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accession-icon GSE12100
hsa-mir-26b and hsa-mir-98 overexpression
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

MicroRNA target prediction by expression analysis of host genes.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE51236
Expression data from MTF mutant roots
  • organism-icon Arabidopsis thaliana
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Mutation of MTF in Arabidopsis increases Agrobacterium-mediated transformation susceptibility. Being a putative transcription factor, different genes controlling transformation may be regulated by MTF.

Publication Title

Cytokinins secreted by Agrobacterium promote transformation by repressing a plant myb transcription factor.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE12091
Profiling gene expression in HeLa cells by hsa-mir-26b overexpression
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Total RNA samples from three biological replicates in which the hsa-mir-26b was overexpressed in HeLa cells were profiled by gene expression. As negative control, we used total RNA samples from HeLa cells transfected with cel-mir-67

Publication Title

MicroRNA target prediction by expression analysis of host genes.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE12092
Profiling gene expression in HeLa cells by hsa-mir-98 overexpression
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Total RNA samples from three biological replicates in which the hsa-mir-98 was overexpressed in HeLa cells were profiled by gene expression. As negative control, we used total RNA samples from HeLa cells transfected with cel-mir-67

Publication Title

MicroRNA target prediction by expression analysis of host genes.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE53480
Expression data from Tg4510 and Wild-type mice after AAVTFEB injection
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We used microarrays to detail the global programme of gene expression after 4 months of TFEB overexpression in the brain.

Publication Title

Selective clearance of aberrant tau proteins and rescue of neurotoxicity by transcription factor EB.

Sample Metadata Fields

Specimen part, Treatment

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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

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accession-icon SRP061429
How C/EBPa creates an elite cell state for reprogramming to pluripotency [RNAseq]
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Mouse Bcell, upon ectopic expression of the transcription factor Cebpa for 18h, can be reprogrammed to iPS with extremely high efficiency. To understand the molecular control of this phenomena we performed multiple high throughtput functionnal genomic analysis. Overall design: Transcriptomic by RNAseqencing (polyA+, non stranded) in Bcell, Bcell+Cebpa18h, Bcell+Cebpa18h+OKSM1d, Bcell+Cebpa18h+OKSM2d, ES cells

Publication Title

C/EBPα creates elite cells for iPSC reprogramming by upregulating Klf4 and increasing the levels of Lsd1 and Brd4.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP095604
Genome-wide transcriptome profiles in Control and Schizophrenia hiPSC-dervied NPC [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We Report the genome-wide RNA expression levels in control and schizophrenia hiPSC dervied NPC treated with neuronal media for 2 days. In total about 15,000 gene expression were detected in all samples, of which 1349 were dysregualted. Overall design: Examination, identification and comparision of mRNA expression profliles in control and schizophrenia npc

Publication Title

Common developmental genome deprogramming in schizophrenia - Role of Integrative Nuclear FGFR1 Signaling (INFS).

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon SRP162537
AMPK activation protects against diet induced obesity through Ucp1-independent thermogenesis in subcutaneous white adipose
  • organism-icon Mus musculus
  • sample-icon 111 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Purpose: To investigate alterations in subcutaneous white adipose gene expression induced by genetic AMPK activation in vivo, in mice fed a chow or a high-fat diet. Methods: Subcutaneous white adipose tissue mRNA profiles of wild-type transgenic (WT-Tg) mice and mice expressing a gain-of-function AMPK mutant gamma1 subunit (D316A-Tg) were generated by deep sequencing. Results: RNA sequencing revealed over 3000 differentially expressed genes between WT-Tg and D316A-Tg subcutaneous white adipose tissue (WATsc) from mice fed a high fat diet (HFD), of which many were classified as 'skeletal muscle-associated'. Interestingly, uncoupling protein 1 (UCP1), associated with 'beige' adipocyte formation in WATsc, was not differentially expressed. On a chow diet, many differentially expressed genes were also identified, with gene ontology analysis identifiying glycolysis, TCA cycle and brown fat differentiation as highly enriched; key features of brown adipocyte identity. HFD-associated skeletal-muscle associated gene expression was either not significantly altered, or significantly down-regulated on a chow diet, indicating a diet-induced gene signature in D316A-Tg WATsc. Conclusions: Our study revealed gene signatures indicative of brown adipocyte development on a chow diet, where no overt metabolic phenotype was observed in gain-of-function animals. When fed a HFD, WATsc from D316A-Tg mice displayed a muscle-like gene signature, expressing key components of creatine and calcium thermogenic cycles including Ckmt2 (creatine kinase, mitochondrial 2) Atp2a1 (SERCA1-sarco/endoplasmic reticulum ATPase 1) and ryr1 (ryanodine receptor 1). UCP1 expression was not altered between WT-Tg and D316A-Tg mice fed a HFD. Our findings suggest a novel role for AMPK in the regulation of white adipocyte identity and a potentially novel cell population that, when metabolically challenged, preferrentially utilise muscle-like thermogenic futile cycles independent of UCP1 to mediate whole organism energy expenditure. Overall design: Whole subcutaneous white adipose tissue mRNA profiles were generated from mice fed either chow or 45% high-fat diet.

Publication Title

AMPK activation protects against diet induced obesity through Ucp1-independent thermogenesis in subcutaneous white adipose tissue.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

View Samples
accession-icon GSE39733
Microarray analysis of gene expression changes in human A549 lung cancer cells upon siRNA knockdown of FAM60A and SDS3
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The Sin3 histone deacetylase (HDAC) complex is a 1.2 MDa chromatin modifying complex that can repress transcription by binding to gene promoters and deacetylating histones. The Sin3/HDAC complex can affect cell cycle progression through multiple mechanisms and is among the targets of anticancer drugs, called HDAC inhibitors. We describe the identification of a new subunit of the Sin3 complex named family with sequence similarity 60 member A (FAM60A). We show that FAM60A/Sin3 complexes normally suppress the epithelial-to-mesenchymal transition (EMT) and cell migration. This occurs through transcriptional repression of genes that encode components of the TGF-beta signaling pathway. This work reveals that FAM60A and the Sin3 complex are upstream repressors of TGF-beta signaling, EMT and cell migration and extends the known biological roles of the Sin3 complex. This experiment investigates the role of FAM60A in gene expression by comparing A549 lung cancer cells treated with or without siRNA against FAM60A.

Publication Title

Human family with sequence similarity 60 member A (FAM60A) protein: a new subunit of the Sin3 deacetylase complex.

Sample Metadata Fields

Specimen part, Cell line

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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