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accession-icon SRP092788
RNA-seq transcriptome analysis in naïve and TNF-a-treated Sirt6-silenced YAMC cells to enrich for direct Sirt6 targets associated with inflammatory stimulation.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

By comparing Sirt6-silenced YAMC cells to siControl-transfected YAMC cells, we found that there were 916 and 1,026 differentially expressed genes in the naïve and TNF-a treatment conditions respectively. We also found that there were 302 genes that were co-expressed differentially in both naïve and TNF-a treatment conditions between Sirt6-silenced and siControl-transfected YAMC cells. Overall design: YAMC cells were transfected with Sirt6 siRNA (siSirt6, 50 nM) and negative control siRNA (siControl, 50 nM) respectively using lipofectamine 2000. Forty-eight hours after transfections, the cells were cultured with medium containing TNFa (100 ng/mL) and medium alone respectively for additional 24 h. At the end of treatments, cells were harvested for RNA extraction followed by RNA-seq transcriptome analysis.

Publication Title

Sirtuin-6 preserves R-spondin-1 expression and increases resistance of intestinal epithelium to injury in mice.

Alternate Accession IDs

GSE89620

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE8671
Transcriptome profile of human colorectal adenomas.
  • organism-icon Homo sapiens
  • sample-icon 61 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background: Colorectal cancers are believed to arise predominantly from adenomas. Although these precancerous lesions have been subjected to extensive clinical, pathological, and molecular analyses, little is currently known about the global gene expression changes accompanying their formation. Results: To characterize the molecular processes underlying the transformation of normal colonic epithelium, we compared the transcriptomes of 32 prospectively collected adenomas with those of normal mucosa from the same individuals. Important differences emerged not only between the expression profiles of normal and adenomatous tissues, but also between those of small and large adenomas. A key feature of the transformation process was the remodeling of the Wnt pathway reflected in patent over- and underexpression of 78 known components of this signaling cascade. Conclusions: Our transcriptomic profiles of normal colonic mucosa and colorectal adenomas shed new light on the early stages of colorectal tumorigenesis.

Publication Title

Transcriptome profile of human colorectal adenomas.

Alternate Accession IDs

E-GEOD-8671

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE62210
Depletion of p62 reduces nuclear inclusions and paradoxically ameliorates disease phenotypes in Huntingtons model mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Huntingtons disease (HD) is a dominantly inherited genetic disease caused by mutant huntingtin (htt) protein with expanded polyglutamine tracts. A neuropathological hallmark of HD is the presence of neuronal inclusions of mutant htt. p62 is an important regulatory protein in selective autophagy, a process by which aggregated proteins are degraded, and it is associated with several neurodegenerative disorders including HD. Here we investigated the effect of p62 depletion in three HD model mice: R6/2, HD190QG and HD120QG mice. We found that loss of p62 in these models led to longer lifespans and reduced nuclear inclusions, although cytoplasmic inclusions increased with polyglutamine length. In mouse embryonic fibroblasts (MEFs) with or without p62, mutant htt with a nuclear localization signal (NLS) showed no difference in nuclear inclusion between the two MEF types. In the case of mutant htt without NLS, however, p62 depletion increased cytoplasmic inclusions. Furthermore, to examine the effect of impaired autophagy in HD model mice, we crossed R6/2 mice with Atg5 conditional knockout mice. These mice also showed decreased nuclear inclusions and increased cytoplasmic inclusions, similar to HD mice lacking p62. These data suggest that the genetic ablation of p62 in HD model mice enhances cytoplasmic inclusion formation by interrupting autophagic clearance of polyQ inclusions. This reduces polyQ nuclear influx and paradoxically ameliorates disease phenotypes by decreasing toxic nuclear inclusions.

Publication Title

Depletion of p62 reduces nuclear inclusions and paradoxically ameliorates disease phenotypes in Huntington's model mice.

Alternate Accession IDs

E-GEOD-62210

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE42538
Knockdown of mineralocorticoid receptor or glucocorticoid receptor on human endometrial stromal cells and decidualization
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

To clarify mineralcorticoid receptor and glucocorticoid receptor-dependent gene networks in decidualizing human endometrial stromal cells.

Publication Title

Induction of 11β-HSD 1 and activation of distinct mineralocorticoid receptor- and glucocorticoid receptor-dependent gene networks in decidualizing human endometrial stromal cells.

