refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 220 results
Sort by

Filters

Technology

Platform

accession-icon GSE57720
Ingestion of Cryptococcus neoformans by macrophages damages multiple host cellular processes
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Human infection with Cryptococcus neoformans (Cn), a prevalent fungal pathogen, occurs by inhalation and deposition in the lung alveoli of infectious particles. The subsequent host pathogen interaction is multifactorial and can result either in eradication, latency or extra-pulmonary dissemination. Successful control of Cn infection is dependent on host macrophages as shown by numerous studies. However in vitro macrophages display little ability to kill Cn. Recently, we reported that ingestion of Cn by macrophages induces early cell cycle progression that is subsequently followed by mitotic arrest, an event that almost certainly reflects damage to the host cell. The goal of the present work was to understand macrophage pathways affected by Cn toxicity. Infection of J774.16 macrophage-like cell line macrophages by Cn in vitro was associated with changes in gene pattern expression. Concomitantly we observed depolarization of macrophage mitochondria and alterations in protein translation rate. Our results indicate that Cn infection impairs multiple host cellular functions. Therefore we conclude Cn intracellular residence in macrophages undermines the health of these critical phagocytic cells interfering with their ability to clear the fungal pathogen.

Publication Title

Macrophage mitochondrial and stress response to ingestion of Cryptococcus neoformans.

Sample Metadata Fields

Specimen part, Cell line, Time

View Samples
accession-icon GSE13171
Alterations in total and in polysomal mRNA fraction in response to expression of RNA binding motif protein 35A
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95A Array (hgu95a)

Description

The gene coding for RNA binding motif protein 35A (RBM35A) is inactivated by frameshift mutations in an LS180 colon carcinoma cell line and in approximately in 50% of colon tumors with microsatellite instability. To get insight into the mechanism of action of these putative tumor suppressor gene we expressed functional copy of the RBM35A cDNA in the LS180 cells. We analyzed alterations in mRNA profiles in total and in polysomal fraction of mRNA in LS180 cells in response to expressing RBM35A gene under Tet off tetracycline inducible promoter.

Publication Title

RNA-binding motif protein 35A is a novel tumor suppressor for colorectal cancer.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE3334
Genomic Profiling of Mixer and Sox17beta Targets During Xenopus Endoderm Development
  • organism-icon Xenopus laevis
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome Array (xenopuslaevis)

Description

The transcription factors Mixer and Sox17beta have well characterized roles in endoderm specification during Xenopus embryogenesis. In order to more thoroughly understand the mechanisms by which these endodermal regulators act, we expressed Mixer and Sox17beta in nave ectodermal tissue and, using oligonucleotide-based microarrays, compared their genomic transcriptional profile to that of unaffected tissue. Using this novel approach, we identified 71 transcripts that are upregulated by Mixer or Sox17beta, 63 of which have previously uncharacterized roles in endoderm development. Furthermore, an in situ hybridization screen using antisense probes for several of these clones identified six targets of Mixer and/or Sox17beta that are expressed in the endoderm during gastrula stages, providing new and regional markers of the endoderm. Our results contribute further insight into the functions of Mixer and Sox17beta and bring us closer to understanding at the molecular level the pathways that regulate endoderm development.

Publication Title

Genomic profiling of mixer and Sox17beta targets during Xenopus endoderm development.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE45725
Internal validation cohort of breast cancers for development of ClinicoMolecular Triad Classification
  • organism-icon Homo sapiens
  • sample-icon 340 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

In our early study (PMID: 21939527), we have created a ClinicoMolecular Triad Classification (CMTC) to improve prediction and prognostication of breast cancer by using a training cohort contained 161 breast cancer patients (2003 to 2008). Here, a supplemental internal validation cohort contained 340 breast cancer patients was collected (2008 to 2010) for development of the CMTC.

Publication Title

Validation of the prognostic gene portfolio, ClinicoMolecular Triad Classification, using an independent prospective breast cancer cohort and external patient populations.

