be preferentially over-expressed in developing mgb-/- bladders. Immunohistochemical studies indicated that the spatial distribution of Urp was altered in mgb-/- bladders, while biochemical studies suggested a potential role for Urp in modifying smooth muscle cell phenotype in vitro. Pathway analysis of mgb microarray data showed dysregulation of at least 60 gene products associated with the differentiation of smooth muscle. In conclusion, the results of this study indicate that the molecular pathways controlling normal smooth muscle development are severely altered in mgb-/- bladders, and provide the first evidence that Urp may play a critical role in bladder smooth muscle development.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE11859
Acquisition of granule neuron precursor identity and Hedgehog-induced medulloblastoma in mice.
  • organism-icon Mus musculus
  • sample-icon 27 Downloadable Samples
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Description

Origins of the brain tumor, medulloblastoma, from stem cells or restricted pro-genitor cells are unclear. To investigate this, we activated oncogenic Hedgehog signaling in multipotent and lineage-restricted CNS progenitors. We observed that normal unipo-tent cerebellar granule neuron precursors (CGNP) derive from hGFAP+ and Olig2+ rhombic lip progenitors. Hedgehog activation in a spectrum of early and late stage CNS progenitors generated similar medulloblastomas, but not other brain cancers, indicating that acquisition of CGNP identity is essential for tumorigenesis. We show in human and mouse medulloblastoma that cells expressing the glia-associated markers Gfap and Olig2 are neoplastic and that they retain features of embryonic-type granule lineage progenitors. Thus, oncogenic Hedgehog signaling promotes medulloblastoma from lineage-restricted granule cell progenitors.

Publication Title

Acquisition of granule neuron precursor identity is a critical determinant of progenitor cell competence to form Shh-induced medulloblastoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE13874
microRNA-1 negatively regulates expression of the hypertrophy-associated genes calmodulin and Mef2a
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon

Description

Calcium signaling is a central regulator of cardiomyocyte growth and function. Calmodulin is a critical mediator of calcium signals. Because the amount of calmodulin within cardiomyocytes is limiting, precise regulation of calmodulin expression may be an important for regulation of calcium signaling. In this study, we show for the first time that calmodulin levels are regulated post-transcriptionally in heart failure. The cardiomyocyte-restricted microRNA miR-1 inhibited translation of calmodulin-encoding mRNAs via highly conserved target sites within their 3-untranslated regions. In keeping with its effect on calmodulin expression, miR-1 downregulated calcium-calmodulin signaling through the calcineurin to NFAT. miR-1 also negatively regulated expression of Mef2a and Gata4, key transcription factors that mediate calcium-dependent changes in gene expression. Consistent with downregulation of these hypertrophy-associated genes, miR-1 attenuated cardiomyocyte hypertrophy in cultured neonatal rat cardiomyocytes and in the intact adult heart. Our data indicate that miR-1 regulates cardiomyocyte growth responses by negatively regulating the calcium-signaling components calmodulin, Mef2a, and Gata4.

Publication Title

No associated publication

Sample Metadata Fields

Cell line, Treatment, Time

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accession-icon GSE13285
Human Fetal Hemoglobin Expression is Regulated by the Developmental Stage-Specific Repressor BCL11A
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Human fetal hemoglobin expression is regulated by the developmental stage-specific repressor BCL11A.

Sample Metadata Fields

No sample metadata fields

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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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Developed by the Childhood Cancer Data Lab

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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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