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accession-icon GSE84569
Transcriptomic analyses of IXR1 gene deletion in Saccharomyces cerevisiae and its increased resistance to cisplatin treatment.
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Ixr1 is a transcriptional factor from Saccharomyces cerevisae with high affinity to cisplatin-DNA adducts through their two HMG-box DNA binding domains. Its transcriptional regulation is essential in the cytotoxicity caused by cisplatin, although the molecular mechanisms supporting this function are not understood. We present a transcriptome analysis discriminating between RNA changes induced by cisplatin which are dependent or independent of the Ixr1 function.

Publication Title

Ixr1 Regulates Ribosomal Gene Transcription and Yeast Response to Cisplatin.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE41094
Transcript analyses of cisplatin and Sky1 effects in Saccharomyces cerevisiae
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Sky1 is a Saccharomyces cerevisiae rich serine-arginine (SR) protein-specific kinase and its enzymatic activity is essential in the cytotoxicity caused by cisplatin, although the molecular mechanisms supporting this function are not understood. We present a transcriptome analysis discriminating between RNA changes induced by cisplatin which are dependent or independent of the Sky1 function.

Publication Title

Sky1 regulates the expression of sulfur metabolism genes in response to cisplatin.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE38829
Expression data from MCF7 and MCF7-LTED cells treated with YC-1
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

To identify novel therapeutic opportunities for patients with acquired resistance to endocrine treatments in breast cancer, we applied a high-throughput drug screen. The IC50 values were determined for MCF7 and MCF7-LTED cells.

Publication Title

VAV3 mediates resistance to breast cancer endocrine therapy.

Sample Metadata Fields

Cell line

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accession-icon SRP116025
Time-course transcriptome of regeneration [RNA-Seq]
  • organism-icon Drosophila melanogaster
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

The ability to regenerate or recover from injuries varies greatly not only between species but also between tissues and organs or developmental stages of the same species. The mechanisms behind these different regenerative capabilities are ultimately dependent on the control of genome activity, determined by a complex interplay of regulatory elements functioning at the level of chromatin. Resetting of gene expression patterns during injury responses is, thus, shaped by the coordinated action of genomic regions (enhancers, silencers) that integrate the activity of multiple sequence-specific DNA binding proteins (transcription factors and cofactors). Using  genome- wide approaches to interrogate chromatin function here we identify the regulatory elements governing tissue recovery in Drosophila wing imaginal discs, which show a high regenerative capacity after genetically induced cell death. Our findings point to a global co-regulation of gene expression and provide evidence for Damage Responding Regulatory Elements (DRRE), some of which are novel whereas others are also used in other tissues or developmental stages. Overall design: We collected data at different time points (0, 15 and 25h) after apoptosis induction. These time periods were selected because they included the most important transcriptional responses to apoptosis, ranging from the earliest gene expression up to complete re-patterning. Discs kept at the same conditions without inducing cell death were used as controls.

Publication Title

Damage-responsive elements in <i>Drosophila</i> regeneration.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE65570
CNV and expression patterns in matched human melanoma tissues and cell lines with different invasive property.
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Altered integrin expression patterns shown by microarray in human cutaneous melanoma.

Sample Metadata Fields

Specimen part, Disease, Cell line

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accession-icon GSE65568
Altered integrin expression patterns revealed by microarray in matched human melanomas (mRNA)
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Metastatic process is considered the predominant cause of melanoma-specific death, decreasing survival dramatically, and resulting in difficulties in the effective treatment. Large variety of molecular pathways associated with disease development and progression suggests that no individual molecular alteration is crucial in these processes per se.

Publication Title

Altered integrin expression patterns shown by microarray in human cutaneous melanoma.

Sample Metadata Fields

Specimen part, Disease, Cell line

View Samples
accession-icon SRP198959
Small extracellular vesicles are key regulators of non-cell autonomous intercellular communication in senescence via the interferon protein, IFITM3
  • organism-icon Homo sapiens
  • sample-icon 45 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Senescence is a cellular phenotype present in health and disease, characterized by a stable cell cycle arrest and an inflammatory response, denominated senescence-associated secretory phenotype (SASP). The SASP is important in influencing the behaviour of neighbouring cells and altering the microenvironment; yet, this role has been mainly attributed to soluble factors. Here, we show that both the soluble factors in addition to small extracellular vesicles (sEV) are capable of transmitting paracrine senescence to nearby cells. Analysis of individual cells internalizing sEV, using a Cre-reporter system, show a positive correlation between sEV uptake and senescence activation. Interestingly, we find an increase in the number of multivesicular bodies during senescence in vivo. sEV protein characterization by mass spectrometry (MS) followed by a functional siRNA screen identify the Interferon Induced Transmembrane Protein 3 (IFITM3) as partially responsible for transmitting senescence to normal cells. Altogether, we found that sEV contribute to paracrine senescence. Overall design: SASP related mRNA transcripts in HFFF2 treated with sEV from iRAS cells in comparison with HFFF2 treated with sEV from iC cells

