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accession-icon GSE61399
Activation of the JAK/STAT pathway in Behcets Disease
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Th1/Th17-type T-cell responses are upregulated in Behcets disease (BD). However, signaling pathways associated with this aberrant immune response are not clarified. Whole-genome microarray profiling was performed with human U133 (Plus 2.0) chips using mRNA of isolated CD14+ monocytes and CD4+ T-cells from PBMC in patients with BD (n=9) and healthy controls (HC) (n=9). Flow cytometric analysis of unstimulated (US) and stimulated (PHA) STAT3 and pSTAT3 expressions of PBMCs were also analysed (BD and HC, both n=26). JAK1 was observed to be upregulated in both CD14+ monocytes (1.94 fold) and CD4+ T-lymphocytes (1.40 fold) of BD patients. Using canonical pathway enrichment analysis, JAK/STAT signaling was identified as activated in both CD14+ monocytes (p=2.95E-06) and in CD4+ lymphocytes (p=8.13E-04) in BD. Interferon (p=1.02E-07) and IL-6 (p=8.91E-03) signaling pathways were also prominent in CD14+ monocytes. Basal unstimulated total STAT3 expression was significantly higher in BD (1.2 vs 3.45, p<0.05). The JAK1/STAT3 signaling pathway is activated in BD, possibly through the activation of Th1/Th17-type cytokines such as IL-2, IFN, IL-6, IL-17 and IL-23.

Publication Title

Activation of the JAK/STAT pathway in Behcet's disease.

Alternate Accession IDs

E-GEOD-61399

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon SRP079913
Effects of the expression of a samble mutant of Kif1-Binding Protein (KBP) on the transcriptome of self-renewing ES cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Mouse ES cells were stably transduced with a lentivirus expressing either wild-type KBP or the stable mutant KBP(KK/RR) and maintained in self-renewing growth conditions. RNA-seq was performed to assess mRNA expression differences caused by the stabilization of KBP. Overall design: 6 samples [a triplicate set for ES cells expressing wild-type KBP and a triplicate set expressing KBP(KK/RR)] were analyzed.

Publication Title

The TDH-GCN5L1-Fbxo15-KBP axis limits mitochondrial biogenesis in mouse embryonic stem cells.

Alternate Accession IDs

GSE84861

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon SRP090923
Next-gen RNA sequencing of mouse osteosarcoma tumors
  • organism-icon Mus musculus
  • sample-icon 175 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Trascriptome analysis of osteosarcoma samples were performed Overall design: Tumor samples were obtained from a previously published Sleeping Beauty forward genetic screen, cell lines were derived from previous primary tumors and sequenced using Illumina HiSeq 2000

Publication Title

Comparative Transcriptome Analysis Quantifies Immune Cell Transcript Levels, Metastatic Progression, and Survival in Osteosarcoma.

Alternate Accession IDs

GSE87685

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP111653
CD95L derived si- and shRNAs kill cancer cells through an RNAi mechanism by targeting survival genes [shL3.shR6.RNAseq.lg]
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

The death receptor CD95/Fas can be activated by immune cells to kill cancer cells. However, most siRNAs or shRNAs targeting either CD95 or CD95L induce DICE (Death Induced by CD95/CD95L Elimination), a form of cell death in which a combination of different cell death pathways are activated, that is selective for transformed cells, and that preferentially affects cancer stem cells. We now provide evidence that both CD95 and CD95L are part of a network of genes that contain sequences that when expressed as either siRNAs or shRNAs are toxic to cancer cells. They act through canonical RNAi by targeting the 3''UTRs of critical survival genes. We propose that these embedded toxic sequences are part of a conserved mechanism that regulates cell death, and we predict the existence of endogenous siRNAs, that when produced, induce cell death to regulate genome fidelity. Our data have implications for cancer therapy and the use of RNAi. Overall design: 293T (shL3 site deleted) cells were infected with either pTIP-shScr or pTIP-shL3 and following puromycin selection large RNAs were analyzed by deep sequencing 50 or 100hrs after addition of doxycycline/HeyA8 (shR6 site deleted) cells were infected with either pLKO-shScr or pLKO-shR6 and following puromycin selection large RNAs were analyzed by deep sequencing 50 or 100hrs after addition of selection.

Publication Title

Many si/shRNAs can kill cancer cells by targeting multiple survival genes through an off-target mechanism.