Sample Metadata Fields

Age, Disease stage

View Samples
accession-icon GSE37165
Gene expression data from time course of fin regeneration in Danio rerio
  • organism-icon Danio rerio
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon GSE37164
Gene expression data from time course of fin regeneration in Danio rerio (part 2)
  • organism-icon Danio rerio
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Olsen et al (2010) have shown that induced Diabetes mellitus (DM) in adult Zebrafish results in an impairment of tissue regeneration as monitored by caudal fin regeneration. In those studies, streptozocin was used to induce hyperglycemia in adult zebrafish, and then, following streptozocin withdrawal, a recovery phase was allowed to re-establish euglycemia, due to pancreatic b-cell regeneration. DM-associated impaired fin regeneration continued indefinitely in the metabolic memory state (MM); allowing for subsequent molecular analysis of the underlying mechanisms of MM. This study focuses on elucidating the molecular basis explaining DM-associated impaired fin regeneration and why it persists into the MM state. The analysis of microarray data indicated that of the 14,900 transcripts analyzed, aberrant expression of 71 genes relating to tissue developmental and regeneration processes were identified in DM fish and the aberrant expression of these 71 genes persisted into the MM state. Key regulatory genes of major signal transduction pathways were identified among this group of 71; and therefore, these findings provide a possible explanation for how hyperglycemia induces impaired fin regeneration and why it continues into the MM state.

Publication Title

Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon GSE37163
Gene expression data from time course of fin regeneration in Danio rerio (part 1)
  • organism-icon Danio rerio
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Olsen et al (2010) have shown that induced Diabetes mellitus (DM) in adult Zebrafish results in an impairment of tissue regeneration as monitored by caudal fin regeneration. In those studies, streptozocin was used to induce hyperglycemia in adult zebrafish, and then, following streptozocin withdrawal, a recovery phase was allowed to re-establish euglycemia, due to pancreatic b-cell regeneration. DM-associated impaired fin regeneration continued indefinitely in the metabolic memory state (MM); allowing for subsequent molecular analysis of the underlying mechanisms of MM. This study focuses on elucidating the molecular basis explaining DM-associated impaired fin regeneration and why it persists into the MM state. The analysis of microarray data indicated that of the 14,900 transcripts analyzed, aberrant expression of 71 genes relating to tissue developmental and regeneration processes were identified in DM fish and the aberrant expression of these 71 genes persisted into the MM state. Key regulatory genes of major signal transduction pathways were identified among this group of 71; and therefore, these findings provide a possible explanation for how hyperglycemia induces impaired fin regeneration and why it continues into the MM state.

Publication Title

Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon GSE44857
Transcriptional profile of AML xenografts treated with either PBS or a combination of decitabine and cytarabine
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The Affymetrix Human Genome U133 Plus 2.0 Array was used to examine the Genome wide transcriptional changes which follow the treatment of AML xenografts with either PBS control or combination of decitabine (DAC) and cytarabine (Ara-C). Animals were treated with PBS, DAC alone, Ara-C alone, DAC and Ara-C combined (D+A), DAC followed by Ara-C (D/A) or Ara-C followed by DAC (A/D).

Publication Title

Sequential treatment with cytarabine and decitabine has an increased anti-leukemia effect compared to cytarabine alone in xenograft models of childhood acute myeloid leukemia.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE72439
Effect of summer daylight exposure and genetic background on growth in growth hormone deficient children
  • organism-icon Homo sapiens
  • sample-icon 60 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The response to growth hormone in humans is dependent on phenotypic, genetic and environmental factors. The present study in children with growth hormone deficiency (GHD) collected worldwide characterised gene-environment interactions on growth response to recombinant human growth hormone (r-hGH). Growth responses in children are linked to latitude, and we found that a correlation of latitude, summer daylight exposure (SDE) was a key environmental factor related to growth response to r-hGH. In turn growth response was determined by an interaction between both SDE and genes known to affect growth response to r-hGH. In addition analysis of associated networks of gene expression implicated a role for circadian clock pathways and specifically the developmental transcription factor NANOG. This work provides the first observation of gene-environment interactions in children treated with r-hGH.

Publication Title

Effect of summer daylight exposure and genetic background on growth in growth hormone-deficient children.

Sample Metadata Fields

Sex, Age

View Samples
accession-icon GSE42135
Expression data from preimplantation mouse embryos
  • organism-icon Mus musculus
  • sample-icon 42 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Landmark events occur in a coordinated manner during preimplantation development of the mammalian embryo, yet the regulatory network that orchestrates these events remains largely unknown.

Publication Title

An Oct4-Sall4-Nanog network controls developmental progression in the pre-implantation mouse embryo.

Sample Metadata Fields

No sample metadata fields

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