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accession-icon GSE75802
Double-stranded microRNA mimics can induce length- and passenger strand-dependent effects in a cell type-specific manner (RNA 2015)
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Double-stranded microRNA mimics can induce length- and passenger strand-dependent effects in a cell type-specific manner.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE75800
Double-stranded microRNA mimics can induce length- and passenger strand-dependent effects in a cell type-specific manner (RNA 2015), Exp 1
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Experiment 1 - miR-155 and miR-199 Phenotype

Publication Title

Double-stranded microRNA mimics can induce length- and passenger strand-dependent effects in a cell type-specific manner.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE75801
Double-stranded microRNA mimics can induce length- and passenger strand-dependent effects in a cell type-specific manner (RNA 2015), Exp 2
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Experiment 2 - MiRNA mimics have a length and passenger strand specific effect

Publication Title

Double-stranded microRNA mimics can induce length- and passenger strand-dependent effects in a cell type-specific manner.

Sample Metadata Fields

Cell line

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accession-icon SRP090566
The transcription factor Sp3 cooperates with HDAC2 to regulate synaptic function and plasticity in neurons
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The histone deacetylase HDAC2, which negatively regulates neuronal plasticity and synaptic gene expression, is upregulated both in Alzheimer’s disease (AD) patients and mouse models (Graff et al., 2012). Therapeutics targeting HDAC2 are speculated to be a promising avenue for ameliorating AD related cognitive impairment. However, attempts to generate HDAC2-specific inhibitors have not been successful. Here, we take a novel approach utilizing integrative genomics to identify proteins that mediate HDAC2 recruitment to synaptic plasticity genes. Functional screening revealed that knockdown of the transcription factor Sp3 phenocopied HDAC2 knockdown, and that Sp3 facilitated the recruitment of HDAC2 to synaptic genes. Importantly, like HDAC2, Sp3 expression was elevated in AD patients and mouse models, where Sp3 knockdown ameliorated synaptic dysfunction. Furthermore, exogenous expression of an HDAC2 fragment containing the Sp3 binding domain fully restored synaptic plasticity and memory in a mouse model with severe neurodegeneration. Our findings indicate that targeting the HDAC2-Sp3 complex could enhance synaptic and cognitive function, without affecting HDAC2 function in other processes. Overall design: We profiled gene expression levels in primary neurons treated with HDAC2 or Sp3 shRNAs through RNA-Seq to examine whether HDAC2 and Sp3 cooperatively regulate a set of genes.

Publication Title

The Transcription Factor Sp3 Cooperates with HDAC2 to Regulate Synaptic Function and Plasticity in Neurons.

Sample Metadata Fields

Specimen part, Treatment, Subject

View Samples
accession-icon GSE48931
Master regulators of FGFR2 signalling and breast cancer risk
  • organism-icon Homo sapiens
  • sample-icon 260 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Master regulators of FGFR2 signalling and breast cancer risk.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE48927
Over-expression of FGFR2b from a tetracycline-inducible expression vector
  • organism-icon Homo sapiens
  • sample-icon 125 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Genome-wide association studies for breast cancer have identified over 80 different risk regions in the genome, with the FGFR2 locus consistently identified as the most strongly associated locus. However, we know little about the mechanisms by which the FGFR2 locus mediates risk or the pathways in which multiple risk loci may combine to cause disease. Here we use a systems biology approach to elucidate the regulatory networks operating in breast cancer and examine the role of FGFR2 in mediating risk. Using model systems we identify FGFR2-regulated genes and, combining variant set enrichment and eQTL analysis, show that these are preferentially linked to breast cancer risk loci. Our results support the concept that cancer-risk associated genes cluster in pathways

