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accession-icon GSE73484
Expression data of LPS-induced genes in bone marrow derived macrophages
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon

Description

TLR ligands consistently induce expression of two Hes family members Hes1 and Hey1 in macrophages.To evaluate the effects of these two factors on inflammatory responses, we generated mice lacking both Hes1 and Hey1 (DKO). WT and DKO BMDMs were then untreated or exposed to LPS for 3 hours, and microarray was performed to examine global gene expression profiles to identify Hes1 and Hey1-regulated inflammatory genes

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE56345
Therapeutic potential of spleen tyrosine kinase inhibition for treatment of high-risk precursor B-cell acute lymphoblastic leukemia
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

This study revealed pathogenic role of pre-BCR-independent SYK activation in high-risk B-ALL.

Publication Title

Therapeutic potential of spleen tyrosine kinase inhibition for treating high-risk precursor B cell acute lymphoblastic leukemia.

Sample Metadata Fields

Specimen part

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accession-icon GSE112449
Microarray analysis comparing gene expression of callus tissue extracted from either Cyp24a1-null mice or their control heterozygous littermates
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

The 24R,25-dihydroxyvitamin D metabolite (24R,25D) has long been suspected of participating to bone fracture repair. We used Cyp24a1-deficient mice, unable to produce 24R25D, to observe gene expression in callus tissue compared to that of control littermates.

Publication Title

Optimal bone fracture repair requires 24R,25-dihydroxyvitamin D3 and its effector molecule FAM57B2.

Sample Metadata Fields

Age, Specimen part, Treatment, Time

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accession-icon GSE15894
Comparison of gene expression in whole blood of mice subjected to normobaric hypoxia in vivo.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

To determine hypoxia mediated changes in whole blood, normal C57Bl/10 mice were gradually exposed to a chronic hypoxic environment, equivalent to an altitude of 6500m, for 2 weeks in vivo. Control, age-matched mice were maintained under normoxic, normobaric conditions by exposing them to ambient air in Philadelphia (c. 50 mts above sea level).

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE15902
Comparison of gene expression in whole blood of mice subjected to chemical hypoxia in vivo.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

To understand hypoxia mediated changes in whole blood, normal C57Bl/10 mice were gradually exposed to a chronic chemical hypoxic environment, for 2 weeks. Control, age-machted mice were maintained under normoxic conditions.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE15901
Comparison of gene expression in whole blood of mice subjected to hypobaric hypoxia at Mt. Everest in vivo.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

To determine hypoxia mediated changes in whole blood, normal swiss webster mice were gradually exposed to a chronic hypobaric hypoxic environment up to 8500m, for 2 weeks in vivo. Control, age-matched mice were maintained under normoxic conditions in Kathmandu (c. 1300 mts above sea level).

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 GSE39388
Distinct transcriptional programs controlled by ERG and ETV1 in prostate cells
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

ETV1 directs androgen metabolism and confers aggressive prostate cancer in targeted mice and patients.

Sample Metadata Fields

Specimen part, 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
  • Technology Badge Icon

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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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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