refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 104 results
Sort by

Filters

Technology

Platform

accession-icon GSE87678
Transcriptional response of small intestinal epithelial cells (S-IECs) to bacterial monocolonization
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Here we analyzed the transcriptional profile of S-IECs sorted from GF and monocolonized mice (C. histolyticum and B. adolescentis), as well as SPF mice colonized with SFB or not.

Publication Title

Identifying species of symbiont bacteria from the human gut that, alone, can induce intestinal Th17 cells in mice.

Sample Metadata Fields

Sex, Age

View Samples
accession-icon SRP092209
Transcriptional response of small-intestinal lamina propria CD4+ T cells to bacterial colonization
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We analyzed the transcriptional profile of small-intestinal lamina propria (SI-LP) CD4+ T cells isolated from germ-free and mice monocolonized with Bifidobacterium adolescentis, SFB, and Nexabiotic (a 23-strain, Th17-inducing, probiotic mix). Overall design: CD4+ T cells were double-sorted from mice directly into lysis buffer.

Publication Title

Identifying species of symbiont bacteria from the human gut that, alone, can induce intestinal Th17 cells in mice.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Subject

View Samples
accession-icon GSE73329
Identification of drugs that enhance skin repair using dermal stem cell-based screens
  • organism-icon Mus musculus, Rattus norvegicus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st), Affymetrix Rat Gene 2.0 ST Array (ragene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Identification of Drugs that Regulate Dermal Stem Cells and Enhance Skin Repair.

Sample Metadata Fields

Treatment

View Samples
accession-icon GSE73327
Identification of drugs that enhance skin repair using dermal stem cell-based screens [Mouse]
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Here, we asked whether we could identify pharmacological agents that enhance endogenous stem cell function to promote skin repair, focusing on SKPs (skin-derived precursors) a dermal precursor cell population. Libraries of compounds already used in humans were screened for their ability to enhance the self-renewal of human and rodent SKPs. We identified and validated 5 such compounds, and showed that two of them, alprostadil and trimebutine maleate, enhanced the repair of full thickness skin wounds in middle-aged mice. Moreover, SKPs isolated from drug-treated skin displayed long-term increases in self-renewal when cultured in basal growth medium without drugs. Both alprostadil and trimebutine maleate likely mediated increases in SKPs self-renewal by moderate hyperactivation of the MEK-ERK pathway. These findings identify candidates for potential clinical use in human skin repair, and provide support for the idea that pharmacological activation of endogenous tissue precursors represents a viable therapeutic strategy.

Publication Title

Identification of Drugs that Regulate Dermal Stem Cells and Enhance Skin Repair.

Sample Metadata Fields

Treatment

View Samples
accession-icon GSE73328
Identification of drugs that enhance skin repair using dermal stem cell-based screens [Rat]
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 2.0 ST Array (ragene20st), Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Here, we asked whether we could identify pharmacological agents that enhance endogenous stem cell function to promote skin repair, focusing on SKPs (skin-derived precursors) a dermal precursor cell population. Libraries of compounds already used in humans were screened for their ability to enhance the self-renewal of human and rodent SKPs. We identified and validated 5 such compounds, and showed that two of them, alprostadil and trimebutine maleate, enhanced the repair of full thickness skin wounds in middle-aged mice. Moreover, SKPs isolated from drug-treated skin displayed long-term increases in self-renewal when cultured in basal growth medium without drugs. Both alprostadil and trimebutine maleate likely mediated increases in SKPs self-renewal by moderate hyperactivation of the MEK-ERK pathway. These findings identify candidates for potential clinical use in human skin repair, and provide support for the idea that pharmacological activation of endogenous tissue precursors represents a viable therapeutic strategy.

Publication Title

Identification of Drugs that Regulate Dermal Stem Cells and Enhance Skin Repair.

Sample Metadata Fields

Treatment

View Samples
accession-icon GSE114887
Expression data from Astro-D2KO mice experiencing a Status Epilepticus (SE)
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Status Epilepticus (SE) is an abnormally prolonged seizure that results from either a failure of mechanisms that terminate seizures or from initiating mechanisms that inherently lead to prolonged seizures.

Publication Title

Induction of Type 2 Iodothyronine Deiodinase After Status Epilepticus Modifies Hippocampal Gene Expression in Male Mice.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE55653
Gene expression during priming-induced resistance to fusarium head blight in wheat as revealed by two distinct mutants of Fusarium graminearum
  • organism-icon Triticum aestivum
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Wheat Genome Array (wheat)

Description

Fusarium head blight (FHB) is a major disease of cereal crops caused by the fungus Fusarium graminearum (Fg). FHB affects the flowering heads (or spikes) and developing seeds. This study compare the gene expression profile in wheat spikelets (spk 2) inoculated with either water (mock treatment) or a pathogenic strain of Fusarium graminearum (WT); spikelets 2 were inoculated 24 hrs after a neighbour spikelet (spk 0) was treated with either water or F. graminerum mutant strain Tri6 or NoxAB. Spikelets 2 were sampled 8 and 24 hrs after the second treatment.

