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accession-icon GSE56251
Expression data from Escherichia coli after treatment with nalidixic acid (NA)
  • organism-icon Escherichia coli
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Having found that LexA degradation was significantly higher under apoptotic like death (ALD) than under SOS conditions, we hypothesized that additional genes tightly regulated by LexA would be transcribed under ALD conditions.

Publication Title

Apoptosis-like death, an extreme SOS response in Escherichia coli.

Sample Metadata Fields

Disease, Treatment

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accession-icon GSE62167
Expression data from the T-DNA insertion line atpip1;2-1
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Arabidopsis Gene 1.0 ST Array (aragene10st)

Description

Some aquaporins do not show a pronounced function as water diffusion facilitators but act as small molecule transport facilitators for substances such as urea, glycerol, boron or gases such as CO2 . Transcriptome analysis provided distinguishable, specific profiles for water stress or for conditions of increased or decreased CO2 concentrations

Publication Title

T-DNA insertion in aquaporin gene AtPIP1;2 generates transcription profiles reminiscent of a low CO2 response.

Sample Metadata Fields

Specimen part

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accession-icon GSE48365
S-adenosylmethionine modifies cocaine-induced DNA methylation and increases locomotor sensitization in mice
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

The aim of the study was to investigate whether environmental factors like S-adenosylmethionine (SAM) via affecting epigenome could alter cocaine-induced gene expression and locomotor sensitization in mice.

Publication Title

S-adenosylmethionine modifies cocaine-induced DNA methylation and increases locomotor sensitization in mice.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE74145
Intermittent neonatal hypoxia elicits the upregulation of inflammatory-related genes in the adult rat through long-lasting programming effects
  • organism-icon Rattus norvegicus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

The long-term effects of neonatal intermittent hypoxia (IH), an accepted model of apnea-induced hypoxia, are unclear. We have previously shown lasting programming effects on the HPA axis in adult rats exposed to neonatal IH. We hypothesized that neonatal rat exposure to IH will subsequently result in a heightened inflammatory state in the adult. Rat pups were exposed to normoxia (control) or six cycles of 5% IH or 10% IH over one hour daily from postnatal day 2 6. Plasma samples from blood obtained at 114 days of age were analyzed by assessing the capacity to induce transcription in a healthy peripheral blood mononuclear cell (PBMC) population and read using a high-density microarray. The analysis of plasma from adult rats previously exposed to neonatal 5% IH vs. 10% IH resulted in 2,579 significantly regulated genes including increased expression of Cxcl1, Cxcl2, Ccl3, Il1a, and Il1b. We conclude that neonatal exposure to intermittent hypoxia elicits a long-lasting programming effect in the adult resulting in an upregulation of inflammatory-related genes.

Publication Title

Intermittent neonatal hypoxia elicits the upregulation of inflammatory-related genes in adult male rats through long-lasting programming effects.

Sample Metadata Fields

Sex

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accession-icon GSE71730
Plasma induced signatures reveal an extracellular milieu possessing an immunoregulatory bias in treatment nave inflammatory bowel disease
  • organism-icon Homo sapiens
  • sample-icon 42 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The complex milieu of inflammatory mediators associated with many diseases is often too dilute to directly measure in the periphery, necessitating development of more sensitive measurements suitable for mechanistic studies, earlier diagnosis, guiding selection of therapy, and monitoring interventions. Previously, we determined that plasma of recent-onset (RO) Type 1 diabetes (T1D) patients induce a proinflammatory transcriptional signature in fresh peripheral blood mononuclear cells (PBMC) relative to that of unrelated healthy controls (HC). Here, using an optimized cryopreserved PBMC-based protocol, we apply this approach to inflammatory bowel disease by examining groups of Crohn's disease (CD) and ulcerative colitus (UC) patients. The induced plasma induced signatures are compared to those of Type 1 diabetes patients (RO T1D) as well as unrelated healthy controls (uHC).

Publication Title

Plasma-induced signatures reveal an extracellular milieu possessing an immunoregulatory bias in treatment-naive paediatric inflammatory bowel disease.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE24147
Sera-induced transcriptional signatures in human leukemia cell lines
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Inflammation is common to many disorders and responsible for tissue and organ damage. However, the associated peripheral cytokine milieu is frequently dilute and difficult to measure, necessitating development of more sensitive and informative biomarkers for mechanistic studies, earlier diagnosis, and monitoring therapeutic interventions. Previously, we have shown that sera from type 1 diabetes (T1D) patients induces a unique disease-specific pro-inflammatory transcriptional profile in fresh peripheral blood mononuclear cells (PBMCs) compared to sera of healthy controls.

Publication Title

Use of transcriptional signatures induced in lymphoid and myeloid cell lines as an inflammatory biomarker in Type 1 diabetes.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE5846
NCI-60 Cancer Cell Line
  • organism-icon Homo sapiens
  • sample-icon 60 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

NCI-60 cancer cell lines were profiled with their genome-wide gene expression patterns using Affymetrix HG-U133A chips.

Publication Title

A strategy for predicting the chemosensitivity of human cancers and its application to drug discovery.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE5845
Bladder Cancer 40 Cell Lines
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

40 bladder cancer cell lines were profiled with their genome-wide gene expression patterns using Affymetrix HG-U133A chips.

Publication Title

A strategy for predicting the chemosensitivity of human cancers and its application to drug discovery.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE40498
Temporal induction of immunoregulatory processes coincides with age-dependent resistance to viral-induced type 1 diabetes
  • organism-icon Homo sapiens, Rattus norvegicus
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Temporal induction of immunoregulatory processes coincides with age-dependent resistance to viral-induced type 1 diabetes.

Sample Metadata Fields

Sex

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accession-icon GSE40497
Temporal induction of immunoregulatory processes coincides with age-dependent resistance to viral-induced type 1 diabetes [Rat]
  • organism-icon Rattus norvegicus
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A need exists for biomarkers in T1D that can 1) sensitively and specifically detect disease-related immune activity prior to, and independent of, measurement of auto-antibodies towards islet cell antigens; 2) define immunopathological mechanisms; and 3) monitor changes in the inflammatory state associated with disease progression or response to therapeutic intervention. In an effort to fill this gap, we have applied a novel bioassay to both human and BB rat T1D whereby the complex milieu of inflammatory mediators present in plasma can be indirectly detected through their ability to drive transcription in peripheral blood mononuclear cells (PBMCs) drawn from healthy, unrelated donors. The resultant gene expressions are comprehensively measured with a microarray. In our human studies, we find that plasma of recent-onset T1D patients induces expression of a pro-inflammatory signature consisting in part of many interleukin-1 (IL-1) regulated genes related to immunological activation and immunocyte chemotaxis compared to unrelated healthy controls. This signature has been found to resolve in long-standing T1D subjects (>10 years post-onset), thus associating it with active autoimmunity. Importantly, this signature has been detected in pre-onset samples of progressors to T1D years prior to onset and prior to development of auto-antibodies directed towards islet antigens.

Publication Title

Temporal induction of immunoregulatory processes coincides with age-dependent resistance to viral-induced type 1 diabetes.

Sample Metadata Fields

Sex

View Samples
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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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