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accession-icon GSE32540
Identification of novel tissue-specific transcription arising from E-cadherin/CDH1 intron2: a novel protein isoform increases gastric cancer cell invasion and angiogenesis.
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

E-cadherin, a protein encoded by the CDH1 gene is the dominant epithelial cell adhesion molecule playing a crucial role in epithelial tissue polarity and structural integrity. The progression of 90% or more carcinomas is believed to be mediated by disruption of normal E-cadherin expression, subcellular localization or function. Despite the strong correlation between E-cadherin loss and malignancy the mechanism through how this occurs is not known in most sporadic and hereditary epithelial carcinomas. Previous works have shown the importance of CDH1 intron 2 sequences for proper gene and protein expression supporting the possibility of these being cis-modulators of E-cadherin expression/function. but when co-expressed it led to reduced cell-cell adhesiveness, increased invasion and angiogenesis. By expression array analysis, IFITM1 and IFI27 levels were found to be increased upon CDH1a overexpression. Importantly, CDH1a was found to be de novo expressed in gastric cancer cell lines when compared to normal stomach.

Publication Title

Transcription initiation arising from E-cadherin/CDH1 intron2: a novel protein isoform that increases gastric cancer cell invasion and angiogenesis.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP105773
Gene expression profiling of the octuple jazQ mycT mutant shows that the MYC transcription factors control expression of many genes mis-regulated in jazQ, and also identifies some MYC-indepedent expression changes
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The quintuple jaz mutant jazQ and the triple myc mutant mycT affect plant defense and growth. We used RNA-sequencing to query the transcriptomes of jazQ and mycT, as well as the combined jazQ mycT octuple mutatant, and examined how these mutations alter the expression of genes mis-regulated in jazQ. The data highlight how jasmonate signaling pathways are largely governed by MYC transcription factors, but also highlight some MYC-independent expression patterns. Overall design: Analysis of Col-0 (wildtype), jazQ, mycT, and jazQ mycT (four genotypes), with three biological replicates per genotype - 12 total samples. This series contains the re-use of 6 samples from GSE79012 (Col-0 and jazQ).

Publication Title

Regulation of growth-defense balance by the JASMONATE ZIM-DOMAIN (JAZ)-MYC transcriptional module.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon E-MTAB-4908
Transcriptional responses in bovine skin during blood feeding of the cattle tick, Rhipicephalus microplus
  • organism-icon Bos indicus, Bos taurus
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Bovine Genome Array (bovine)

Description

We examined gene expression induced by Rhipicephalus microplus bites on host skin of tick-resistant and tick-susceptible breeds of bovines, Nelore and Holstein respectively, when they underwent a primary infestation.

Publication Title

Immune and biochemical responses in skin differ between bovine hosts genetically susceptible and resistant to the cattle tick Rhipicephalus microplus.

Sample Metadata Fields

Sex, Specimen part, Subject, Time

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accession-icon GSE22255
Blood genomic expression profile for ischemic stroke (IS)
  • organism-icon Homo sapiens
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Stroke is a brain attack cutting off vital blood, and consequently the nutrients and oxygen vital to the brain cells that control everything we do. Stroke is a complex disease with unclear pathogenesis resulting from environmental and genetic factors.

Publication Title

TTC7B emerges as a novel risk factor for ischemic stroke through the convergence of several genome-wide approaches.

Sample Metadata Fields

Sex

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accession-icon SRP058128
Montelukast counteracts the influenza virus-induced block in unfolded protein stress response and reduces virus multiplication
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Influenza A viruses generate annual epidemics and occasional pandemics of respiratory disease with important consequences for human health and economy. Therefore, a large effort has been devoted to the development of new anti-influenza drugs directed to viral targets, as well as to the identification of cellular targets amenable for anti-influenza therapy. Here we describe a new approach to identify such potential cellular targets by screening collections of drugs approved for human use. We reasoned that this would most probably ensure addressing a cellular target and, if successful, the compound would have a well known pharmacological profile. In addition, we reasoned that a screening using a GFP-based recombinant replicon system would address virus trancription/replication and/or gene expression, and hence address a stage in virus infection more useful for inhibition. By using such strategy we identified Montelukast as an inhibitor of virus gene expression, which reduced virus multiplication in virus-infected cells but did not alter virus RNA synthesis in vitro or viral RNA accumulation in vivo. By deep sequencing of RNA isolated from mock- and virus-infected human cells, treated or not with Montelukast, we identified the PERK-mediated unfolded protein response as the pathway responsible for Montelukast action. Accordingly, PERK phosphorylation was inhibited in infected cells but stimulated in Montelukast-treated cells. These results suggest the PERK-mediated unfolded protein response as a potential cellular target to modulate influenza virus infection. Overall design: Comparison of gene expression measured by deep sequencing (single-ends, 50nt, RNA-seq) of "Infected", "Not infected", "Infected+Montelukast" and "Not infect+Montelukast" in human A549 cells. Infected means "Infected with influenza virus".

Publication Title

Chemical Genomics Identifies the PERK-Mediated Unfolded Protein Stress Response as a Cellular Target for Influenza Virus Inhibition.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE44053
Identification of heat stress-targets of translational control by large scale analysis of Arabidopsis trancriptome and translatome.
  • organism-icon Arabidopsis thaliana
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Heat stress is one of the most prominent and deleterious environmental threads affecting plant growth and development. Upon high temperatures, plants launch specialized gene expression programs that promote stress protection and survival. These programs involve global and specific changes at the transcriptional and translational levels. However the coordination of these processes and their specific role in the establishment of the heat stress response is not fully elucidated.

Publication Title

Analysis of genome-wide changes in the translatome of Arabidopsis seedlings subjected to heat stress.

Sample Metadata Fields

Specimen part

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accession-icon SRP115415
RNA seq_A375 gSMARCB1 + A549 etoposide, Aurora kinases inhibitors treated
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To study the senescence gene signatures in the cells, which were genetic SMARCB1 depleted or treated with aurora kinase inhibitors or etoposide, we performed next generation RNA sequencing on these cell, and ''FRIDMAN_SENESCENCE_UP'' geneset was used to determine the enrichment of senescence-related genes. The RNA sequencing results include (1) A375 cells and SMARCB1 depleted counterparts. (2) A549 cells and aurora kinase inhibitor (Alisertib, barasertib or tozasertib) or etoposide treated counterparts. Overall design: RNA seq data of A375_gSMARCB1 + A549_etoposide, Aurora kinases inhibitors treated, to check senescence gene expression signature one replicate of A375 cells parental V.S SMARCB1 KO (by CRISPR) + duplicates of A549 parental V.S etoposide, or 3 indepdent aurora kinase inhibitors (MLN8237/Alisertib, VX680/Tozasertib, AZD1132/Barasertib)

Publication Title

High-Throughput Functional Genetic and Compound Screens Identify Targets for Senescence Induction in Cancer.

Sample Metadata Fields

Disease, Disease stage, Cell line, Subject

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accession-icon GSE113736
Gene expression profiling of mesenchymal stem cells from bone marrow of multiple myeloma patients and normal donors
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [AltAnalyz probeset-to-Ensembl mapping (huex10st)

Description

A growing body of evidence points to the essential role of bone marrow (BM) tumor microenvironment in Multiple Myeloma (MM) maintenance and progression. Mesenchymal stem cells (MSC) are one of the most important players in this scenario. Through direct and indirect interactions, these cells support MM cells by promoting increase of proliferation, migration, survival, and drug resistance. Additionally, an increasing number of evidence has been demonstrating that MSC from MM patients (MM-MSC) have several abnormalities when compared with their normal counterpart from normal donors (ND-MSC). Therefore, the aimed of our study was to explore the differences between MM-MSC and ND-MSC through gene expression analysis.

Publication Title

Transcriptome Analysis of Mesenchymal Stem Cells from Multiple Myeloma Patients Reveals Downregulation of Genes Involved in Cell Cycle Progression, Immune Response, and Bone Metabolism.

Sample Metadata Fields

Sex, Age, Specimen part, Disease stage, Subject

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accession-icon GSE56549
Perception of fight outcome is needed to activate socially driven changes in brain transcriptome
  • organism-icon Danio rerio
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Group living animals must be able to express different behavior profiles depending on their social status. This implies that the same genotype may translate into different behavioral phenotypes through socially driven differential gene expression. Here we show for the first time that what triggers the switch between status-specific neurogenomic states is not the objective structure of the social interaction but rather the subjects perception of its outcome. For this purpose we had male zebrafish fight either a real opponent or their own image on a mirror. Massive changes in the brain transcriptome were observed in real opponent fighters, which experience either a victory or a defeat. In contrast, mirror fighters, which had no information on fight outcome despite expressing aggressive behavior, failed to activate a neurogenomic response. These results indicate that, even in cognitively simple organisms such as zebrafish, neurogenomic responses underlying changes in social status rely on cognitive appraisal.

Publication Title

Assessment of fight outcome is needed to activate socially driven transcriptional changes in the zebrafish brain.

Sample Metadata Fields

Specimen part

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accession-icon GSE57999
Expression data from baseline and post-endurance training in human PBMCs
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

There is an association between transcriptome and the exercise-related phenotype. Peripheral blood cells suffer alterations in the gene expression pattern in response to perturbations caused by exercise. The acute response to endurance activates stress and inflammation, as well as growth and tissue repair responses.

Publication Title

PBMCs express a transcriptome signature predictor of oxygen uptake responsiveness to endurance exercise training in men.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage, Treatment, Subject, Time

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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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