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accession-icon GSE49237
Analysis of TBR1 downnstream target genes in embryonic forebrains
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

TBR1 is a forebrain specific T-box transcription factor. Tbr1-/- mice have been characterized by defective axonal projections from cerebral cortex and abnormal neuronal migration of cerebral cortex and amygdala.

Publication Title

Tbr1 haploinsufficiency impairs amygdalar axonal projections and results in cognitive abnormality.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE22927
Hierarchical synergy of Pten, p53 and Rb pathways in high-grade astrocytoma induced in adult brain
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

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.

Publication Title

Cooperativity within and among Pten, p53, and Rb pathways induces high-grade astrocytoma in adult brain.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE32034
Tissue-specific differences in PPAR control of macrophage function.
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

PPAR is known for its anti-inflammatory actions in macrophages. However, which macrophage populations express PPAR in vivo and how it regulates tissue homeostasis in the steady state and during inflammation is not completely understood. We show that lung and spleen macrophages constitutively expressed PPAR, while other macrophage populations did not. Recruitment of monocytes to sites of inflammation was associated with induction of PPAR as they differentiated to macrophages. Its absence in these macrophages led to failed resolution of inflammation, characterized by persistent, low-level recruitment of leukocytes. Conversely, PPAR agonists supported an earlier cessation in leukocyte recruitment during resolution of acute inflammation and likewise suppressed monocyte recruitment to chronically inflamed atherosclerotic vessels. In the steady state, PPAR deficiency in macrophages had no obvious impact in the spleen but profoundly altered cellular lipid homeostasis in lung macrophages. Reminiscent of pulmonary alveolar proteinosis, LysM-Cre x PPARflox/flox mice displayed mild leukocytic inflammation in the steady-state lung and succumbed faster to mortality upon infection with S. pneumoniae. Surprisingly, this mortality was not due to overly exuberant inflammation, but instead to impaired bacterial clearance. Thus, in addition to its anti-inflammatory role in promoting resolution of inflammation, PPAR sustains functionality in lung macrophages and thereby has a pivotal role in supporting pulmonary host defense.

Publication Title

Systemic analysis of PPARγ in mouse macrophage populations reveals marked diversity in expression with critical roles in resolution of inflammation and airway immunity.

Sample Metadata Fields

Sex, Treatment

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accession-icon GSE35805
Gene expression analysis of WT and Flt3-ITD multipotent progenitors
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

FLT3-ITDs Introduce a Myeloid Differentiation and Transformation Bias in Lympho-myeloid Multipotent Progenitors

Publication Title

FLT3-ITDs instruct a myeloid differentiation and transformation bias in lymphomyeloid multipotent progenitors.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE49129
Otitis Media Impact on Ear
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Otitis media impacts hundreds of mouse middle and inner ear genes.

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon GSE49128
Otitis Media Impact on Middle Ear
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon

Description

Objective: Otitis media is known to alter expression of cytokine and other genes in the mouse middle ear and inner ear. However, whole mouse genome studies of gene expression in otitis media have not previously been undertaken. Ninety-nine percent of mouse genes are shared in the human, so these studies are relevant to the human condition.

Publication Title

Otitis media impacts hundreds of mouse middle and inner ear genes.

Sample Metadata Fields

Age, Specimen part, Treatment

View Samples
accession-icon GSE49122
Otitis Media Impact on Inner Ear
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon

Description

Objective: Otitis media is known to alter expression of cytokine and other genes in the mouse middle ear and inner ear. However, whole mouse genome studies of gene expression in otitis media have not previously been undertaken. Ninety-nine percent of mouse genes are shared in the human, so these studies are relevant to the human condition.

Publication Title

Otitis media impacts hundreds of mouse middle and inner ear genes.

Sample Metadata Fields

Age, Specimen part, Treatment

View Samples
accession-icon GSE20500
T cell genes regulated by retinoic acid
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

This is to determine the T cell genes regulated by retinoic acid.

Publication Title

Complementary roles of retinoic acid and TGF-β1 in coordinated expression of mucosal integrins by T cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE52024
Genome wide analysis of transcriptome and microRNAs in early stage of Alzheimer's disease
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Prediction of miRNA-mRNA associations in Alzheimer's disease mice using network topology.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE12609
Transcription factor Arx null brains (fulp-affy-mouse-364520)
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Arx is a paired-box homeodomain transcription factor and the vertebrate ortholog to the Drosophila aristaless (al) gene. Mutations in Arx are associated with a variety of human diseases, including X-linked infantile spasm syndrome (OMIM: 308350), X-linked myoclonic epilepsy with mental retardation and spasticity (OMIM: 300432), X-linked lissencephaly with ambiguous genitalia (OMIM: 300215), X-linked mental retardation 54 (OMIM: 300419), and agenesis of the corpus callosum with abnormal genitalia (OMIM: 300004). Arx-deficient mice exhibit a complex, pleiotrophic phenotype, including decreased proliferation of neuroepithelial cells of the cortex, dysgenesis of the thalamus and olfactory bulbs, and abnormal nonradial migration of GABAergic interneurons. It has been suggested that deficits in interneuron specification, migration, or function lead to loss of inhibitory neurotransmission, which then fails to control excitatory activity and leads to epilepsy or spasticities. Given that Arx mutations are associated with developmental disorders in which epilepsy and spasticity predominate and that Arx-deficient mice exhibit deficits in interneuron migration, understanding the function of Arx in interneuron migration will prove crucial to understanding the pathology underlying interneuronopathies. Yet, downstream transcriptional targets of Arx, to date, remain unidentified.

Publication Title

Identification of Arx transcriptional targets in the developing basal forebrain.

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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