refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
    0
github link
Build and Download Custom Datasets
refine.bio helps you build ready-to-use datasets with normalized transcriptome data from all of the world’s genetic databases.
Showing
of 184 results
Sort by

Filters

Technology

Platform

accession-icon GSE87223
Airn isoforms are important for the functions of cardiomyocytes
  • organism-icon Mus musculus
  • sample-icon 30 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

<i>Airn</i> Regulates Igf2bp2 Translation in Cardiomyocytes.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE87221
Airn isoforms are important for the functions of cardiomyocytes (RIP-chip-Igf2bp2)
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

To elucidate the function of Airn isoforms in the heart, we conducted RNA immunoprecipitation experiment followed by microarray (RIP-chip) in murine cardiomoycyte cell line HL-1.

Publication Title

<i>Airn</i> Regulates Igf2bp2 Translation in Cardiomyocytes.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE87222
Airn isoforms are important for the functions of cardiomyocytes (Gene_Array-Airn)
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

To elucidate the function of Airn isoforms in the heart, we conducted loss-of-function experiments in murine cardiomoycyte cell line HL-1.

Publication Title

<i>Airn</i> Regulates Igf2bp2 Translation in Cardiomyocytes.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE110147
Gene expression profiling of idiopathic pulmonary fibrosis and non-specific interstitial pneumonia
  • organism-icon Homo sapiens
  • sample-icon 46 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Idiopathic pulmonary fibrosis (IPF) and non-specific interstitial pneumonia (NSIP) are the 2 most common forms of idiopathic interstitial pneumonia. Response to therapy and prognosis are remarkably different. The clinical-radiographic distinction between IPF and NSIP may be challenging. We sought to investigate the gene expression profile of IPF vs. NSIP

Publication Title

Comprehensive gene expression profiling identifies distinct and overlapping transcriptional profiles in non-specific interstitial pneumonia and idiopathic pulmonary fibrosis.

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon GSE69530
A novel long non-coding RNA Myolinc regulates myogenesis through TDP-43 and Filip1
  • organism-icon Mus musculus
  • sample-icon 24 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 novel long non-coding RNA Myolinc regulates myogenesis through TDP-43 and Filip1.

Sample Metadata Fields

Cell line, Time

View Samples
accession-icon GSE69451
An Evolutionarily-Conserved Long Noncoding RNA Myolinc Regulates muscle differentiation [array_knockdown]
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Myogenesis is a complex process required for skeletal muscle formation during embryonic development and for regeneration and growth of myofibers in adults. Accumulating evidence suggests that long non-coding RNAs (lncRNAs) play key roles in regulating cell fate decision and function in various tissues. However, the role of lncRNAs in the regulation of myogenesis remains poorly understood. In this study, we identified a novel muscle-enriched lncRNA called "Myolinc (AK142388)", which we functionally characterized in the C2C12 myoblast cell line. Myolinc is predominately localized in the nucleus, and its levels increase upon induction of the differentiation. Knockdown of Myolinc impairs the expression of myogenic regulatory factors and formation of multinucleated myotubes in cultured myoblasts. Myolinc also regulates the expression of Filip1 in a cis-manner. Similar to Myolinc, knockdown of Filip1 inhibits myogenic differentiation. Furthermore, Myolinc binds to TAR DNA-binding protein 43 (TDP-43), a DNA/RNA-binding protein that regulates the expression of muscle genes (e.g. Acta1 and MyoD). Knockdown of TDP-43 inhibits myogenic differentiation. We also show that Myolinc-TDP-43 interaction is essential for the binding of TDP-43 to the promoter regions of muscle marker genes. Finally, we show that silencing of Myolinc inhibits skeletal muscle regeneration in adult mice. Altogether, our study identifies a novel lncRNA that controls key regulatory networks of myogenesis.

Publication Title

A novel long non-coding RNA Myolinc regulates myogenesis through TDP-43 and Filip1.

Sample Metadata Fields

Cell line, Time

View Samples
accession-icon GSE69455
An Evolutionarily-Conserved Long Noncoding RNA Myolinc Regulates muscle differentiation [array_overexpression]
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Myogenesis is a complex process required for skeletal muscle formation during embryonic development and for regeneration and growth of myofibers in adults. Accumulating evidence suggests that long non-coding RNAs (lncRNAs) play key roles in regulating cell fate decision and function in various tissues. However, the role of lncRNAs in the regulation of myogenesis remains poorly understood. In this study, we identified a novel muscle-enriched lncRNA called "Myolinc (AK142388)", which we functionally characterized in the C2C12 myoblast cell line. Myolinc is predominately localized in the nucleus, and its levels increase upon induction of the differentiation. Knockdown of Myolinc impairs the expression of myogenic regulatory factors and formation of multinucleated myotubes in cultured myoblasts. Myolinc also regulates the expression of Filip1 in a cis-manner. Similar to Myolinc, knockdown of Filip1 inhibits myogenic differentiation. Furthermore, Myolinc binds to TAR DNA-binding protein 43 (TDP-43), a DNA/RNA-binding protein that regulates the expression of muscle genes (e.g. Acta1 and MyoD). Knockdown of TDP-43 inhibits myogenic differentiation. We also show that Myolinc-TDP-43 interaction is essential for the binding of TDP-43 to the promoter regions of muscle marker genes. Finally, we show that silencing of Myolinc inhibits skeletal muscle regeneration in adult mice. Altogether, our study identifies a novel lncRNA that controls key regulatory networks of myogenesis.

Publication Title

A novel long non-coding RNA Myolinc regulates myogenesis through TDP-43 and Filip1.

Sample Metadata Fields

Cell line

View Samples
accession-icon SRP047289
Dosage compensation can buffer copy-number variation in wild yeast
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 59 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Illumina HiSeq 2500

Description

We show that aneuploidy is common in wild isolates of yeast, which are inherently tolerant to chromosome amplification and down-regulate expression at 40% of amplified genes.  To dissect the mechanism of this dosage response, we generated isogenic strain panels in which diploid cells carried either two, three, or four copies of the affected chromosomes.  Using a mixture of linear regression (MLR) model to classify genes, we find that expression is actively down regulated in proportion to increased gene copy at up to 30% of genes. Genes subject to dosage control are under higher expression constraint – but show elevated rates of gene amplification – in wild populations, suggesting that dosage compensation buffers copy number variation (CNV) at toxic genes Overall design: RNA-seq and transcriptome analysis of S. cerevisiae natural isolates having aneuploidy. Technical triplicate was performed for isogenic diploid strains having 2, 3 and 4 copies of a given chromosome (strain panels), while technical duplicate or singulate was performed on all other aneuploids.

Publication Title

Dosage compensation can buffer copy-number variation in wild yeast.

Sample Metadata Fields

Subject

View Samples
accession-icon GSE89997
Expression data from 2 cohorts of human pancreatic ductal adenocarcinoma (PDAC) tumors
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

In this dataset, we included expression data obtained from 30 resected human PDAC tumors, to examine what genes are differentially expressed in different cohorts that might lead to various outcomes

Publication Title

Identification of unique neoantigen qualities in long-term survivors of pancreatic cancer.

Sample Metadata Fields

Specimen part

View Samples
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

View Samples
...

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

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact