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accession-icon GSE72425
Systematic identification of changes in the yeast protein interaction network in response to environmental, chemical, and genetic perturbation
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Quantitative analysis of protein interaction network dynamics in yeast.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE72423
Systematic identification of changes in the yeast protein interaction network in response to environmental, chemical, and genetic perturbation [transcriptome data]
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

To understand the principles underlying protein-protein interaction (PPI) complex changes in response to external perturbations, we created a highly multiplexed version of the murine dihydrofolate reductase protein complementation assay (mDHFR PCA) in Saccharomyces cerevisiae, allowing quantitative PPI complex profiling in vivo. We investigated the effects of 14 different conditions (including small molecules, abiotic stress factors, and nutrient composition) on a total of 1383 PPIs. More than half of PPIs (758) were found to be variable, and their Gene Ontology (GO) annotations were found to be informative of both the nature of the perturbation within each condition, as well as the overall variability of the interactions across conditions. Many perturbations triggered network changes characterized by large connected modules centered around highly connected proteins ('hubs'), suggesting that cellular control of a few proteins (e.g., by mRNA levels) can induce widespread PPI remodeling. Under a diauxic shift from glucose to ethanol as the main carbon source, we found a striking relationship between PPI changes measured by our assay and those predicted by mRNA expression under a simple law of mass action based model.

Publication Title

Quantitative analysis of protein interaction network dynamics in yeast.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP062144
Integrated analysis of MLL-AF9 AML patients and model leukemias highlights RET and other novel therapeutic targets (RNA-seq AML development)
  • organism-icon Homo sapiens
  • sample-icon 83 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Next generation DNA sequencing of acute myeloid leukemia (AML) patient samples has revealed novel recurrent mutations while at the same time highlighting the genetic heterogeneity of the disease. These observations suggest that an extraordinarily large number of combinations of mutations can contribute to leukemogenesis. In order to address the question of the contribution of patient genetic background to AML we have developed a model system to generate multiple human leukemias in a single donor’s genetic background. Stepwise RNA-seq data from this model shows that in the context of AML driven by the MLL-AF9 (MA9) oncogene, the genetic background of the donor does not have a detectable effect. Comparison of these model leukemias from multiple single donors to AML patient samples containing MA9 translocations revealed conserved gene expression patterns not previously highlighted in this genetic sub-type. We further demonstrate that the expression of one of these genes, RET, is essential both in vivo and in vitro growth of MA9 AMLs . Overall design: study of transcriptome during the development of MLL-AF9 AML

Publication Title

Modeling human MLL-AF9 translocated acute myeloid leukemia from single donors reveals RET as a potential therapeutic target.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP062170
Integrated analysis of MLL-AF9 AML patients and model leukemias highlights RET and other novel therapeutic targets (RNA-seq B-ALL)
  • organism-icon Homo sapiens
  • sample-icon 63 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Next generation DNA sequencing of acute myeloid leukemia (AML) patient samples has revealed novel recurrent mutations while at the same time highlighting the genetic heterogeneity of the disease. These observations suggest that an extraordinarily large number of combinations of mutations can contribute to leukemogenesis. In order to address the question of the contribution of patient genetic background to AML we have developed a model system to generate multiple human leukemias in a single donor’s genetic background. Stepwise RNA-seq data from this model shows that in the context of AML driven by the MLL-AF9 (MA9) oncogene, the genetic background of the donor does not have a detectable effect. Comparison of these model leukemias from multiple single donors to AML patient samples containing MA9 translocations revealed conserved gene expression patterns not previously highlighted in this genetic sub-type. We further demonstrate that the expression of one of these genes, RET, is essential both in vivo and in vitro growth of MA9 AMLs . Overall design: study of transcriptome during the development of MLL-AF9 B-ALL

Publication Title

Modeling human MLL-AF9 translocated acute myeloid leukemia from single donors reveals RET as a potential therapeutic target.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP061972
Integrated analysis of MLL-AF9 AML patients and model leukemias highlights RET and other novel therapeutic targets [RNA-Seq_AML]
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Next generation DNA sequencing of acute myeloid leukemia (AML) patient samples has revealed novel recurrent mutations while at the same time highlighting the genetic heterogeneity of the disease. These observations suggest that an extraordinarily large number of combinations of mutations can contribute to leukemogenesis. In order to address the question of the contribution of patient genetic background to AML we have developed a model system to generate multiple human leukemias in a single donor’s genetic background. Stepwise RNA-seq data from this model shows that in the context of AML driven by the MLL-AF9 (MA9) oncogene, the genetic background of the donor does not have a detectable effect. Comparison of these model leukemias from multiple single donors to AML patient samples containing MA9 translocations revealed conserved gene expression patterns not previously highlighted in this genetic sub-type. We further demonstrate that the expression of one of these genes, RET, is essential both in vivo and in vitro growth of MA9 AMLs . Overall design: Transcriptome of several AML cell lines

