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accession-icon GSE72755
Toxicogenomics on mice liver of coumarins from Calophyllum brasiliense
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

A toxicogenomic analysis from liver of different pharmacological active coumarins (mammea A/BA+A/BB 3:1 and soulatrolide ) was performed on mice treated (20mg/kg/daily) for a whole week to evaluate if such compounds possess or could develop a hazardous profile on liver.

Publication Title

Toxicogenomic analysis of pharmacological active coumarins isolated from Calophyllum brasiliense.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE72157
Expression data from pooled biological replicates (n=6) from MEF2D knockdown in neonatal rat ventricular myocytes (NRVMs)
  • organism-icon Rattus norvegicus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Differentiation and maintenance of cardiac muscle is a complex biological process. MEF2D appears to play an important role in the regulation of cardiomyocyte homeostasis.

Publication Title

MEF2D deficiency in neonatal cardiomyocytes triggers cell cycle re-entry and programmed cell death in vitro.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE63798
Expression data from individual MEF2A isoform knockdown in C2C12 myotubes
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Differentiation of muscle tissue is regulated by a complex network of transcription factors. The MEF2 family of transcription factors are important players in muscle development and differentiation.

Publication Title

MEF2 transcription factors regulate distinct gene programs in mammalian skeletal muscle differentiation.

Sample Metadata Fields

Cell line

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accession-icon GSE41871
Dysregulated gene expression in Mef2a knockout mice subjected to cardiotoxin-induced muscle injury
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We identified genes expressed in mouse skeletal muscle, during the process of muscle regeneration after injury, which are dysregulated in the absence of Mef2a expression. MEF2A is a member of the evolutionarily conserved MEF2 transcription factor family which has known roles in cardiac muscle development and function, but is not well studied in skeletal muscle. We performed a comparison of gene expression profiles in wild type and MEF2A knockout tibialis anterior muscle, seven days post-injury with cardiotoxin. The results indicated that a variety of genes expressed during muscle regeneration, predominantly microRNAs in the Gtl2-Dio3 locus, are dysregulated by the loss of MEF2A expression.

Publication Title

MEF2A regulates the Gtl2-Dio3 microRNA mega-cluster to modulate WNT signaling in skeletal muscle regeneration.

Sample Metadata Fields

Specimen part

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accession-icon SRP172824
RNA-seq of WT and Nocturnin knockout A549 cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

mRNA regulation by the circadian protein Nocturnin in A549 cells. Overall design: Total RNA from WT and NOCT KO A549 cells were subject to poly-A pulldown and RNA-seq.

Publication Title

The metabolites NADP<sup>+</sup> and NADPH are the targets of the circadian protein Nocturnin (Curled).

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE32892
A genome-wide and dose-dependent inhibition map of androgen receptor binding by small molecules reveals its regulatory program upon antagonism
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The androgen receptor plays a critical role throughout the progression of prostate cancer and is an important drug target for this disease. While chromatin immunoprecipitation coupled with massively parallel sequencing (ChIP-Seq) is becoming an essential tool in studying transcription and chromatin modification factors, it has rarely been employed in the context of drug discovery. Here we report the first publicly available genome-wide and dose-dependent inhibition landscape of AR binding by drug-like small molecules including correlation with binding strength using ChIP-Seq. Integration of sequence analysis, transcriptome profiling, cell viability assays and in vivo tumor inhibition studies enabled us to establish a direct cistrome-activity relationship for two novel potent AR antagonists. By selectively occupying the strongest binding sites, AR signaling remains active even when low androgen levels are low, a scenario characteristic of first-line androgen ablation therapy. Coupled cistrome and transcriptome profiling upon small molecule antagonism led to the identification of not only key direct downstream effectors of AR but also their mode of regulation: unbiased pathway mapping revealed that AR is a key modulator of steroid metabolism by forming a tightly controlled feedback loop with other nuclear receptor family members. Furthermore, we found AR has an extensive role in negative gene regulation and estrogen (related) receptor likely mediates its function as a transcriptional repressor. In conclusion, our study provides a global and dynamic view of ARs regulatory program upon antagonism, which may serve as a molecular basis for deciphering and developing AR therapeutics.

