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accession-icon GSE4885
Role of coactivator SRC-1/NcoA-1 for IL-6 target gene induction in HepG2 cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This experiment series addresses the role of coactivator SRC-1/NcoA-1 for the induction of interleukin-6 (IL-6) target genes in HepG2 cells. For that purpose, HepG2 human hepatocellular carcinoma cells were manipulated to stably express an shRNA that knocks down SRC-1 expression yielding the HepG2-Src1 cells. Either unmanipulated HepG2 or HepG2-Src1 cells were then treated for various periods with IL-6.

Publication Title

Co-activator SRC-1 is dispensable for transcriptional control by STAT3.

Sample Metadata Fields

No sample metadata fields

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accession-icon E-MEXP-401
Transcription profiling of mouse myoblast samples treated with a panel of compounds known to affect cellular differentiation or its reversal
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

A Single Cell Analysis of Myogenic Dedifferentiation Induced by Small Molecules An important direction in chemical biology is the derivation of compounds that affect cellular differentiation or its reversal. The fragmentation of multinucleate myofibers into viable mononucleates (called cellularisation) occurs during limb regeneration in urodele amphibians and the isolation of myoseverin, a tri-substituted purine that could apparently activate this pathway of myogenic dedifferentiation in mammalian cells, generated considerable interest. We have explored the mechanism and outcome of cellularisation at a single cell level, and report findings that significantly extend the previous work with myoseverin. Using a panel of compounds, including a novel triazine compound called 109 with structural similarity and comparable activity to myoseverin, we have identified microtubule disruption as critical for activation of the response. Our analysis has included the related control triazine compound 401, and the microtubule disrupting agent nocodazole. Time-lapse microscopy has enabled us to analyse the fate of identified mononucleate progeny, and directly assess the extent of dedifferentiation.

Publication Title

A single-cell analysis of myogenic dedifferentiation induced by small molecules.

Sample Metadata Fields

Specimen part, Cell line, Compound, Time

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accession-icon GSE4817
Sphingosine 1-phosphate effect on glioblastoma cells in vitro
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Abstract

Publication Title

Text mining of full-text journal articles combined with gene expression analysis reveals a relationship between sphingosine-1-phosphate and invasiveness of a glioblastoma cell line.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE40438
Gene expression profiling of resistant and vulnerable motor neuron subtypes in amyotrophic lateral sclerosis
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A consistent clinical feature of amyotrophic lateral sclerosis (ALS) is the sparing of eye movements. Pathological studies have confirmed that there is relative sparing of the cranial motor nuclei of the oculomotor, trochlear and abducens nerves, although pathological changes resembling those seen in anterior horn cells are present to a lesser degree. The aim of the present study is to combine LCM and microarray analysis to study the differences between motor neurons that are selectively resistant (oculomotor neurons) and those that are vulnerable (lumbar spinal motor neurons) to the disease process in amyotrophic lateral sclerosis.

Publication Title

Unravelling the enigma of selective vulnerability in neurodegeneration: motor neurons resistant to degeneration in ALS show distinct gene expression characteristics and decreased susceptibility to excitotoxicity.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE19332
Mutations in CHMP2B in lower motor neuron predominant amyotrophic lateral sclerosis (ALS)
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression profiling has been performed on motor cortex and spinal cord homogenates and of sporadic ALS cases and controls, to identify genes and pathways differentially expressed in ALS. More recent studies have combined the use of laser capture microdissection (LCM) with gene expression profiling to isolate the motor neurons from the surrounding cells, such as microglia and astrocytes, in order to determine those genes differentially expressed in the vulnerable cell population i.e. motor neuron.

Publication Title

Mutations in CHMP2B in lower motor neuron predominant amyotrophic lateral sclerosis (ALS).