Publication Title

Components of priming-induced resistance to Fusarium head blight in wheat revealed by two distinct mutants of Fusarium graminearum.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE139601
Transcriptomic profiling of the white adipose tissue (WAT) in ApoE3L.CETP mice fed a high fat diet (HFD) or a low fat diet (LFD) for three different time periods, or chow diet at baseline
  • organism-icon Mus musculus
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

The metabolic syndrome (MetS) is characterized by the presence of metabolic abnormalities that include abdominal obesity, dyslipidemia, hypertension, increased blood glucose/insulin resistance, hypertriglyceridemia and increased risk for cardiovascular disease (CVD). The ApoE*3Leiden.human Cholesteryl Ester Transfer Protein (ApoE3L.CETP) mouse model manifests several features of the MetS upon high fat diet (HFD) feeding. Moreover, the physiological changes in the white adipose tissue (WAT) contribute to MetS comorbidities. The aim of this study was to identify transcriptomic signatures in the gonadal WAT of ApoE3L.CETP mice in discrete stages of diet-induced MetS.

Publication Title

Transcriptome analysis of the adipose tissue in a mouse model of metabolic syndrome identifies gene signatures related to disease pathogenesis.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE5817
marsh-affy-mouse-232749
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Malformations of cortical development are the underlying eitiology of many cases of Mental Retardation and Epilepsy. Subtle, below the resolution of current MRI, cortical dysplasias are probably involved in many cases of MR, Epilepsy and Autism for which no diagnosis can currently be made. Therefore, understanding the process of cortical development will be vital in diagnosing and eventual treatment of many patients with these conditions. More specifically, the cortex forms from two major populations of neuroblasts which reach their final destination in the cortex by differerent mechanisms. One is radial migration from ventricular neuroblasts to the cortical plate. These cells are excititory projection neurons and glia. The second pathway is from the ventral ganglionic eminences and tangential migration of the interneuronal population of primarily inhibitory neurons. Much less is known about the control of the latter process, and many of these currently undiagnosed subtle malformations may stem from abnormalities of this tangential migration. This project focuses on the understanding the control of the tangentially migrating inhibitory interneurons.

Publication Title

Identification of Arx transcriptional targets in the developing basal forebrain.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP093840
Histone deacetylase inhibitor MS-275 augments expression of a subset of IFN-?-regulated genes in Toxoplasma gondii-infected macrophages but does not improve parasite control
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Toxoplasma gondii is a ubiquitous apicomplexan parasite of mammals and birds and an important pathogen of humans. IFN-g is the major mediator of host resistance against T. gondii but intriguingly, parasite-infected host cells including macrophages are severely impaired to respond to IFN-g due to defective transcriptional activation of target genes. Here, we tested the possibility that the impaired responsiveness of T. gondii-infected macrophages to IFN-g can be restored by inhibiting histone deacetylases (HDACs) using the class I-specific inhibitor MS-275. Treatment of RAW264.7 cells with MS-275 indeed increased MHC class II surface expression in infected and non-infected cells and largely abolished the inhibition of IFN-g-regulated MHC class II expression exerted by T. gondii. Genome-wide transcriptome profiling revealed that MS-275 increased mean mRNA levels of IFN-g-regulated genes particularly in non-infected macrophages. Transcript levels of 33% of IFN-g secondary response genes but only those of a few primary response genes were also increased by MS-275 in T. gondii-infected cells. Importantly, the unresponsiveness of parasite-infected cells to IFN-g was however not abolished by MS-275. Furthermore, MS-275 also up-regulated several anti-inflammatory cytokines or signaling molecules in T. gondii-infected macrophages. It additionally regulated expression of more than 2500 genes in non-infected macrophages expression of which was surprisingly counteracted by prior infection with T. gondii. FACS analysis and immunofluorescence microscopy revealed that MS-275 did not considerably diminish the number of parasite-positive cells or the intracellular replication in macrophages stimulated or not with IFN-g. Thus, a supportive therapy using MS-275 appears inappropriate for treatment of toxoplasmosis. Overall design: High throughput RNA profiles from IFN-g-activated monocytic cells infected with Toxoplasma gondii and treated with MS-275 and control cells were generated by Illumina sequencing. Five experimental conditions with 2 biological replicates each were analysed.

Publication Title

Histone deacetylase inhibitor MS-275 augments expression of a subset of IFN-γ-regulated genes in Toxoplasma gondii-infected macrophages but does not improve parasite control.

Sample Metadata Fields

Subject

View Samples
...

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact