refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
    0
github link
Build and Download Custom Datasets
refine.bio helps you build ready-to-use datasets with normalized transcriptome data from all of the world’s genetic databases.
Showing
of 132 results
Sort by

Filters

Technology

Platform

accession-icon GSE22186
Phosphorylation of p53 Serine 46 contributes to target gene selectivity of p53
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Role of p53 serine 46 in p53 target gene regulation.

Sample Metadata Fields

Specimen part, Cell line, Compound

View Samples
accession-icon GSE22184
Phosphorylation of p53 Serine 46 contributes to target gene selectivity of p53 (Exon)
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

The tumor suppressor p53 plays a crucial role in cellular growth control inducing a plethora of cellular response pathways. The molecular mechanisms that discriminate between the distinct p53-responses towards different stress treatments have remained largely elusive. Here, we have analyzed the p53-regulated pathways induced by two chemotherapeutical treatments, Actinomycin D inducing growth arrest and Etoposide resulting in apoptosis. We found that the genome-wide p53-binding patterns are almost identical upon both treatments notwithstanding transcriptional differences that we observed in genome-wide transcriptome analysis. To assess the role of post-translational modifications in target gene choice and activation we investigated the extent of phosphorylation of Serine 46 of p53 bound to DNA (p53-pS46), a modification that has been linked to apoptosis-pathways, and the extent of phosphorylation of Serine 15 (p53-pS15), a general p53-activation mark. Interestingly, the overall extent of S46 phosphorylation of p53 bound to DNA is considerably higher in cells directed towards apoptosis while the degree of phosphorylation at S15 of DNA bound p53 remains highly similar upon both treatments. Moreover, our data suggest that, following different chemotherapeutical treatments, the extent of chromatin-associated p53 phosphorylated at S46 but not at pS15 is higher on certain apoptosis related target genes, including the BAX and PUMA genes. These data provide evidence that cell fate decisions are not made primarily on the level of general p53 DNA-binding, but possibly through post-translational modifications of chromatin bound p53.

Publication Title

Role of p53 serine 46 in p53 target gene regulation.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE114639
Inhibition of TOR Represses Nutrient Consumption, Which Improves Greening after Extended Periods of Etiolation
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Arabidopsis Gene 1.0 ST Array (aragene10st)

Description

Upon illumination, etiolated seedlings experience a transition from heterotrophic to photoautotrophic growth. During this process, the tetrapyrrole biosynthesis pathway provides chlorophyll for photosynthesis. This pathway has to be tightly controlled to prevent the accumulation of photoreactive metabolites and to provide stoichiometric amounts of chlorophyll for its incorporation into photosynthetic protein complexes. Therefore, plants have evolved regulatory mechanisms to synchronize the biosynthesis of chlorophyll and chlorophyll-binding proteins. Two phytochrome-interacting factors (PIF1 and PIF3) and the DELLA proteins, which are controlled by the gibberellin pathway, are key regulators of this process. Here, we show that impairment of TARGET OF RAPAMYCIN (TOR) activity in Arabidopsis (Arabidopsis thaliana), either by mutation of the TOR complex component RAPTOR1B or by treatment with TOR inhibitors, leads to a significantly reduced accumulation of the photoreactive chlorophyll precursor protochlorophyllide in darkness but an increased greening rate of etiolated seedlings after exposure to light. Detailed profiling of metabolic, transcriptomic, and physiological parameters revealed that the TOR-repressed lines not only grow slower, they grow in a nutrient-saving mode, which allows them to resist longer periods of low nutrient availability. Our results also indicated that RAPTOR1B acts upstream of the gibberellin-DELLA pathway and its mutation complements the repressed greening phenotype of pif1 and pif3 after etiolation.

Publication Title

Inhibition of TOR Represses Nutrient Consumption, Which Improves Greening after Extended Periods of Etiolation.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE85963
Carbon starvation along the maize leaf gradient
  • organism-icon Zea mays
  • sample-icon 43 Downloadable Samples
  • Technology Badge Icon Affymetrix Maize Genome Array (maize)

Description

gene expression profiling in different zones along the gradient of the growing maize leaf balde aover a time course of dirunal cycle and carbon starvation by extension of the night

Publication Title

The Interplay between Carbon Availability and Growth in Different Zones of the Growing Maize Leaf.