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE15822
High-fat diet leads to tissue-specific changes reflecting risk factors for diseases in DBA/2J mice
  • organism-icon Mus musculus
  • sample-icon 96 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchip

Description

Analysis of tissues of DBA/2 mice fed a standard breeding diet (SBD) and high fat diet (HFD) revealed tissue specific roles in inflammation and disease, and altered communication between tissues. The tissues surveyed incuded adipose tissues (brown, inguinal, mesenteric, retro-peritoneal, subcutaneious and gonadal), muscle and liver.

Publication Title

High-fat diet leads to tissue-specific changes reflecting risk factors for diseases in DBA/2J mice.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE50813
Prevention of mammary tumor progression by silencing HoxA1 via intraductal injection of nanoparticle-formulated siRNA
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Silencing HoxA1 in vivo by intraductal delivery of nanoparticle-formulated siRNA reduced mammary tumor incidence by 75% , reduced cell proliferation, and prevented loss of ER and PR expression.

Publication Title

Silencing HoxA1 by intraductal injection of siRNA lipidoid nanoparticles prevents mammary tumor progression in mice.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE108904
Heart tissue expression data from dTGR rats treated with or without BAY 41-8543 and Sprague Dawley control rats
  • organism-icon Rattus norvegicus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 2.1 ST Array (ragene21st)

Description

We aimed to characterize the complex cardiovascular effects of NOsGC stimulation using NO-independent stimulator BAY 41-8543 in a double transgenic rat (dTGR) model of HFpEF.

Publication Title

Nitric oxide-sensitive guanylyl cyclase stimulation improves experimental heart failure with preserved ejection fraction.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon SRP136127
Nascent transcription of E14, PWWP2AKO, and PWWP2A/B DKO
  • organism-icon Mus musculus
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Transcriptional regulation by chromatin is a highly dynamic process directed through the recruitment and coordinated action of epigenetic modifiers and readers of these modifications. Using an unbiased proteomic approach to find interactors of H3K36me3, a modification enriched on active chromatin, here we identify PWWP2A and HDAC2 among the top interactors. PWWP2A and its paralog PWWP2B form a stable complex with NuRD subunits MTA1/2/3:HDAC1/2:RBBP4/7, but not with MBD2/3, p66a/ß, and CHD3/4. PWWP2A competes with MBD3 for binding to MTA1, thus defining a new variant NuRD complex that is mutually exclusive with the MBD2/3-containing NuRD. In mESCs, PWWP2A/B is most enriched at highly transcribed genes. Loss of PWWP2A/B leads to increases in histone acetylation predominantly at highly expressed genes, accompanied by decreases in Pol II elongation. Collectively, these findings suggest a role for PWWP2A/B in regulating transcription through the fine-tuning of histone acetylation dynamics at actively transcribed genes. Overall design: In order to explore the influence of PWWP2A/B on nascent transcription, we isolated the 4sU-labelled nascent transcripts, followed by deep sequencing. Three cell lines, E14, PWWP2A KO, and PWWP2A/B double knockout, and three biological replicates.

Publication Title

A variant NuRD complex containing PWWP2A/B excludes MBD2/3 to regulate transcription at active genes.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP106321
mRNA-seq data from murine colon adenomas and non-adenoma tissues
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We report that colon adenomas from ApcMin/+ mice not only exhibit similarities in gene expression profile to colon adenomas from azoxymethane / dextran sulfate sodium-treated mice (with activating Ctnnb1 mutations) due to the activation of canonical WNT signaling, but also unique transcriptional changes in the pathways regulating cell cycle progression / proliferation, chromosome segregation / cytoskeletal organization and apoptosis. Subsequent experiments characterized changes in gene expression unique to colon adenomas from ApcMin/+ mice including increases in the H2afv, Map6 and Nsmf transcripts. Overall design: Examination of gene expression profiles in 2 different colon adenoma types with activated canonical WNT signaling, relative to their respective non-adenoma controls

Publication Title

Mutational Mechanisms That Activate Wnt Signaling and Predict Outcomes in Colorectal Cancer Patients.

Sample Metadata Fields

Cell line, Treatment, Subject

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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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