Publication Title

Master regulators of FGFR2 signalling and breast cancer risk.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE48925
Activation of FGFR2-kinase domain (iF2 construct)
  • organism-icon Homo sapiens
  • sample-icon 71 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Genome-wide association studies for breast cancer have identified over 80 different risk regions in the genome, with the FGFR2 locus consistently identified as the most strongly associated locus. However, we know little about the mechanisms by which the FGFR2 locus mediates risk or the pathways in which multiple risk loci may combine to cause disease. Here we use a systems biology approach to elucidate the regulatory networks operating in breast cancer and examine the role of FGFR2 in mediating risk. Using model systems we identify FGFR2-regulated genes and, combining variant set enrichment and eQTL analysis, show that these are preferentially linked to breast cancer risk loci. Our results support the concept that cancer-risk associated genes cluster in pathways

Publication Title

Master regulators of FGFR2 signalling and breast cancer risk.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE48924
Stimulation of endogenous FGFR1b and FGFR2b
  • organism-icon Homo sapiens
  • sample-icon 46 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Genome-wide association studies for breast cancer have identified over 80 different risk regions in the genome, with the FGFR2 locus consistently identified as the most strongly associated locus. However, we know little about the mechanisms by which the FGFR2 locus mediates risk or the pathways in which multiple risk loci may combine to cause disease. Here we use a systems biology approach to elucidate the regulatory networks operating in breast cancer and examine the role of FGFR2 in mediating risk. Using model systems we identify FGFR2-regulated genes and, combining variant set enrichment and eQTL analysis, show that these are preferentially linked to breast cancer risk loci. Our results support the concept that cancer-risk associated genes cluster in pathways

Publication Title

Master regulators of FGFR2 signalling and breast cancer risk.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE48928
Knockdown of breast cancer master regulators: siRNA targeting PTTG1 and SPDEF in MCF-7 cells.
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Genome-wide association studies for breast cancer have identified over 80 different risk regions in the genome, with the FGFR2 locus consistently identified as the most strongly associated locus. However, we know little about the mechanisms by which the FGFR2 locus mediates risk or the pathways in which multiple risk loci may combine to cause disease. Here we use a systems biology approach to elucidate the regulatory networks operating in breast cancer and examine the role of FGFR2 in mediating risk. Using model systems we identify FGFR2-regulated genes and, combining variant set enrichment and eQTL analysis, show that these are preferentially linked to breast cancer risk loci. Our results support the concept that cancer-risk associated genes cluster in pathways

Publication Title

Master regulators of FGFR2 signalling and breast cancer risk.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP065965
Gene expression profile in Ronin (Thap11) conditional knock out retina through RNA-sequencing
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Conditional knockout of the transcription factor Ronin (Thap11) in retinal progenitor cells (RPCs) results in a profound failure cell proliferation resulting in a hypoplastic adult retina that also suffers from photoreceptor degeneration. The goal of this study was to determine which genes are deregulated in response to loss of Ronin transcription factor activity in the developing retina. We generated Ronin flox/flox (Control) and Chx10-Cre::GFP+/tg; Ronin flox/flox (CKO) mice, in which Ronin loss occurs specifically within RPCs, and performed RNA-Seq analysis of embryonic day E14.5 (E14.5) retinae. Three independent pools of control and Ronin CKO retinae were collected consisting of a minimum of 10 retinae per pool and total RNA was extracted followed by polyA selection, fractionation (200-500 nucleotide range) and generation of cDNA. The resulting DNA was then used for standard Illumina adaptor ligation and sequencing. This experiment revealed decreased expression of a large group of mitochondrial genes including components of the electron transport chain (ETC), which have been recently implicated as direct regulators of the cell cycle. Overall design: Retinal mRNA profiles of embryonic day 14.5 (E14.5) Control (Ronin flox/flox) and Ronin CKO (Chx10-Cre::GFP+/tg; Ronin flox/flox) mice were generated by deep sequencing, in triplicate using Illumina HiSeq2500

Publication Title

RONIN Is an Essential Transcriptional Regulator of Genes Required for Mitochondrial Function in the Developing Retina.

Sample Metadata Fields

Specimen part, 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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