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accession-icon GSE106271
Treatment of insulin resistant 3T3-L1 adipose cells with MnTBAP
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
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Description

MnTBAP reversed insulin resistance without significant alteration to gene expression

Publication Title

The transcriptional response to oxidative stress is part of, but not sufficient for, insulin resistance in adipocytes.

Sample Metadata Fields

Specimen part

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accession-icon GSE90673
Expression profiles of retinal neuronal cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Satb1 Regulates Contactin 5 to Pattern Dendrites of a Mammalian Retinal Ganglion Cell.

Sample Metadata Fields

Specimen part

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accession-icon GSE90648
A gene expression database for retinal neuron subtypes
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
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Description

The goal of this experiment was to define gene expression patterns of two mouse retinal ganglion cell subsets, labeled by expression of fluorescent proteins in Hb9-GFP and Drd4-GFP mice, all retinal ganglion cells labeled by anti-Thy1 antibody staining.

Publication Title

Satb1 Regulates Contactin 5 to Pattern Dendrites of a Mammalian Retinal Ganglion Cell.

Sample Metadata Fields

Specimen part

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accession-icon GSE15541
Linkage of Meis1 leukemogenic activity to multiple downstream effectors including Trib2 and Ccl3
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
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Description

OBJECTIVE: MEIS1, a HOX cofactor, collaborates with multiple HOX and NUP98-HOX fusion proteins to accelerate the onset of acute myeloid leukemia (AML) through largely unknown molecular mechanisms. MATERIALS AND METHODS: To further resolve these mechanisms, we conducted a structure-function analysis of MEIS1 and gene-expression profiling, in the context of NUP98-HOXD13 (ND13) leukemogenesis. RESULTS: We show, in a murine bone marrow transplantation model, that the PBX-interaction domain, the homeodomain, and the C-terminal domain of MEIS1, are all required for leukemogenic collaboration with ND13. In contrast, the N-terminal domain of MEIS1 is dispensable for collaboration with ND13, but is required for Flt3 upregulation, indicating additional roles for MEIS1 in induction of leukemia independent of alterations in Flt3 expression. Gene-expression profiling of a cloned ND13 preleukemic cell line transduced with wild-type or Meis1 mutant forms revealed deregulation of multiple genes, including a set not previously implicated as MEIS1 targets. Chromatin immunoprecipitation revealed the in vivo occupancy of MEIS1 on regulatory sequences of Trib2, Flt3, Dlk1, Ccl3, Ccl4, Pf4, and Rgs1. Furthermore, engineered overexpression of Trib2 complements ND13 to induce AML while Ccl3 potentiates the repopulating ability of ND13. CONCLUSION: This study shows that Meis1-induced leukemogenesis with ND13 can occur in the absence of Flt3 upregulation and reveals the existence of other pathways activated by MEIS1 to promote leukemia.

Publication Title

Linkage of Meis1 leukemogenic activity to multiple downstream effectors including Trib2 and Ccl3.

Sample Metadata Fields

Specimen part

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accession-icon GSE100002
Molecular and functional sex differences of noradrenergic neurons in the mouse locus coeruleus [Affymetrix]
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
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Description

Preclinical work has long focused only on male animals, even though sexual divergence in both baseline behaviors and drug responses clearly impact treatment outcomes in patients. Psychiatric disorders are notably divergent, with males showing higher prevalence of ADHD and ASD, and females GAD and MDD. This divergence is reflected in quantitative differences in subclincal behaviors. The Noradrenergic neurotransmitter system is targeted by many psychiatric drugs, but is relatively uncharacterized at a molecular level. We developed a mouse to profile these neurons, defining their both a baseline transcriptome, including druggable receptors, and their molecular response to stimulation. We also discovered a remarkable sexual divergence in their gene expression, including functionally increased expression of the EP3 receptor in females a difference that can be used to modulate stress-induced anxiety in a sex specific manner. These findings underscore the need to conduct preclinical studies in a manner balanced for sex, and suggest that baseline differences in noradrenergic neurons could underlay sexually divergent behaviors.

Publication Title

Molecular and Functional Sex Differences of Noradrenergic Neurons in the Mouse Locus Coeruleus.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE25911
Expression changes after loss of Dot1l in murine MLL-AF9 leukemia cells
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
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Description

MLL-fusions may induce leukemogenic gene expression programs by recruiting the histone H3K79 methyltransferase to MLL-target promoters. We evaluated gene expression changes after cre-mediated loss of Dot1l in leukemia cells obtained from mice injected with MLL-9 transformed lineage negative bone marrow cells.

Publication Title

MLL-rearranged leukemia is dependent on aberrant H3K79 methylation by DOT1L.

Sample Metadata Fields

Specimen part

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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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