Alternate Accession IDs

E-GEOD-42538

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon SRP096690
The transcription factor Foxo1 controls germinal center B cell proliferation in response to T cell help
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1500

Description

Germinal center (GC) B cells cycle between two states, the light zone (LZ) and the dark zone (DZ), and in the latter they proliferate and hypermutate their immunoglobulin genes. How this functional transition takes place is still controversial. In this study, we demonstrate that ablation of Foxo1 after GC development led to the loss of the DZ GC B cells and disruption of the GC architecture. Mechanistically, even upon provision of adequate T cell help, Foxo1-deficient GC B cells showed less proliferative expansion than controls. Moreover, we found that the transcription factor BATF was transiently induced in LZ GC B cells in a Foxo1-dependent manner and that deletion of BATF similarly led to GC disruption. Thus, our results are consistent with a model where the switch from the LZ to the DZ is triggered after receipt of T cell help, and suggest that Foxo1-mediated BATF up-regulation is at least partly involved in this switch. Overall design: mRNA profiles of wild-type DZ, LZ, and Foxo1-deficient GC B cells were generated by deep sequencing in triplicate, using Illumina HiSeq 1500.

Publication Title

The transcription factor Foxo1 controls germinal center B cell proliferation in response to T cell help.

Alternate Accession IDs

GSE93554

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE45665
Expression data (U133 Plus 2.0) from fibroblast like synoviocytes from patients with rheumatoid arthritis (RA-FLS) stimulated by DcR3
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Decoy receptor 3 (DcR3), a member of the tumor necrosis factor receptor (TNFR) superfamily, competitively binds and inhibits members of the TNF family, including Fas ligand (FasL), LIGHT, and TL1A. DcR3 was recently reported not only to act as a decoy receptor for these TNFRs but also to play a role as a ligand for the pathogenesis of RA.

Publication Title

Decoy receptor 3 regulates the expression of various genes in rheumatoid arthritis synovial fibroblasts.

Alternate Accession IDs

E-GEOD-45665

Sample Metadata Fields

Specimen part, Race

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accession-icon SRP073735
Total RNA-seq of HeLa cells upon conventional or improved RNA extraction
  • organism-icon Homo sapiens
  • sample-icon 46 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We devised a novel improved RNA extraction method, and performed total RNA-seq to determine the effect of improved RNA extraction. Overall design: Examination of total RNAs that were derived from the same cell/TRI Reagent solution, split into two and extracted by either a conventional or improved RNA extraction method. Hokkaido System Science, Co.

Publication Title

Unusual semi-extractability as a hallmark of nuclear body-associated architectural noncoding RNAs.

Alternate Accession IDs

GSE80589

Sample Metadata Fields

Subject

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accession-icon GSE11597
Expression data from chicken B cell lymphoma (DT40) cell lines.
  • organism-icon Gallus gallus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Genome Array (chicken)

Description

Global gene expression profiling of the avian B-lymphoma DT40 cell line was used as a model to differentiate among Btk KO and Btk KO cells reconstituted with human Btk. Differences in the gene expression pattern showed statistically significant changes between parental DT40 and all the Btk KO cell populations irrespective of whether they are reconstituted or not. These results imply that in the process of generating a knockout cell line, subclones are selected, which have multiple changes in their gene expression pattern (p<0.01).

Publication Title

Expression profiling of chicken DT40 lymphoma cells indicates clonal selection of knockout and gene reconstituted cells.

Alternate Accession IDs

E-GEOD-11597

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE24574
Expression data from BCL6-YFP-positive Tfh cells, BCL6-YFP-negative Tfh cells, non-Tfh cells, and nave helper T cells.
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We found that a number of Tfh cells downmodulated BCL6 protein after their development, and we sought to compare the gene expression between BCL6-hi Tfh cells and BCL6-low Tfh cells.

Publication Title

Bcl6 protein expression shapes pre-germinal center B cell dynamics and follicular helper T cell heterogeneity.

Alternate Accession IDs

E-GEOD-24574

Sample Metadata Fields

Specimen part

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accession-icon SRP102963
Identify novel muscle fusogenic factors for reconstitution of plasma membrane fusion in non-fusogenic cells
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina HiSeq 2000

Description

Overall goal: To identify genes that will cause non-fusogenic fibroblasts to become fusogenic. Purpose of analysis: To generate transcriptional profile of non-fusogenic fibroblasts, using 10T1/2 fibroblasts transduced with empty retrovirus as model. Experimental structure: The profile generated from the RNAseq analysis would be compared with transcriptional profile of MyoD-expressing fibroblasts (GEO DataSet GSE34907) to identify genes regulating fusion in muscle cells. Overall design: RNAseq analysis of total RNA from 10T1/2 fibroblasts transduced with retrovirus carrying empty pBabe-X retroviral vector was carried out to generate a transcriptional profile of a model of non-fusogenic fibroblasts.

Publication Title

Myomerger induces fusion of non-fusogenic cells and is required for skeletal muscle development.

Alternate Accession IDs

GSE97361

Sample Metadata Fields

Specimen part, Cell line, Subject

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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