Alternate Accession IDs

GSE101234

Sample Metadata Fields

Specimen part, Cell line, Subject, Time

View Samples
accession-icon SRP111526
CD95L derived si- and shRNAs kill cancer cells through an RNAi mechanism by targeting survival genes [shL1.RNAseq.lg]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

We provide evidence that shRNAs and siRNAs derived from CD95 and CD95L preferentially target the 3'' UTRs of survival genes culminating in a very robust mode of cell death we call DISE (Death Induced by Survival gene Elimination) Overall design: 293T cells were infected with either pTIP-shScr or pTIP-shL1 and following puromycin selection RNA was analyzed by deep sequencing 100hrs after addition of doxycycline

Publication Title

Many si/shRNAs can kill cancer cells by targeting multiple survival genes through an off-target mechanism.

Alternate Accession IDs

GSE101157

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject, Time

View Samples
accession-icon SRP080121
Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and FXRalpha-/- testicular Transcriptomes
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The goals of this study are to define the putatitve impacts of FXRalpha deficiency in testicular physiology Overall design: Testis mRNA profiles of 10-day old wild type (WT) and FXralpha-/- mice were generated by deep sequencing, on 5 individual mice for each geneotype, sequence on flowcell HS168.

Publication Title

The Bile Acid Nuclear Receptor FXRα Is a Critical Regulator of Mouse Germ Cell Fate.

Alternate Accession IDs

GSE84945

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon E-MTAB-3558
Transcription profiling by array of Arabidopsis swp73b-1 mutant
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

SWP73 subunits of SWI/SNF chromatin remodeling complexes (CRCs) are involved in key developmental pathways in Arabidopsis. We found, using microarray that inactivation of SWP73B caused altered expression of genes belonging to various regulatory pathways, including leaf and flower development. On the basis of this experiment and our other data we concluded that SWP73B modulates major developmental pathways.

Publication Title

SWP73 Subunits of Arabidopsis SWI/SNF Chromatin Remodeling Complexes Play Distinct Roles in Leaf and Flower Development.

Alternate Accession IDs

None

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE79681
Global transcriptional analysis reveals unique and shared responses in Arabidopsis thaliana exposed to combined drought and pathogen stress
  • organism-icon Arabidopsis thaliana
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Arabidopsis Gene 1.0 ST Array (aragene10st)

Description

With frequent fluctuations in global climate, plants often experience co-occurring dry-wet cycles and pathogen infection and this combination adversely affects plant survival. In the past, some studies indicated that morpho-physiological responses of plants to the combined stress are different from the individual stressed plants. However, interaction of drought stressed or drought recovered plants with pathogen has not been widely studied at molecular level. Such studies are important to understand the defense pathways that operate as part of combined stress tolerance mechanism. In this study, Arabidopsis plants were exposed to individual drought stress (soil drying at 40% FC, D), Pseudomonas syringae pv tomato DC3000 (PStDC3000), infection and their combination. Plants recovered from drought stress were also exposed to PStDC3000. Beside we have also infiltrated P. syringae pv tabaci (PSta, non-host pathogen) individually or in combination with drought stress. Using Affymetrix WT gene 1.0 ST array, global transcriptome profiling of plants leaves under individual drought stress and pathogen infection was compared with their combination. Results implicate that plants exposed to combined drought and pathogen stress experience a new state of stress where each combination of stressor and their timing defines the plant responses and thus should be studied explicitly.

Publication Title

Global Transcriptional Analysis Reveals Unique and Shared Responses in Arabidopsis thaliana Exposed to Combined Drought and Pathogen Stress.

Alternate Accession IDs

E-GEOD-79681

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE37165
Gene expression data from time course of fin regeneration in Danio rerio
  • organism-icon Danio rerio
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.

Alternate Accession IDs

E-GEOD-37165

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon GSE37164
Gene expression data from time course of fin regeneration in Danio rerio (part 2)
  • organism-icon Danio rerio
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Olsen et al (2010) have shown that induced Diabetes mellitus (DM) in adult Zebrafish results in an impairment of tissue regeneration as monitored by caudal fin regeneration. In those studies, streptozocin was used to induce hyperglycemia in adult zebrafish, and then, following streptozocin withdrawal, a recovery phase was allowed to re-establish euglycemia, due to pancreatic b-cell regeneration. DM-associated impaired fin regeneration continued indefinitely in the metabolic memory state (MM); allowing for subsequent molecular analysis of the underlying mechanisms of MM. This study focuses on elucidating the molecular basis explaining DM-associated impaired fin regeneration and why it persists into the MM state. The analysis of microarray data indicated that of the 14,900 transcripts analyzed, aberrant expression of 71 genes relating to tissue developmental and regeneration processes were identified in DM fish and the aberrant expression of these 71 genes persisted into the MM state. Key regulatory genes of major signal transduction pathways were identified among this group of 71; and therefore, these findings provide a possible explanation for how hyperglycemia induces impaired fin regeneration and why it continues into the MM state.

Publication Title

Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.

Alternate Accession IDs

E-GEOD-37164

Sample Metadata Fields

Specimen part, Disease, Disease stage

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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