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accession-icon GSE70174
De novo generation of somatic stem cells from differentiated cells
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Alternate Accession IDs

E-GEOD-70174

Sample Metadata Fields

Specimen part

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accession-icon GSE21927
Expression data from bone marrow derived- and tumor induced- CD11b+ MDSC
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon

Description

Tumor growth is associated with a profound alteration of myelopoiesis, leading to recruitment of immunosuppressive cells known as myeloid-derived suppressor cells (MDSCs). Analyzing the cytokines affecting myelo-monocytic differentiation produced by various experimental tumors, we found that GM-CSF, G-CSF, and IL-6 allowed a rapid generation of MDSCs from precursors present in mouse and human bone marrow (BM). BM-MDSCs induced by GM-CSF+IL-6 possessed the highest tolerogenic activity, as revealed by the ability to impair the priming of IFN- -producing CD8+ T cells upon in vivo adoptive transfer. Moreover, adoptive transfer of syngeneic, GM-CSF+IL-6-conditioned MDSCs to diabetic mice transplanted with allogeneic pancreatic islets resulted in long term acceptance of the allograft and correction of the diabetic status. Cytokines inducing MDSCs acted on a common molecular pathway. Immunoregulatory activity of both tumor-induced and BM-derived MDSCs was entirely dependent on C/EBP transcription factor, a key component of the emergency myelopoiesis triggered by stress and inflammation. Adoptive transfer of tumor antigen-specific CD8+ T lymphocytes resulted in therapy of established tumors only in mice lacking C/EBP in myeloid compartment. These data unveil another link between inflammation and cancer and identify a novel molecular target to control tumor-induced immune suppression.

Publication Title

Tumor-induced tolerance and immune suppression depend on the C/EBPbeta transcription factor.

Alternate Accession IDs

E-GEOD-21927

Sample Metadata Fields

Specimen part

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accession-icon GSE70164
De novo generation of somatic stem cells from differentiated cells [mammary]
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

To investigate the role of YAP/TAZ as factors able to convert differentiated cells into stem cells of the same tissue, we compared the expression profiles of mammary organoids (yOrg) obtained by doxycycline-inducible expression of YAP in luminal differentiated mammary cells with original luminal differentiated mammary cells (Lum) and organoids from native mammary stem cells (Org).

Publication Title

Induction of Expandable Tissue-Specific Stem/Progenitor Cells through Transient Expression of YAP/TAZ.

Alternate Accession IDs

E-GEOD-70164

Sample Metadata Fields

Specimen part

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accession-icon GSE13610
Basal gene expression in bone (mice and rat)
  • organism-icon Mus musculus, Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Adult rat bones maintain distinct regionalized expression of markers associated with their development.

Alternate Accession IDs

E-GEOD-13610

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE13563
Pilot study: Basal gene expression in bone
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Pilot study

Publication Title

Adult rat bones maintain distinct regionalized expression of markers associated with their development.

Alternate Accession IDs

E-GEOD-13563

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE25926
Comparative transcriptome profiling of Amyloid Precursor Protein APP family members in the adult cortex
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon

Description

The -amyloid precursor protein APP and the related APLPs, undergo complex proteolytic processing giving rise to several fragments. Whereas it is well established that A accumulation is a central trigger for Alzheimer disease (AD), the physiological role of APP family members and their diverse proteolytic products is still largely unknown. The secreted APPs ectodomain has been shown to be involved in neuroprotection and synaptic plasticity. The -secretase generated APP intracellular domain AICD, functions as a transciptional regulator in heterologous reporter assays, although its role for endogenous gene regulation has remained controversial. To gain further insight into the molecular changes associated with knockout phenotypes and to elucidate the physiological functions of APP family members including their proposed role as transcriptional regulators we performed a DNA microarray transcriptome profiling of the frontal cortex of adult wild type, APP-/-, APLP2-/- and APPs knockin (KI) mice, APP/, expressing solely the secreted APPs ectodomain. Biological pathways affected by the lack of APP family members included regulation of neurogenesis, regulation of transcription and regulation of neuron projection development. Comparative analysis of transcriptome changes and qPCR validation identified co-regulated gene sets. Interestingly, these included heat shock proteins and plasticity related genes that were down-regulated in knock-out cortices. In contrast, we failed to detect significant differences in expression of previously proposed AICD target genes including Bace1, Kai1, Gsk3b, p53, Tip60 and Vglut2. Only Egfr was slightly up-regulated in APLP2-/- mice. Comparison of APP-/- and APP/ with wild-type mice revealed a high proportion of co-regulated genes indicating an important role of the C-terminus for cellular signaling. Finally, comparison of APLP2-/- on different genetic backgrounds revealed that background related transcriptome changes may dominate over changes due to the knockout of a single gene. Shared transcriptome profiles corroborated closely related physiological functions of APP family members in the adult central nervous system. As expression of proposed AICD target genes was not altered in adult cortex, this may indicate that these genes are not affected by lack of APP under resting conditions or only in a small subset of cells.

Publication Title

Comparative transcriptome profiling of amyloid precursor protein family members in the adult cortex.

Alternate Accession IDs

E-GEOD-25926

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE27888
Comparative transcriptome analysis of APPs-DM and APLP2-KO brains
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon

Description

Despite its key role in Alzheimer pathogenesis, the physiological function(s) of the amyloid precursor protein (APP) and of its proteolytic fragments are still poorly understood. The secreted APPs ectodomain has been shown to be involved in neuroprotection and synaptic plasticity. The -secretase generated APP intracellular domain, AICD, functions as a transcriptional regulator in heterologous reporter assays although its role for endogenous gene regulation has remained controversial. Previously, we have generated APPs knockin (KI) mice expressing solely the secreted ectodomain APPs. Here, we generated double mutants (APPs-DM) by crossing APPs-KI mice onto an APLP2-deficient background and show that APPs rescues the postnatal lethality of the majority of APP/APLP2 double knockout mice. Despite normal CNS morphology and unaltered basal synaptic transmission, young APPs-DM mice already showed pronounced hippocampal dysfunction, impaired spatial learning and a deficit in LTP. To gain further mechanistic insight into which domains/proteolytic fragments are crucial for hippocampal APP/APLP2 mediated functions, we performed a DNA microarray transcriptome profiling of prefrontal cortex and hippocampus of adult APLP2-KO (APLP2-/-) and APPs-DM mice (APP/APLP2-/- mice).Interestingly, this analysis failed to reveal major genotype-related transcriptional differences. Expression differences between cortex and hippocampus were, however, readily detectable.

Publication Title

APP and APLP2 are essential at PNS and CNS synapses for transmission, spatial learning and LTP.

Alternate Accession IDs

E-GEOD-27888

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE16585
Expression profiling of P14 and P28 mouse retina from 4 genotypes: +/+, Rorb-/- , +/+;CrxpNrl and Rorb-/-;CrxpNrl
  • organism-icon Mus musculus
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon

Description

Rorb is essential for rod photoreceptor development in the mouse retina. Using Affymetrix mouse GeneChips, we have generated expression profiles of the +/+, Rorb-/- , +/+;CrxpNrl and Rorb-/-;CrxpNrl retina at P14 and P28.

Publication Title

Retinoid-related orphan nuclear receptor RORbeta is an early-acting factor in rod photoreceptor development.

Alternate Accession IDs

E-GEOD-16585

Sample Metadata Fields

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.

Alternate Accession IDs

E-GEOD-49129

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.

Alternate Accession IDs

E-GEOD-49128

Sample Metadata Fields

Age, Specimen part, Treatment

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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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