Sample Metadata Fields

Time

View Samples
accession-icon GSE18312
Gene Expression in Blood in Scizophrenia and Bipolar Disorder
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Schizophrenia (SCZ) and bipolar disorder (BPD) are polygenic disorders with many genes contributing to their etiologies. The aim of this investigation was to search for dysregulated molecular and cellular pathways for these disorders as well as psychosis. We conducted a blood-based microarray investigation in two independent samples with SCZ and BPD from San Diego (SCZ=13, BPD=9, control=8) and Taiwan [data not included](SCZ=11, BPD=14, control=16). Diagnostic groups were compared to controls, and subjects with a history of psychosis [PSYCH(+): San Diego (n=6), Taiwan (n=14)] were compared to subjects without such history [PSYCH(-): San Diego (n=11), Taiwan (n=14)]. Analyses of covariance comparing mean expression levels on a gene-by-gene basis were conducted to generate the top 100 significantly dysregulated gene lists for both samples by each diagnostic group. Gene lists were imported into Ingenuity Pathway Analysis (IPA) software. Results showed the ubiquitin proteasome pathway (UPS) was listed in the top ten canonical pathways for BPD and psychosis diagnostic groups across both samples with a considerably low likelihood of a chance occurrence (p = .001). No overlap in dysregulated genes populating these pathways was observed between the two independent samples. Findings provide preliminary evidence of UPS dysregulation in BPD and psychosis as well as support further investigation of the UPS and other molecular and cellular pathways for potential biomarkers for SCZ, BPD, and/or psychosis.

Publication Title

Preliminary evidence of ubiquitin proteasome system dysregulation in schizophrenia and bipolar disorder: convergent pathway analysis findings from two independent samples.

Sample Metadata Fields

Sex, Age, Disease

View Samples
accession-icon GSE31415
Comparison of WAT CD34+ vs LAF CD34+
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

A catalytic role has been proposed in neoplastic angiogenesis and cancer progression for bone marrow-derived endothelial progenitor cells (EPCs). However, in preclinical and clinical studies the quantitative role of marrow-derived EPCs in cancer vascularization was found to be extremely variable. Adipose tissue represents an attractive source of autologous adult stem cells due to its abundance and surgical accessibility. CD34+cells from Lipotransfer aspirates (LAs) of patients undergoing breast reconstruction after breast cancer surgery were compared with CD34+ cells from Leucapheresis of normal subjects.

Publication Title

The white adipose tissue used in lipotransfer procedures is a rich reservoir of CD34+ progenitors able to promote cancer progression.

Sample Metadata Fields

Sex

View Samples
accession-icon GSE86198
Reprogramming Mouse Fibroblasts into Engraftable Myeloerythroid and Lymphoid Progenitors: Induction and Underlying Mechanisms
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Reprogramming mouse fibroblasts into engraftable myeloerythroid and lymphoid progenitors.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE86196
Reprogramming Mouse Fibroblasts into Engraftable Myeloerythroid and Lymphoid Progenitors: Induction and Underlying Mechanisms (BeadChip)
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Here we show that hematopoietic transcription factors Scl, Lmo2, Runx1 and Bmi1 can convert a developmentally-distant lineage (fibroblasts) into induced hematopoietic progenitors (iHPs). We analyzed transcriptomic data for cell undergoing the transdifferentiation process at several time-points of the process.

Publication Title

Reprogramming mouse fibroblasts into engraftable myeloerythroid and lymphoid progenitors.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE51270
Genes regulated by TAZ in lung cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

To investigate the roles of TAZ in lung cancer cell proliferation, we compared the expression profiles of A549 and H441 lung adenocarcinoma cell lines transfected with control siRNA and siTAZ.

Publication Title

An integrative analysis of the tumorigenic role of TAZ in human non-small cell lung cancer.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon SRP083073
Roquin suppresses PI3K-mTOR signaling to control T cell differentiation and Treg effector function
  • organism-icon Mus musculus
  • sample-icon 115 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Illumina HiSeq 1500

Description

Roquin proteins are required to preclude spontaneous T cell activation and aberrant T follicular helper (Tfh) or T helper 17 (Th17) differentiation. Here, we show that deletion of Roquin encoding alleles in regulatory T cells (Tregs) also caused the activation of conventional T cells. These Tregs exhibited a follicular Treg phenotype, CD25 downregulation and could not protect from colitis. Mechanistically, Roquin was required for full expression and activity of Pten and Foxo1, two essential signaling molecules in Tregs and effector T cells. Roquin upregulated Pten by interfering with miR-17~92 binding to an overlapping cis-element in the Pten 3' UTR and downregulated the Foxo1-specific E3 ubiquitin ligase Itch. Loss of Roquin enhanced mTOR signaling and global protein synthesis, while inhibition of PI3K or mTOR in Roquin-deficient CD4+ T cells corrected increased Tfh and Th17 differentiation. Thereby, the control of PI3K-mTOR signaling by Roquin prevents autoimmunity through T cell-intrinsic and Treg-mediated regulation. Overall design: Examination of transcriptome and ribosome occupancy in MEF and T cells upon Roquin expression and inhibition. Examination of Roquin binding sites in the mouse transcriptome of MEF cells. Examination of transcriptome in CD25+ and CD25- Treg cells from WT and Roquin DKO mice.

Publication Title

Roquin targets mRNAs in a 3'-UTR-specific manner by different modes of regulation.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
...

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact