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accession-icon GSE18942
TAP-ORC2 and control ChIP experiments in Drosophila Kc167 cells
  • organism-icon Drosophila melanogaster
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Expression data from Kc167 cells under normal conditions. Used to assess expression levels of genes with ORC bound at promoter.

Publication Title

Drosophila ORC localizes to open chromatin and marks sites of cohesin complex loading.

Sample Metadata Fields

Cell line

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accession-icon SRP008977
Expression profile of third instar larval salivary gland tissue
  • organism-icon Drosophila melanogaster
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

We use mRNA-seq to transcriptionally profile larval salivary gland tissue from Drosophila third instar larvae. These data provide insights into tissue physiology and can be used to identify tissue specific transcripts. Overall design: Salivary glands were dissected from 200 wandering third instar larvae and the associated fat body was removed.Salivary glands were transferred to Graces unsupplemented medium on ice prior to RNA extraction with TRIzol reagent. mRNA-seq samples were prepared from 10 ug of total RNA and subject to Illumina based sequencing.

Publication Title

Developmental control of gene copy number by repression of replication initiation and fork progression.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP006898
Expression profile of 16C ovarian follicle cells
  • organism-icon Drosophila melanogaster
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

We use DSN normalized RNA-seq to transcriptionally profile FACS sorted 16C ovarian follicle cells. These data provide insights into the developmental control of gene expression programmed gene amplificaton. Overall design: Follicle cells were isolated from whole ovaries by trypsinization and filtering and stained with Hoescht. 16C follicle cells were isolated by FACS sorting based on DNA content (Hoescht). RNA was extracted with TRIzol reagent and 100ng of total RNA and used to generate a total library. This library was then subjected to DSN normalization prior to Illumina based sequencing.

Publication Title

Integrative analysis of gene amplification in Drosophila follicle cells: parameters of origin activation and repression.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE9088
Drosophila Myb-MuvB/dREAM
  • organism-icon Drosophila melanogaster
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome Array (drosgenome1)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genomic profiling and expression studies reveal both positive and negative activities for the Drosophila Myb MuvB/dREAM complex in proliferating cells.

Sample Metadata Fields

Treatment

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accession-icon GSE8751
Drosophila Myb-MuvB/dREAM (Expression data)
  • organism-icon Drosophila melanogaster
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome Array (drosgenome1)

Description

Myb-MuvB (MMB)/dREAM is a nine subunit complex first described in Drosophila as a repressor of transcription, dependent upon E2F2 and the RBFs. Myb, an integral member of MMB, curiously plays no role in the silencing of the test genes previously analyzed. Moreover, Myb plays an activating role in DNA replication in Drosophila egg chamber follicle cells. The essential functions for Myb are executed as part of MMB. This duality of function lead to the hypothesis that MMB, which contains both known activator and repressor proteins, might function as part of a switching mechanism that is dependent upon DNA sites and developmental context.

Publication Title

Genomic profiling and expression studies reveal both positive and negative activities for the Drosophila Myb MuvB/dREAM complex in proliferating cells.

Sample Metadata Fields

Treatment

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accession-icon SRP004454
X chromosome dosage compensation via enhanced transcriptional elongation in Drosophila males (Untreated)
  • organism-icon Drosophila melanogaster
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

MSL (Male-specific lethal) complex increases transcription on the single X chromosome of Drosophila males in order to equalize expression of X-linked genes between males (XY) and females (XX). The increase in transcript levels correlates with MSL- dependent acetylation of histone H4 at K16 within the bodies of active genes, but identification of the transcriptional step affected has not been possible. In this study, we use global run-on sequencing (GRO-seq) to examine the specific effect of MSL complex on RNA Polymerase II (RNAP II) on a genome-wide level. Results indicate that MSL complex enhances transcription by facilitating the progression of RNAP II across the bodies of active X-linked genes. Improving transcriptional output downstream of typical gene-specific control may explain how dosage compensation can be imposed on the diverse set of genes along an entire chromosome. Overall design: Global Run-On Sequencing (GRO-Seq) reads, i.e., RNA-Seq of nascent RNA transcripts, from D. Melanogaster SL2 cells. Two biological replicates were analyzed.

Publication Title

Comprehensive analysis of the chromatin landscape in Drosophila melanogaster.

Sample Metadata Fields

Subject

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accession-icon GSE61373
The molecular basis of analgesia in congenital insensitivity to pain associated with loss of Nav1.7 function
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Loss of function mutations in the SCN9a gene encoding voltage-gated sodium channel Nav1.7 cause congenital insensitivity to pain (CIP) and anosmia in otherwise normal humans and mice, suggesting that this channel may be a good analgesic drug target. Surprisingly, potent selective antagonists of Nav1.7 are weak analgesics. We therefore investigated whether Nav1.7 , as well as contributing to electrical signalling may have an additional function. Here we report that Nav1.7 deletion has profound effects on the sensory neuron transcriptome, leading to dysregulation of a number of transcription factors as well as upregulation of enkephalin precursor PENK mRNA and down regulation of CEACAM10 mRNA, a protein involved in noxious thermosensation. PENK mRNA is transcriptionally upregulated in Nav1.7 null mutant female sensory neurons, resulting in increased enkephalin expression in the dorsal horn of the spinal cord. PENK expression is down-regulated by addition of the sodium ionophore monensin, suggesting that sodium may play a role as a second messenger. Application of the opioid antagonist naloxone strongly enhances noxious peripheral input into the spinal cord, and dramatically reduces analgesia in both male and female Nav1.7 null mutant mice, as well as in human Nav1.7 null mutants. These data show that loss of Nav1.7 expression increases opioid drive over the lifetime of mice and humans. They further suggest that Nav1.7 channel blockers alone may not replicate the phenotype of null mutant humans and mice, but should be potentiated with exogenous opioids.

Publication Title

Endogenous opioids contribute to insensitivity to pain in humans and mice lacking sodium channel Nav1.7.

Sample Metadata Fields

Specimen part

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accession-icon GSE17784
Gene expression in FACS-purified cortical projection neurons
  • organism-icon Mus musculus
  • sample-icon 38 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302), Affymetrix Mouse Expression 430A Array (moe430a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Novel subtype-specific genes identify distinct subpopulations of callosal projection neurons.

Sample Metadata Fields

Specimen part

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accession-icon GSE47495
Transcriptional profiling of left ventricle and peripheral blood cells in rats with post-myocardial infarction
  • organism-icon Rattus norvegicus
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Myocardial infarction (MI) often results in left ventricular (LV) remodeling followed by heart failure (HF). It is of great clinical importance to understand the molecular mechanisms that trigger transition from compensated LV injury to HF and to identify relevant diagnostic biomarkers. In this study, we performed transcriptional profiling of LVs in rats with a wide range of experimentally induced infarct sizes and of peripheral blood mononuclear cells (PBMCs) in animals that developed HF.

Publication Title

Transcriptional profiling of left ventricle and peripheral blood mononuclear cells in a rat model of postinfarction heart failure.

Sample Metadata Fields

Specimen part

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accession-icon GSE17783
Analysis of gene expression in FACS-purified cortical projection neurons using Affymetrix 430 2.0 microarrays
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a), Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

3 subtypes of cortical projection neurons were purified by fluorescence-activated cell sorting (FACS) at 4 different stages of development from mouse cortex. A detailed description of the data set is described in Arlotta, P et al (2005) and Molyneaux, BJ et al (2009). The hybridization cocktails used here were originally applied to the Affymetrix mouse 430A arrays and submitted as GEO accession number GSE2039. The same hybridization cocktails were then applied to the Affymetrix mouse 430 2.0 arrays, and those data are contained in this series.

Publication Title

Novel subtype-specific genes identify distinct subpopulations of callosal projection neurons.

Sample Metadata Fields

Specimen part

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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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