refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 213 results
Sort by

Filters

Technology

Platform

accession-icon GSE17449
Transcription signature of Multiple Sclerosis
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Learning from nature: pregnancy changes the expression of inflammation-related genes in patients with multiple sclerosis.

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon GSE17410
Pregnancy changes expression in peripheral blood mononuclear cells of Multiple Sclerosis (MS) patients
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Background: pregnancy is associated with reduced activity of multiple sclerosis (MS). However, the biological mechanisms underlying this pregnancy-related decrease in disease activity are poorly understood.

Publication Title

Learning from nature: pregnancy changes the expression of inflammation-related genes in patients with multiple sclerosis.

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon GSE17393
Transcription signature of Multiple Sclerosis in peripheral blood mononuclear cells.
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Background: pregnancy is associated with reduced activity of multiple sclerosis (MS). However, the biological mechanisms underlying this pregnancy-related decrease in disease activity are poorly understood.

Publication Title

Learning from nature: pregnancy changes the expression of inflammation-related genes in patients with multiple sclerosis.

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon GSE17409
Pregnancy changes expression in peripheral blood mononuclear cells of healthy donors
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Background: pregnancy is associated with reduced activity of multiple sclerosis (MS). However, the biological mechanisms underlying this pregnancy-related decrease in disease activity are poorly understood.

Publication Title

Learning from nature: pregnancy changes the expression of inflammation-related genes in patients with multiple sclerosis.

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon GSE34179
Effect of Th-POK deficiency on global gene expression in liver Va14i NKT cells
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We sought to identify genes regulated by the transcription factor Th-POK (Zbtb7b) in liver Va14i NKT cells, by RNA microarray analysis of global gene expression in Va14i NKT cells from mice homozygous for the Th-POK-inactivating hd point mutation as compared with the same cell population isolated from heterozygous or wild-type age-matched mice.

Publication Title

The transcription factor Th-POK negatively regulates Th17 differentiation in Vα14i NKT cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE18991
Overexpression of Hoxd4 transcription factor alters transcriptional profiles in mouse chondrocytes at E18.5
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Homeobox genes of the Hox class are required for proper patterning of skeletal elements and play a role in cartilage differentiation. In transgenic mice with overexpression of Hoxd4 during cartilage development, we observed severe defects, namely physical instability of cartilage, accumulation of immature chondrocytes, and decreased maturation to hypertrophy. To define the molecular basis underlying these defects, we performed gene expression profiling using the Affymetrix microarray platform.

Publication Title

Microarray Analysis of Defective Cartilage in Hoxc8- and Hoxd4-Transgenic Mice.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE18992
Overexpression of Hoxc8 transcription factor alters transcriptional profiles in mouse chondrocytes at E18.5
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Homeobox genes of the Hox class are required for proper patterning of skeletal elements and play a role in cartilage differentiation. In transgenic mice with overexpression of Hoxc8 during cartilage development, we observed severe defects, namely physical instability of cartilage, accumulation of immature chondrocytes, and decreased maturation to hypertrophy. To define the molecular basis underlying these defects, we performed gene expression profiling using the Affymetrix microarray platform.

Publication Title

Microarray Analysis of Defective Cartilage in Hoxc8- and Hoxd4-Transgenic Mice.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE33550
Reverse engineering of TLX oncogenic transcriptional networks identifies RUNX1 as tumor suppressor in T-ALL
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 66 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The TLX1 and TLX3 transcription factor oncogenes play an important role in the pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL)1,2. Here we used reverse engineering of global transcriptional networks to decipher the oncogenic regulatory circuit controlled by TLX1 and TLX3. This Systems Biology analysis defined TLX1 and TLX3 as master regulators of an oncogenic transcriptional circuit governing T-ALL. Notably, network structure analysis of this hierarchical network identified RUNX1 as an important mediator of TLX1 and TLX3 induced T-ALL, and predicted a tumor suppressor role for RUNX1 in T-cell transformation. Consistent with these results, we identified recurrent somatic loss of function mutations in RUNX1 in human T-ALL. Overall, these results place TLX1 and TLX3 atop of an oncogenic transcriptional network controlling leukemia development, demonstrate power of network analysis to identify key elements in the regulatory circuits governing human cancer and identify RUNX1 as a tumor suppressor gene in T-ALL.

Publication Title

Disregulated expression of the transcription factor ThPOK during T-cell development leads to high incidence of T-cell lymphomas.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE33549
Expression data from mouse T-cell lymphomas
  • organism-icon Mus musculus
  • sample-icon 59 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Transgenic expression of key transcritpion factors inducing T-cell leukemias in mice.

Publication Title

Disregulated expression of the transcription factor ThPOK during T-cell development leads to high incidence of T-cell lymphomas.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE33540
Expression data obtained from HPBALL cell line
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The experiment was designed in order to knock down the expression of TLX3 gene in T-ALL cell line

Publication Title

Disregulated expression of the transcription factor ThPOK during T-cell development leads to high incidence of T-cell lymphomas.

Sample Metadata Fields

Cell line

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