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accession-icon GSE43010
HDAC Inhibitors induce tumor cell-selective pro-apoptotic transcriptional responses.
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The identification of recurrent somatic mutations in genes encoding epigenetic enzymes, coupled with biochemical studies demonstrating aberrant recruitment of epigenetic enzymes such as histone deacetylases (HDACs) and histone methyltransferases (HMTs) to promoter regions through association with oncogenic fusion proteins such as PML-RAR and AML1-ETO has provided a strong rationale for the development compounds that target the epigenome for the treatment of cancer. HDAC inhibitors (HDACi) are potent inducers of tumor cell apoptosis but it remains unclear why tumor cells are selectively sensitive to HDACi-induced cell death.

Publication Title

HDAC inhibitors induce tumor-cell-selective pro-apoptotic transcriptional responses.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE6189
Molecular Mechanisms of Early Response in Adaptive Cerebral Arteriogenesis
  • organism-icon Rattus norvegicus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

This study aims at a comprehensive understanding of the genomic program activated during early-phase of collateral vessel growth in a rat model for cerebral adaptive arteriogenesis (3-VO). While arteriogenesis constitutes a promising therapeutic concept for cerebrovascular ischemia, genomic profiles essential for therapeutic target identification were analysed solely for collateral arteries of the heart and periphery. Despite challenging anatomical conditions of the brain the 3-VO model allows identification of differentially expressed genes during adaptive cerebral arteriogenesis by selective removal of the posterior cerebral artery (PCA).

Publication Title

Induction of cerebral arteriogenesis leads to early-phase expression of protease inhibitors in growing collaterals of the brain.

Sample Metadata Fields

Age

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accession-icon GSE63012
Expression data from 2-3 month old brain-specific IB conditional knockout mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The activation of NFkB pathway is commonly observed in many neurodegenerative disease and contributes to the disease pathogenesis. However, with hundreds of target genes expressed in the brain, the mechanism of NFkB signaling transduction pathway is bearly understood.

Publication Title

NFκB-activated astroglial release of complement C3 compromises neuronal morphology and function associated with Alzheimer's disease.

Sample Metadata Fields

Specimen part

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accession-icon SRP065307
Gene expression profiling of sciatic nerves from Zeb2cKO and control mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We performed gene expression pofiling of Zeb2cKO and control sciatic nerves and identified significantly changed genes ZEB2 is also known as SIP1 Overall design: 4 RNA-Seq samples from P7 sciatic nerves of Ctrl and Zeb2 cKO mice (duplicatess, Ctrl and cKO)

Publication Title

Zeb2 recruits HDAC-NuRD to inhibit Notch and controls Schwann cell differentiation and remyelination.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP096081
A Histone Deacetylase 3-Dependent Pathway Delimits Peripheral Myelin Growth and Functional Regeneration [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Schwann cell remyelination defects impair functional restoration after nerve damage, contributing to peripheral neuropathies. The mechanisms that mediate remyelination block remain elusive. Upon small-molecule epigenetic screening, we identified HDAC3, a histone-modifying enzyme, as a potent inhibitor of peripheral myelinogenesis. Inhibition of HDAC3 markedly enhances myelin growth and regeneration, and improves functional recovery after peripheral nerve injury. HDAC3 antagonizes myelinogenic neuregulin/PI3K/AKT signaling axis. Moreover, genome-wide profiling analyses reveal that HDAC3 represses pro-myelinating programs through epigenetic silencing, while coordinating with p300 histone acetyltransferase to activate myelination-inhibitory programs that include HIPPO signaling effector TEAD4 to inhibit myelin growth. Schwann-cell-specific deletion of either Hdac3 or Tead4 results in a profound increase in myelin thickness in sciatic nerves. Thus, our findings identify the HDAC3-TEAD4 network as a dual-function switch of cell-intrinsic inhibitory machinery that counters myelinogenic signals and maintains peripheral myelin homeostasis, highlighting the therapeutic potential of transient HDAC3 inhibition for improving peripheral myelin repair. Overall design: 4 RNA-Seq samples from P6 sciatic nerves of Ctrl and Hdac3-cKO mice (Cnpcre-Ctrl, Cnpcre-cKO, Dhhcre-Ctrl, Dhhcre-cKO)

Publication Title

A histone deacetylase 3-dependent pathway delimits peripheral myelin growth and functional regeneration.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP021535
Minotaur is critical for primary piRNA biogenesis [RNA-Seq]
  • organism-icon Drosophila melanogaster
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

Piwi proteins and their associated small RNAs are essential for fertility in animals. This is due, in part, to their roles in guarding germ cell genomes against the activity of mobile genetic elements. piRNA populations direct Piwi proteins to silence transposon targets and as such form a molecular code that discriminates transposons from endogenous genes. Information ultimately carried by piRNAs is encoded within genomic loci, termed piRNA clusters. These give rise to long, single-stranded, primary transcripts that are processed into piRNAs. Despite the biological importance of this pathway, neither the characteristics that define a locus as a source of piRNAs nor the mechanisms that catalyze primary piRNA biogenesis are well understood. We searched an EMS-mutant collection annotated for fertility phenotypes for genes involved in the piRNA pathway. Twenty-seven homozygous-sterile strains showed transposon-silencing defects. One of these, which strongly impacted primary piRNA biogenesis, harbored a causal mutation in CG5508, a member of the Drosophila glycerol-3-phosphate O-acetyltransferase (GPAT) family. These enzymes catalyze the first acylation step on the path to the production of phosphatidic acid (PA). Though this pointed strongly to a function for phospholipid signaling in the piRNA pathway, a mutant form of CG5508, which lacks the GPAT active site, still functions in piRNA biogenesis. We have named this new biogenesis factor Minotaur. Overall design: Examination of transcriptom profile in heterozygous and homozygous CG5508 mutant ovaries

Publication Title

Minotaur is critical for primary piRNA biogenesis.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP021534
Minotaur is critical for primary piRNA biogenesis [smallRNA-Seq]
  • organism-icon Drosophila melanogaster
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

Piwi proteins and their associated small RNAs are essential for fertility in animals. This is due, in part, to their roles in guarding germ cell genomes against the activity of mobile genetic elements. piRNA populations direct Piwi proteins to silence transposon targets and as such form a molecular code that discriminates transposons from endogenous genes. Information ultimately carried by piRNAs is encoded within genomic loci, termed piRNA clusters. These give rise to long, single-stranded, primary transcripts that are processed into piRNAs. Despite the biological importance of this pathway, neither the characteristics that define a locus as a source of piRNAs nor the mechanisms that catalyze primary piRNA biogenesis are well understood. We searched an EMS-mutant collection annotated for fertility phenotypes for genes involved in the piRNA pathway. Twenty-seven homozygous-sterile strains showed transposon-silencing defects. One of these, which strongly impacted primary piRNA biogenesis, harbored a causal mutation in CG5508, a member of the Drosophila glycerol-3-phosphate O-acetyltransferase (GPAT) family. These enzymes catalyze the first acylation step on the path to the production of phosphatidic acid (PA). Though this pointed strongly to a function for phospholipid signaling in the piRNA pathway, a mutant form of CG5508, which lacks the GPAT active site, still functions in piRNA biogenesis. We have named this new biogenesis factor Minotaur. Overall design: Examination of small RNA profile in heterozygous and homozygous CG5508 mutant ovaries

Publication Title

Minotaur is critical for primary piRNA biogenesis.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE34552
Expression data from mouse kidney tissue
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The role of the renin-angiotensin system in chronic kidney disease involves multiple peptides and receptors. Exerting antipodal pathophysiological mechanisms, renin inhibition and AT1 antagonism ameliorate renal damage.

Publication Title

AT1 antagonism and renin inhibition in mice: pivotal role of targeting angiotensin II in chronic kidney disease.

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon SRP056636
Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type, 4L;C* and Isofagamine treated 4L;C* region specifics mouse brain Transcriptomes (RNA-Seq)
  • organism-icon Mus musculus
  • sample-icon 35 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived brain transcriptome profiling (RNA-seq) in neuropathic region specific Gaucher mouse brain compared with WT and Isofagamine treated mice of the same age and background and secondly to identify the DEmiRNA associated with the DEmRNA before and after treatment This will give us some insights to see if miRNA is also involved in the the regulation of the expression of the genes involved in the disease process before and after treatment. Methods: 42-45 days old 4L;C*, wild-type (WT) and Isofagamine treated 4L;C* mouse brain were generated by deep sequencing, in triplicate, using IlluminaHiseq. The sequence reads that passed quality filters were analyzed at the gene level with two methods: Burrows–Wheeler Aligner (BWA) followed and TopHat followed by DESeq. qRT–PCR validation was performed using TaqMan and SYBR Green assays Overall design: Regional brain mRNA profiles of ~42 -days old wild type (WT) and 4L;C* an d Isofagamine treated mice were generated by deep sequencing, in triplicate, using IlluminaHi Seq.

Publication Title

Signatures of post-zygotic structural genetic aberrations in the cells of histologically normal breast tissue that can predispose to sporadic breast cancer.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE71731
The impact of PPAR activation on whole genome gene expression in human precision-cut liver slices
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

Background: Studies in mice have shown that PPAR is an important regulator of lipid metabolism in liver and a key transcription factor involved in the adaptive response to fasting. However, much less is known about the role of PPAR in human liver. Here we set out to study the function of PPAR in human liver via analysis of whole genome gene regulation in human liver slices treated with the PPAR agonist Wy14643.

Publication Title

The impact of PPARα activation on whole genome gene expression in human precision cut liver slices.

Sample Metadata Fields

Sex, Specimen part, Treatment, Subject, Time

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)

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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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