Publication Title

Dose-dependent effects of small-molecule antagonists on the genomic landscape of androgen receptor binding.

Sample Metadata Fields

Treatment

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accession-icon GSE93832
Lipid Nanoparticle-Mediated Delivery of Anti-miR-17 Family Oligonucleotide Suppresses Hepatocellular Carcinoma Growth
  • organism-icon Homo sapiens
  • sample-icon 6 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

Lipid Nanoparticle-Mediated Delivery of Anti-miR-17 Family Oligonucleotide Suppresses Hepatocellular Carcinoma Growth.

Sample Metadata Fields

Cell line

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accession-icon SRP097126
mRNA Profiling of miR-17 family inhibition using TuD lentiviral vector in HepG2 and SK-Hep1 hepatocellular carcinoma cell lines [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

To functionally characterize the role of miR-17 family in HCC, lentiviral vector-based miR inhibitor TuD was used to inhibit miR-17 family of microRNAs in HepG2 and SK-Hep1 HCC cell lines Overall design: Methods: HepG2 and SK-Hep1 HCC cell lines were acquired from American Type Culture Collection (ATCC) and miR-17 TuD or NC TuD expressing lines were generated. mRNA profiling of miR-17 TuD or NC TuD expressing samples was performed using Illumina NGS. Total RNA was extracted as per manufacturer’s instructions (RNeasy kit, Qiagen). RNA quality was assessed using BioAnalyzer (Agilent). mRNA expression profiles were determined using next-generation sequencing (NGS) on the Illumina HiSeq 2000 platform producing 50bp paired-end reads. Bowtie/TopHat suites were used to align the reads to mouse genome or transcriptome and RSEM were used to quantify gene abundances. Gene level counts were then normalized with the R/Bioconductor package limma using the voom/variance stabilization method.

Publication Title

Lipid Nanoparticle-Mediated Delivery of Anti-miR-17 Family Oligonucleotide Suppresses Hepatocellular Carcinoma Growth.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE93799
mRNA Profiling of miR-17 family inhibition using TuD lentiviral vector in Hep3B hepatocellular carcinoma cell line [array]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To functionally characterize the role of miR-17 family in HCC, lentiviral vector-based miR inhibitor TuD was used to inhibit miR-17 family of microRNAs in Hep3B cell line

Publication Title

Lipid Nanoparticle-Mediated Delivery of Anti-miR-17 Family Oligonucleotide Suppresses Hepatocellular Carcinoma Growth.

Sample Metadata Fields

Cell line

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accession-icon SRP037533
Transcriptional reprogramming of engineered cellobiose-utilizing Saccharomyces cerevisiae in response to cellobiose revealed by RNA-Seq
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

Saccharomyces cerevisiae cannot metabolize cellobiose in nature. Here, S. cerevisiae was engineered to achieve cellobiose utilization by introducing both a cellodextrin transporter gene (cdt-1) and an intracellular ß-glucosidase gene (gh1-1) from Neurospora crassa. We sequenced mRNA from anaerobic exponential cultures of engineered S. cerevisiae grown on cellobiose or glucose as a single carbon source in biological triplicate. Differences in gene expression between cellobiose and glucose metabolism revealed by RNA deep sequencing indicated that cellobiose metabolism induced mitochondrial activation and reduced amino acid biosynthesis under fermentation conditions. Overall design: mRNA levels in cellobiose-grown and glucose-grown cells of engineered cellobiose-utilizing Saccharomyces cerevisiae were examined by deep sequencing, in triplicate, using Illumina Genome Analyzer-II. We sequenced 3 samples from cellobiose-grown cells and 3 samples from glucose-grown cells and identified differential expressions in the cellobiose versus glucose fermentations by using mRNA levels of glucose-grown cells as a reference.

Publication Title

Leveraging transcription factors to speed cellobiose fermentation by Saccharomyces cerevisiae.

Sample Metadata Fields

Cell line, Subject

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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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