refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 253 results
Sort by

Filters

Technology

Platform

accession-icon GSE6526
Expression time course data HEY2 KO and WT MASMC treated with PDGF
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The cardiovascular restricted transcription factor CHF1/Hey2 has been previously shown to regulate the smooth muscle response to growth factors. To determine how CHF1/Hey2 affects the smooth muscle response to growth factors, we performed a genomic screen for transcripts that are differentially expressed in wild type and knockout smooth muscle cells after stimulation with platelet derived growth factor.

Publication Title

Transcription factor CHF1/Hey2 regulates the global transcriptional response to platelet-derived growth factor in vascular smooth muscle cells.

Sample Metadata Fields

No sample metadata fields

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
accession-icon GSE33539
Expression data obtained from ALLSIL cell line
  • organism-icon Homo sapiens
  • sample-icon 3 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 TLX1 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
accession-icon SRP012317
Zea mays Transcriptome or Gene expression
  • organism-icon Zea mays
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx, Illumina HiSeq 2000, Illumina Genome Analyzer

Description

Small RNAs (sRNAs) are hypothesized to contribute to hybrid vigor because they maintain genome integrity, contribute to genetic diversity, and control gene expression. We used Illumina sequencing to assess how sRNA populations vary between two maize inbred lines (B73, Mo17) and their hybrid. We sampled sRNAs from the seedling shoot apex and the developing ear, two rapidly growing tissues that program the greater growth of maize hybrids. We found that parental differences in siRNAs primarily originate from repeat regions. Although the maize genome contains greater number and complexity of repeats compared to Arabidopsis or rice, we confirmed that like these simpler plant genomes, 24-nt siRNAs whose abundance differs between maize parents also show a trend of downregulation following hybridization. Surprisingly, hybrid vigor is fully maintained when 24-nt siRNAs are globally reduced by mutation of the RNA-dependent RNA polymerase2 (RDR2) encoded by modifier of paramutation1 (mop1). We also discovered that 21-22nt siRNAs derived from a number of distinct retrotransposon families differentially accumulate between B73 and Mo17 as well as their hybrid. Thus, maize possesses a novel source of genetic variation for regulating both transposons and genes at a genomic scale, which may contribute to its high degree of observed heterosis. Overall design: sRNA libraries were derived from RNA isolated from the seedling shoot apex and developing ear tissues from B73, Mo17, B73xMo17 and Mo17xB73. The shoot apex was chosen because it is enriched for meristematic tissue where cell proliferation occurs, rates of organ initiation are determined, and organ size is specified. The developing ear was examined because it is enriched in meristematic tissue and is undergoing rapid growth, and also because the mature ear shows the highest degree of heterosis. Total RNA was isolated and separated on a 15% TBE-Urea polyacrylamide gel. Using a 10-bp ladder, the sRNA fraction representing 10-40-bp was excised. sRNA libraries were prepared according to Lu et al. (2007) or manufacturer''s instructitions (Illumina). A combination of Perl scripts and FASTX toolkit scripts were used to remove adapters, collapse identical sequences and count reads per sequence. Supplementary processed data text files contain the distinct sRNA sequences for all of the genotypes analyzed in that experiment. Abundance (reads per million) was calculated for each distinct sequence by dividing the number of reads of distinct sRNA in a library by the total number of sRNA reads for that library and multiplying this by 1 million. Genome builds: B73 genome, maizesequence.org release 4a.53 (October, 2009); Mo17 whole genome shotgun clones.

Publication Title

Repeat associated small RNAs vary among parents and following hybridization in maize.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE18824
Expression data from 17 day old testes of wild type and UBR2-/- mice
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Ubiquitylation of histones provides an important mechanism regulating chromatin remodeling and gene expression. Recent studies have revealed ubiquitin ligases involved in histone ubiquitylation, yet the responsible enzymes and the function of histone ubiquitination in spermatogenesis remain unclear. Here we show that the ubiquitin ligase UBR2, one of the recognition E3 components of the N-end rule proteolytic pathway, localizes to meiotic chromatin regions, including unsynapsed axial elements linked to chromatin inactivation, and mediates, in combination with the ubiquitin-conjugating enzyme HR6B, the ubiquitination of histone H2A. UBR2 interacts with HR6B and H2A and promotes the HR6B-H2A interaction and the HR6B-to-H2A transfer of ubiquitin. UBR2 and ubiquitinated H2A (uH2A) spatiotemporally mark meiotic chromatin regions subject to transcriptional silencing, and UBR2-deficient spermatocytes fail to induce the ubiquitination of H2A during meiosis. UBR2-deficient spermatocytes are profoundly impaired in transcriptional silencing of genes linked to unsynapsed axes of the X and Y chromosomes. We propose a model, in which UBR2 on axial elements of the X-Y pair enables HR6B on the linked chromatin domain to repeat histone ubiquitination cycles while scanning a string of nucleosomes. Our results suggest that histone ubiquitination in germ cells may be mediated by E3-E2 pairs distinct from those in somatic cells, providing a new insight into chromatin remodeling and gene expression regulation.

Publication Title

UBR2 mediates transcriptional silencing during spermatogenesis via histone ubiquitination.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE21419
Laser Capture Microdissection of Hyperlipidemic Mouse Aorta Atherosclerosis
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302), Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Atherosclerosis is a transmural chronic inflammatory condition of small and large arteries that is associated with adaptive immune responses at all disease stages. However, impacts of adaptive immune reactions on clinically apparent atherosclerosis such as intima lesion (plaque) rupture, thrombosis, myocardial infarction, and aneurysm largely remain to be identified. It is increasingly recognized that leukocyte infiltrates in plaque, media, and adventitia are distinct but their specific roles have not been defined. To map these infiltrates, we employed laser capture microdissection (LCM) to isolate the three arterial wall laminae using apoE-/- mouse aorta as a model. RNA from LCM-separated tissues was extracted and large scale whole genome expression microarrays were prepared. We observed that the quality of the resulting gene expression maps was compromised by tissue RNA carried over from adjacent laminae during LCM. To account for these flaws, we established quality controls and algorithms to improve the predictive power of LCM-derived microarray data. Our approach creates robust transcriptome atlases of normal and atherosclerotic aorta. Assessing LCM transcriptomes for immunity-related mRNAs indicated markedly distinctive gene expression patterns in the three laminae of the atherosclerotic aorta. These mouse mRNA expression data banks can now be mined to address a wide range of questions in cardiovascular biology.

Publication Title

The lamina adventitia is the major site of immune cell accumulation in standard chow-fed apolipoprotein E-deficient mice.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE101476
Global expression of sebacous gland carcinoma
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

MicroRNA and transcriptome analysis in periocular Sebaceous Gland Carcinoma.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE101474
Global expression of sebacous gland carcinoma [mRNA]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Samples were taken from patients undergoing cancer excision for pagetoid (wide) sebaceous gland carcinoma (SGC) and different individuals undergoing excision for nodular (local) SGC.

Publication Title

MicroRNA and transcriptome analysis in periocular Sebaceous Gland Carcinoma.

Sample Metadata Fields

Specimen part

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