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accession-icon E-MEXP-515
Transcription profiling of diabetic neuropathy in dorsal root ganglia from streptozotocin-diabetic male wistar rats over the first 8 weeks of diabetes
  • organism-icon Rattus norvegicus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302), UNKNOWN

Description

A study of diabetic neuropathy in dorsal root ganglia from streptozotocin-diabetic male wistar rats over the first 8 weeks of diabetes

Publication Title

Identification of changes in gene expression in dorsal root ganglia in diabetic neuropathy: correlation with functional deficits.

Alternate Accession IDs

None

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage, Time

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accession-icon GSE21578
Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP
  • organism-icon Homo sapiens
  • sample-icon 14 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

Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP.

Alternate Accession IDs

E-GEOD-21578

Sample Metadata Fields

Cell line

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accession-icon GSE21574
Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP: QKI data
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To assess whether the transcripts identified by PAR-CLIP are regulated by the RNA-binding protein (RBP) Quaking (QKI), we analyzed the mRNA levels of mock-transfected and QKI-specific siRNA-transfected cells with microarrays. Transcripts crosslinked to QKI were significantly upregulated upon siRNA transfection, indicating that QKI negatively regulates bound mRNAs (Figure 3H of PMID 20371350), consistent with previous reports of QKI being a repressor.

Publication Title

Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP.

Alternate Accession IDs

E-GEOD-21574

Sample Metadata Fields

Cell line

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accession-icon GSE21575
Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP: IGF2BP data
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To test the influence of IGF2BPs on the stability of their interacting mRNAs, as reported previously for some targets (Yisraeli, 2005), we simultaneously depleted all three IGF2BP family members using siRNAs and compared the cellular RNA from knockdown and mock-transfected cells on microarrays. The levels of transcripts identified by PAR-CLIP decreased in IGF2BP-depleted cells, indicating that IGF2BP proteins stabilize their target mRNAs. Moreover, transcripts that yielded clusters with the highest T to C mutation frequency were most destabilized (Figure 4G of PMID 20371350), indicating that the ranking criterion that we derived based on the analysis of PUM2 and QKI data generalizes to other RNA-binding proteins (RBPs).

Publication Title

Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP.

Alternate Accession IDs

E-GEOD-21575

Sample Metadata Fields

Cell line

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accession-icon GSE21577
Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP: miRNA inhibition data
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To obtain evidence that Argonaute (AGO) crosslink-centered regions (CCRs) indeed contain functional miRNA-binding sites, we blocked 25 of the most abundant miRNAs in HEK 293 cells (Figure 5C of PMID 20371350) by transfection of a cocktail of 2'-O-methyl-modified antisense oligoribonucleotides and monitored the changes in mRNA stability by microarrays (Figure 7A of PMID 20371350). Consistent with previous studies of individual miRNAs (Grimson et al., 2007), the magnitude of the destabilization effects of transcripts containing at least one CCR depended on the length of the seed-complementary region and dropped from 9-mer to 8-mer to 7-mer to 6-mer matches (Figure 7B of PMID 20371350). We did not find evidence for significant destabilization of transcripts that only contained imperfectly paired seed regions.

Publication Title

Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP.

Alternate Accession IDs

E-GEOD-21577

Sample Metadata Fields

Cell line

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accession-icon GSE61562
Murine Norovirus Effect on Cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Changes in gene expression on MNV infection of RAW264.7 cells

Publication Title

Murine norovirus replication induces G0/G1 cell cycle arrest in asynchronously growing cells.

Alternate Accession IDs

E-GEOD-61562

Sample Metadata Fields

Cell line

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accession-icon GSE35428
Transcriptional profiling of clinically relevant SERMs and SERM/estradiol complexes in a cellular model of breast cancer
  • organism-icon Homo sapiens
  • sample-icon 106 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In this study, we have utilized microarray analysis to directly compare a subset of structurally distinct, clinically relevant SERMs in the presence and absence of estradiol, using a high replicate number (10) to ensure detection of modestly regulated genes.

Publication Title

Research resource: Transcriptional profiling in a cellular model of breast cancer reveals functional and mechanistic differences between clinically relevant SERM and between SERM/estrogen complexes.

Alternate Accession IDs

E-GEOD-35428

Sample Metadata Fields

Cell line

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accession-icon GSE47346
Identification of differentially expressed genes due to LBH589 treatment in aromatase inhibitor-resistant tumors
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

In order to validate the utility of a novel pathway algorithm (BD-Func), we test if an LBH589 signature based data from 3 cell lines (GSE36509) in an independent experiment in vivo.

Publication Title

BD-Func: a streamlined algorithm for predicting activation and inhibition of pathways.

Alternate Accession IDs

E-GEOD-47346

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP092584
PC1/3 deficiency impacts POMC processing in human embryonic stem cell-derived hypothalamic neurons
  • organism-icon Homo sapiens
  • sample-icon 89 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We developed a technique for generating hypothalamic neurons from human pluripotent stem cells. Here, as proof-of-principle, we examine the use of these cells in modeling of a monogenic form of severe obesity: PCSK1 deficiency. We generated PCSK1 (PC1/3)-deficient human embryonic stem cell (hESC) lines using both shRNA and CRISPR-Cas9, and investigated pro-opiomelanocortin (POMC) processing using hESC-differentiated hypothalamic neurons. Overall design: We tried to idenitify transcripitional profiles and specific transcription factors that involved in of different stages during hypothalamic neuron differentiation from single cell sequencing for hESC-derived Day27 hypothalamic neurons, Day 12 neuron progenitors and undifferentiated stem cells

Publication Title

PC1/3 Deficiency Impacts Pro-opiomelanocortin Processing in Human Embryonic Stem Cell-Derived Hypothalamic Neurons.

Alternate Accession IDs

GSE89503

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon GSE38053
Host Response Signature to Staphylococcus aureus alpha-Hemolysin
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Staphylococcus aureus pneumonia causes significant morbidity and mortality. Alpha-hemolysin (Hla), a pore-forming cytotoxin of S. aureus, has been identified through animal models of pneumonia as a critical virulence factor that induces lung injury. In spite of considerable molecular knowledge of how this cytotoxin injures the host, the precise host response to Hla in the context of infection remains poorly understood. We employed whole-genome expression profiling of infected lung to define the host response to wild-type S. aureus compared with an Hla-deficient isogenic mutant in experimental pneumonia. These data provide a complete expression profile at four and at twenty-four hours post-infection, revealing a unique response to the toxin-expressing strain. Gene ontogeny analysis revealed significant differences in the extracellular matrix and cardiomyopathy pathways, both of which govern cellular interactions in the tissue microenvironment. Evaluation of individual transcript responses to Hla-secreting bacteria was notable for upregulation of host cytokine and chemokine genes, including the p19 subunit of interleukin-23. Consistent with this observation, the cellular immune response to infection was characterized by a prominent TH17 response to wild-type staphylococci. These findings define specific host mRNA responses to Hla-producing S. aureus, coupling the pulmonary TH17 response to the presence of this cytotoxin. Expression profiling to define the host response to a single virulence factor proved to be a valuable tool in identifying pathways for further investigation in S. aureus pneumonia. This approach may be broadly applicable to the study of bacterial toxins, defining host pathways that can be targeted to mitigate toxin-induced disease.

Publication Title

Host response signature to Staphylococcus aureus alpha-hemolysin implicates pulmonary Th17 response.

Alternate Accession IDs

E-GEOD-38053

Sample Metadata Fields

Sex, 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)

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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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