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accession-icon SRP063054
Circular RNAs are down-regulated in KRAS mutant colon cancer cells and can be transferred to exosomes
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Recent studies have shown that circular RNAs (circRNAs) are abundant, widely expressed in mammals, and can display cell-type specific expression. However, how production of circRNAs is regulated and their precise biological function remains largely unknown. To study how circRNAs might be regulated during colorectal cancer progression, we used three isogenic colon cancer cell lines that differ only in KRAS mutation status. Cellular RNAs from the parental DLD-1 cells that contain both wild-type and G13D mutant KRAS alleles and isogenically-matched derivative cell lines, DKO-1 (mutant KRAS allele only) and DKs-8 (wild-type KRAS allele only) were analyzed using RNA-Seq. We developed a bioinformatics pipeline to identify and evaluate circRNA candidates from RNA-Seq data. Hundreds of high-quality circRNA candidates were identified in each cell line. Remarkably, circRNAs were significantly down-regulated at a global level in DLD-1 and DKO-1 cells compared to DKs-8 cells, indicating a widespread effect of mutant KRAS on circRNA abundance. This finding was confirmed in two independent colon cancer cell lines HCT116 (KRAS mutant) and HKe3 (KRAS WT). In all three cell lines, circRNAs were also found in secreted extracellular-vesicles, and circRNAs were more abundant in exosomes than cells. Our results suggest that circRNAs may serve as promising cancer biomarkers. Overall design: RNAseq deep sequencing for both cell and exosome mRNAs

Publication Title

Circular RNAs are down-regulated in KRAS mutant colon cancer cells and can be transferred to exosomes.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE68608
C9ORF72 GGGGCC expanded repeats produce splicing dysregulation which correlates with disease severity in amyotrophic lateral sclerosis
  • 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

C9ORF72 GGGGCC Expanded Repeats Produce Splicing Dysregulation which Correlates with Disease Severity in Amyotrophic Lateral Sclerosis.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE68605
C9ORF72 GGGGCC expanded repeats produce splicing dysregulation which correlates with disease severity in amyotrophic lateral sclerosis [HG-U133_Plus_2]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Objective: An intronic GGGGCC-repeat expansion of C9ORF72 is the most common genetic variant of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. The mechanism of neurodegeneration is unknown, but a direct effect on RNA processing mediated by RNA foci transcribed from the repeat sequence has been proposed.

Publication Title

C9ORF72 GGGGCC Expanded Repeats Produce Splicing Dysregulation which Correlates with Disease Severity in Amyotrophic Lateral Sclerosis.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE56504
Loss of nuclear TDP-43 in ALS causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurons
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Loss of nuclear TDP-43 in amyotrophic lateral sclerosis (ALS) causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurones.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE33855
Loss of nuclear TDP-43 in ALS causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurons [fibroblasts]
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

Aims: Loss of nuclear TDP-43 characterises sporadic and most familial forms of amyotrophic lateral sclerosis (ALS). TDP-43 (encoded by TARDBP) has multiple roles in RNA processing. We aimed to determine whether 1) RNA splicing dysregulation is present in lower motor neurons in ALS and in a motor neuron-like cell model, and 2) TARDBP mutations (mtTARDBP) are associated with aberrant RNA splicing using patient-derived fibroblasts.

Publication Title

Loss of nuclear TDP-43 in amyotrophic lateral sclerosis (ALS) causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurones.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE56500
Loss of nuclear TDP-43 in ALS causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurons [LCM]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

Aims: Loss of nuclear TDP-43 characterises sporadic and most familial forms of amyotrophic lateral sclerosis (ALS). TDP-43 (encoded by TARDBP) has multiple roles in RNA processing. We aimed to determine whether 1) RNA splicing dysregulation is present in lower motor neurons in ALS and in a motor neuron-like cell model, and 2) TARDBP mutations (mtTARDBP) are associated with aberrant RNA splicing using patient-derived fibroblasts.

Publication Title

Loss of nuclear TDP-43 in amyotrophic lateral sclerosis (ALS) causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurones.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE11542
Expression data from rat mixed tissues samples
  • organism-icon Rattus norvegicus
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

To evaluate gene expression changes in mixed tissue samples used as process controls in male Sprague Dawley rats over time.

Publication Title

Assessment of repeated microarray experiments using mixed tissue RNA reference samples.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE44765
Global profiling of human hair follicle scalp dermal papilla cells using Affymetrix microarrays
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Dermal papilla cells isolated from the human hair follicle are capable of inducing hair growth in recipient epithelia. However, demonstrating disparity from rodent dermal papilla, human cells lose this inductive competance immediately upon growth in culture under normal growth conditions. We grew dermal papilla cells in hanging drop cultures that are morphologically akin to intact dermal papilla, and found that by enhancing the environment for aggregation, we could restore the inductive capacity of human dermal papilla cells in culture. The underlying genes that regulate the inductive potential of dermal papilla cells is not well understood, and we sought to use global profiling to identify key genes and pathways related to inductive competance within dermal papilla cells.

Publication Title

Microenvironmental reprogramming by three-dimensional culture enables dermal papilla cells to induce de novo human hair-follicle growth.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon GSE47820
Gene expression changes of Saccharomyces cerevisiae to linoleic acid hydroperoxide
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Reactive oxygen species, generated in vivo or exogenously encountered, constantly challenge living organisms. Oxidation of polyunsaturated fatty acids (PUFA), which are susceptible to oxidant attack, can lead to initiation of lipid peroxidation and in turn rapid production of toxic lipid hydroperoxides. Eukaryotic microorganisms such as Saccharomyces cerevisiae can survive harsh industrial conditions that contain high levels of the PUFA linoleic acid and its oxidised derivative, linoleic acid hydroperoxide (LoaOOH). The precise signalling and response mechanisms induced by yeast to overcome lipid hydroperoxide stress are ill understood.

Publication Title

Transcriptomic insights into the molecular response of Saccharomyces cerevisiae to linoleic acid hydroperoxide.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE19320
Zebrafish early eye development
  • organism-icon Danio rerio
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Gene expression profiling of zebrafish early eye development on 3 to 5 days post fertilization (dpf)

Publication Title

Integrating multiple genome annotation databases improves the interpretation of microarray gene expression data.

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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