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accession-icon GSE44148
Analysis of Drosophila salivary glands and Kc cells with depleted levels of linker histone H1
  • organism-icon Drosophila melanogaster
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Drosophila H1 regulates the genetic activity of heterochromatin by recruitment of Su(var)3-9.

Sample Metadata Fields

Specimen part

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accession-icon GSE44398
Analysis of Drosophila salivary glands and Kc cells with depleted levels of linker histone H1 [Affymetrix Expression]
  • organism-icon Drosophila melanogaster
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Indicated cells were subjected to RNAi against linker histone H1, Nautilus (control), or GFP (control). RNA was isolated and subjected to Affymetrix GeneChIP Drosophila Genome 2.0 arrays

Publication Title

Drosophila H1 regulates the genetic activity of heterochromatin by recruitment of Su(var)3-9.

Sample Metadata Fields

Specimen part

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accession-icon SRP018798
Analysis of Drosophila salivary glands and Kc cells with depleted levels of linker histone H1 (Illumina smRNA-Seq]
  • organism-icon Drosophila melanogaster
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

Salivary glands or larval ovaries were isolated from transgenic flies expressing RNAi targeting Nautilus (control) or linker histone H1 using a Tub-Gal4 driver. Overall design: ~200 larvae were used to isolate salivary glands or ovaries, independently. Total RNA was isolated using Trizol reagent following manufacturer''s guidelines. Then 5 µg of total RNA was separated on a polyacrylamide gel, and 18-29 nt small RNAs were isolated for cloning.

Publication Title

Drosophila H1 regulates the genetic activity of heterochromatin by recruitment of Su(var)3-9.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE35385
GATA-1 in proliferating and differentiating murine ES cell derived erythroid progenitors
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A core erythroid transcriptional network is repressed by a master regulator of myelo-lymphoid differentiation.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE35384
Transcriptome analysis of differentiating normal and leukemic erythroid progenitors
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We compared the transcriptomes of differentiating cultures of ES cell derived erythroid progentor cells (ES-EP) and murine erythroleukemia (MEL) cells stably transfected with GATA-1 fused to ER.

Publication Title

A core erythroid transcriptional network is repressed by a master regulator of myelo-lymphoid differentiation.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE21953
PU.1 in normal erythroid progenitors and erythroleukemia cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A large gene network in immature erythroid cells is controlled by the myeloid and B cell transcriptional regulator PU.1.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE21949
Transcriptome analysis of normal erythroid progenitors and erythroleukemia cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We compared the transcriptomes of ES cell derived erythroid progentor cells (ES-EP) and murine erythroleukemia (MEL) cells stably transfected with Gata-1 fused to ER.

Publication Title

A large gene network in immature erythroid cells is controlled by the myeloid and B cell transcriptional regulator PU.1.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE25913
Gene expression profiling of the classical (CD14++CD16-), intermediate (CD14++CD16+) and nonclassical (CD14+CD16+) human monocyte subsets
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina human-6 v2.0 expression beadchip

Description

The new official nomenclature subdivides human monocytes into three subsets, classical (CD14++CD16-), intermediate (CD14++CD16+) and nonclassical (CD14+CD16+). Here, we comprehensively define relationships and unique characteristics of the three human monocyte subsets using microarray and flow cytometry analysis. Our analysis revealed that the intermediate and nonclassical monocyte subsets were most closely related. For the intermediate subset, majority of genes and surface markers were expressed at an intermediary level between the classical and nonclassical subset. There features therefore indicate a close and direct lineage relationship between the intermediate and nonclassical subset. From gene expression profiles, we define unique characteristics for each monocyte subset. Classical monocytes were functionally versatile, due to the expression of a wide range of sensing receptors and several members of the AP-1 transcription factor family. The intermediate subset was distinguished by high expression of MHC class II associated genes. The nonclassical subset were most highly differentiated and defined by genes involved in cytoskeleton rearrangement that explains their highly motile patrolling behavior in vivo. Additionally, we identify unique surface markers, CLEC4D, IL-13RA1 for classical, GFRA2, CLEC10A for intermediate and GPR44 for nonclassical. Our study hence defines the fundamental features of monocyte subsets necessary for future research on monocyte heterogeneity.

Publication Title

Gene expression profiling reveals the defining features of the classical, intermediate, and nonclassical human monocyte subsets.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE45414
Low-dose actinomycin D preferentially disrupts EWS-FLI1DNA binding.
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Fusion of the EWS gene to FLI1 produces a fusion oncoprotein that drives an aberrant gene expression program responsible for the development of Ewing sarcoma. We used a homogenous proximity assay to screen for compounds that disrupt the binding of EWS-FLI1 to its cognate DNA targets. A number of DNA-binding chemotherapeutic agents were found to non-specifically disrupt protein binding to DNA. In contrast, actinomycin D was found to preferentially disrupt EWS-FLI1 binding by comparison to p53 binding to their respective cognate DNA targets in vitro. In cell-based assays, low concentrations of actinomycin preferentially blocked EWS-FLI1 binding to chromatin, and disrupted EWS-FLI1-mediated gene expression. Higher concentrations of actinomycin globally repressed transcription. These results demonstrate that actinomycin preferentially disrupts EWS-FLI1 binding to DNA at selected concentrations. Although the window between this preferential effect and global suppression is too narrow to exploit in a therapeutic manner, these results suggest that base-preferences may be exploited to find DNA-binding compounds that preferentially disrupt subclasses of transcription factors.

Publication Title

Differential disruption of EWS-FLI1 binding by DNA-binding agents.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE46928
Downstream Signaling Modeling of Cancer Signaling Pathways Enables Systematic Drug Respositioning for Subtypes of Breast Cancer Metastases
  • organism-icon Homo sapiens
  • sample-icon 51 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Gene Expression Profiling of Breast Cancer Patients with Brain Metastases Brain metastases confer the worst prognosis of breast cancer as no therapy exists that prevents or eliminates the cancer from spreading to the brain. We developed a new computational modeling method to derive specific downstream signaling pathways that reveal unknown target-disease connections and new mechanisms for specific cancer subtypes. The model enables us to reposition drugs based on available gene expression data of patients. We applied this model to repurpose known or shelved drugs for brain, lung, and bone metastases of breast cancer with the hypothesis that cancer subtypes have their own specific signaling mechanisms. To test the hypothesis, we addressed the specific CSBs for each metastasis that satisfy that (1) CSB proteins are activated by the maximal number of enriched signaling pathways specific to this metastasis, and (2) CSB proteins involve in the most differential expressed coding-genes specific to the specific breast cancer metastasis. The identified signaling networks for the three types of metastases contain 31, 15, and 18 proteins, respectively, and are used to reposition 15, 9, and 2 drug candidates for the brain, lung, and bone metastases of breast cancer. We performed in vitro and in vivo preclinical experiments as well as analysis on patient tumor specimens to evaluate the targets and repositioned drugs. Two known drugs, Sunitinib (FDA approved for renal cell carcinoma and imatinib-resistant gastrointestinal stromal tumor) and Dasatinib (FDA approved for chronic myelogenous leukemia (CML) after imatinib treatment and Philadelphia chromosome-positive acute lymphoblastic leukemia), were shown to prohibit the metastatic colonization in brain.

Publication Title

Novel modeling of cancer cell signaling pathways enables systematic drug repositioning for distinct breast cancer metastases.

Sample Metadata Fields

Time

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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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