Publication Title

Small Extracellular Vesicles Are Key Regulators of Non-cell Autonomous Intercellular Communication in Senescence via the Interferon Protein IFITM3.

Sample Metadata Fields

Disease, Subject

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accession-icon GSE35383
INTEGRATIVE ONCOGENOMIC AND HIGH-THROUGHPUT SEQUENCING ANALYSES OF THE COMMONLY DELETED REGION IN CHROMOSOME 7q32 IN SPLENIC MARGINAL ZONE LYMPHOMA
  • organism-icon Homo sapiens
  • sample-icon 9 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

High-throughput sequencing analysis of the chromosome 7q32 deletion reveals IRF5 as a potential tumour suppressor in splenic marginal-zone lymphoma.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon SRP057021
Myc and SAGA Rewire an Alternative Splicing Network During Early Somatic Cell Reprogramming [Reprogramming_RNASEQ]
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Embryonic stem cells are maintained in a self-renewing and pluripotent state by multiple regulatory pathways. Pluripotent-specific transcriptional networks are sequentially reactivated as somatic cells reprogram to achieve pluripotency. How epigenetic regulators modulate this process and contribute to somatic cell reprogramming is not clear. Here we perform a functional RNAi screen to identify the earliest epigenetic regulators required for reprogramming. We identify components of the SAGA histone acetyltransferase complex, in particular Gcn5, as critical regulators of reprogramming initiation. Furthermore, we show in mouse pluripotent stem cells that Gcn5 strongly associates with Myc and that upon initiation of somatic reprogramming, Gcn5 and Myc form a positive feed forward loop that activates a distinct alternative splicing network and the early acquisition of pluripotency-associated splicing events. These studies expose a Myc-SAGA pathway that drives expression of an essential alternative splicing regulatory network during somatic cell reprogramming. Overall design: Examination of expression level changes at D0 and D2 MEFs

Publication Title

Myc and SAGA rewire an alternative splicing network during early somatic cell reprogramming.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE35082
INTEGRATIVE ONCOGENOMIC AND HIGH-THROUGHPUT SEQUENCING ANALYSES OF THE COMMONLY DELETED REGION IN CHROMOSOME 7q32 IN SPLENIC MARGINAL ZONE LYMPHOMA (expression)
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Using high-resolution genomic microarray analysis, a distinct genomic profile was defined in 114 samples from patients with splenic marginal zone lymphoma (SMZL). Notably, deletion or uniparental disomy of chromosome 7q were detected in 39% of SMZLs but in only 9 of 170 (5%) mature B-cell lymphomas (p<10-6). The presence of unmutated IgVH genes, genomic complexity, 17p13-P53 deletion and 8q gain including MYC gene, but not 7q deletion, were correlated with shorter overall survival. Extensive mapping analyses narrowed down the commonly deleted region to 2.7 Mb. in 7q32.1-q32.2 from SND1 to COPG2 genes. High-throughput sequencing analysis of the 7q32 deleted segment in SMZL cells did not identify bi-allelic deletions, insertions or clear pathogenic mutations, but detected six single nucleotide changes in IRF5 (n=2), TMEM209 (n=2), CALU (n=1) and ZC3HC1 (n=1). Comparative expression analysis found that IRF5, TMEM209 and CALU genes had down-regulated expression in lymphomas with 7q32 deletion vs. non-deleted tumors. Ectopic expression of IRF5 in marginal-zone lymphoma cells decreased cell proliferation and induced apoptosis. These results indicate that small deletions, insertions and/or point mutations inactivating genes within 7q32 are not common events in SMZL. Further studies are required to evaluate the putative role of IRF5 in SMZL pathogenesis.

Publication Title

High-throughput sequencing analysis of the chromosome 7q32 deletion reveals IRF5 as a potential tumour suppressor in splenic marginal-zone lymphoma.

Sample Metadata Fields

Disease, Disease stage

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)

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Developed by the Childhood Cancer Data Lab

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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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