Publication Title

Modeling human MLL-AF9 translocated acute myeloid leukemia from single donors reveals RET as a potential therapeutic target.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP061973
Integrated analysis of MLL-AF9 AML patients and model leukemias highlights RET and other novel therapeutic targets [RNA-Seq_normal]
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Next generation DNA sequencing of acute myeloid leukemia (AML) patient samples has revealed novel recurrent mutations while at the same time highlighting the genetic heterogeneity of the disease. These observations suggest that an extraordinarily large number of combinations of mutations can contribute to leukemogenesis. In order to address the question of the contribution of patient genetic background to AML we have developed a model system to generate multiple human leukemias in a single donor’s genetic background. Stepwise RNA-seq data from this model shows that in the context of AML driven by the MLL-AF9 (MA9) oncogene, the genetic background of the donor does not have a detectable effect. Comparison of these model leukemias from multiple single donors to AML patient samples containing MA9 translocations revealed conserved gene expression patterns not previously highlighted in this genetic sub-type. We further demonstrate that the expression of one of these genes, RET, is essential both in vivo and in vitro growth of MA9 AMLs . Overall design: Transcriptome of normal cells (CD34+) from different donors

Publication Title

Modeling human MLL-AF9 translocated acute myeloid leukemia from single donors reveals RET as a potential therapeutic target.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP062417
Integrated analysis of MLL-AF9 AML patients and model leukemias highlights RET and other novel therapeutic targets (Leukemia Cell Bank)
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Next generation DNA sequencing of acute myeloid leukemia (AML) patient samples has revealed novel recurrent mutations while at the same time highlighting the genetic heterogeneity of the disease. These observations suggest that an extraordinarily large number of combinations of mutations can contribute to leukemogenesis. In order to address the question of the contribution of patient genetic background to AML we have developed a model system to generate multiple human leukemias in a single donor’s genetic background. Stepwise RNA-seq data from this model shows that in the context of AML driven by the MLL-AF9 (MA9) oncogene, the genetic background of the donor does not have a detectable effect. Comparison of these model leukemias from multiple single donors to AML patient samples containing MA9 translocations revealed conserved gene expression patterns not previously highlighted in this genetic sub-type. We further demonstrate that the expression of one of these genes, RET, is essential both in vivo and in vitro growth of MA9 AMLs . Overall design: Transcriptome of MLL-AF9 AML pediatric patients

Publication Title

Modeling human MLL-AF9 translocated acute myeloid leukemia from single donors reveals RET as a potential therapeutic target.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE92955
Whole transcriptome analysis of the ventrolateral hypothalamic parvafox nucleus in mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

The ventrolateral hypothalamic parvafox (formerly called PV1-Foxb1) nucleus is an anatomical entity of recent discovery and unknown function. With a view to gaining an insight into its putative functional role(s), we conducted a gene-microarray analysis.

Publication Title

Parvalbumin-Neurons of the Ventrolateral Hypothalamic Parvafox Nucleus Receive a Glycinergic Input: A Gene-Microarray Study.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE13766
Expression analysis of the Saccharomyces cerevisiae hst3hst4 mutant
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

The hst3hst4 strain (FY background) has the HST3 and HST4 genes, encoding putative NAD-dependent deacetylases that regulate histone 3 K56 acetylation, deleted. Expression profiling using Affymetrix microarrays was used to assess the change in the gene expression in this strain in comparison to wild-type under normal growth conditions.

Publication Title

Histone H3 K56 hyperacetylation perturbs replisomes and causes DNA damage.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE54837
Altered gene expression in blood and sputum from COPD patients with frequent exacerbations
  • organism-icon Homo sapiens
  • sample-icon 218 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Investigation of gene expression profiles among patients with COPD frequent exacerbations and to find gene targets as predictors of exacerbations

Publication Title

Altered gene expression in blood and sputum in COPD frequent exacerbators in the ECLIPSE cohort.

Sample Metadata Fields

Sex, Age, Specimen part

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)

fund-icon Fund the CCDL

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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