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accession-icon GSE30487
Expression profile of high yielding rice introgression line
  • organism-icon Oryza sativa
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rice Genome Array (rice)

Description

Leaves and panicles from recurrent parent KMR3 and a high yielding KMR3-O.rufipogon introgression line were used

Publication Title

Os11Gsk gene from a wild rice, Oryza rufipogon improves yield in rice.

Sample Metadata Fields

Specimen part

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accession-icon SRP125821
RNA-seq to compare wild type, db/+ and db/db islets
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Purpose: RNA seq analysis were to compare and contrast the gene expression profile involved in the dedifferentiation of db/db islets in type 2 diabetes Methods: Islets of wild type, db/+ and db/db were purified using perfusion from 12 week old mice and RNA were isolated. Islated RNA were used in RNA seq to understand the expression pattern Results: Using an optimized data analysis workflow, we mapped about 10 million sequence reads per sample to the mouse genome (build mm9) and identified 16,014 transcripts WT, db/+ and db/db mice islets with TopHat workflow. Hierarchical clustering of differentially expressed genes uncovered there role in type 2 diabetes. Data analysis with TopHat workflows revealed a significant overlap yet provided complementary insights in transcriptome profiling. Conclusions: We characterised and identified genes involved in dedifferentiation of islets. Overall design: Islets of mRNA 12 weeks old wild type (WT), db/+ and db/db mice were generated by deep sequencing, in triplicate, using Illumina Hiseq 2500 platform.

Publication Title

RNA-Seq Analysis of Islets to Characterise the Dedifferentiation in Type 2 Diabetes Model Mice db/db.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon GSE52840
Transcription factor Achaete-Scute homologue 2 initiates T follicular helper cell development
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Transcription factor achaete-scute homologue 2 initiates follicular T-helper-cell development.

Sample Metadata Fields

Specimen part

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accession-icon GSE52838
Transcription factor Achaete-Scute homologue 2 initiates T follicular helper cell development [array]
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

In immune responses, activated T cells migrate to B cell follicles and develop to T follicular helper (Tfh) cells, a new subset of CD4+ T cells specialized in providing help to B lymphocytes in the induction of germinal centers 1-3. Although Bcl6 has been shown to be essential in Tfh cell function, it may not regulate the initial migration of T cells 4 or the induction of Tfh program as exampled by CXCR5 upregulation 5. Here, we show that the Achaete-Scute homologue 2 (Ascl2) gene that encodes a basic helix-loop-helix (bHLH) transcription factor 6, is selectively upregulated in its expression in Tfh cells. Ectopic expression of Ascl2 uniquely upregulates CXCR5 but not Bcl6 and downregulates CCR7 expression in T cells in vitro and accelerates T cell migration to the follicles and Tfh cell development in vivo. Combined transcriptome profiling and genome-wide occupancy analysis indicate that Ascl2 directly regulates Tfh-related genes while inhibits expression of Th1 and Th17 genes. Acute deletion of Ascl2 as well as blockade of its function with the Id3 protein in peripheral CD4+ T cells results in a failure in Tfh cell development and the germinal center response. Conversely, mutation of Id3, known to cause antibody-mediated autoimmunity, greatly enhances Tfh cell generation. Thus, Ascl2 critically and directly initiates Tfh cell development.

Publication Title

Transcription factor achaete-scute homologue 2 initiates follicular T-helper-cell development.

Sample Metadata Fields

Specimen part

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accession-icon GSE55902
Expression data from Rice leaves
  • organism-icon Oryza sativa
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rice Genome Array (rice)

Description

Senescence is a developmental process and chlorophyll is an indicator of leaf senescene. In plants cytokinin plays a role in delaying leaf senescence. Chlorophyll degradation is tightly regulated during senescence and cytokinin might interplay in the chrorophyll degradation pathway to regulate leaf greening.

Publication Title

Cytokinin delays dark-induced senescence in rice by maintaining the chlorophyll cycle and photosynthetic complexes.

Sample Metadata Fields

Specimen part

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accession-icon GSE68091
Effects of ONC201 on mantle cell lymphoma cell lines
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The small molecule ONC201 is toxic in vitro to multiple cell lines and primary tumor samples of mantle cell lymphoma (MCL) and acute myeloid leukemia, even ones with unfavorable genetic features (notably including TP53 inactivation) or acquired resistance to other agents. Because the mechanism of action in these malignant hematologic cells appeared to differ from that in solid tumors, we performed gene expression profiling (GEP) studies on MCL lines treated with ONC201 and other agents with known mechanisms of action. Treatment of JeKo-1 cells with 5 uM ONC201 showed consistent and progressive increases or decreases over time in two sets of genes: upregulated genes, which implicated an ER stress response and mTOR pathway inhibition, and downregulated genes, which implicated reduced proliferation. These implicated effects of ONC201 were validated by confirmatory experiments. Similar GEP changes were observed in ONC201-naive Z138 cells after 24 hr of ONC201 treatment, but were not seen in Z138 cells made ONC201-resistant by chronic exposure. Finally, the GEP effects of ONC201 in JeKo-1 cells were mimicked by the ER stress inducer tunicamycin, but not by the direct MTOR inhibition rapamycin, further confirming an ER stress response and suggesting that inhibition of the mTOR pathway was by an indirect mechanism.

Publication Title

ATF4 induction through an atypical integrated stress response to ONC201 triggers p53-independent apoptosis in hematological malignancies.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE50686
Role of MITF in melanoma
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Enhancer-targeted genome editing selectively blocks innate resistance to oncokinase inhibition.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE50649
COLO829 treatment with PLX4032 and/or MITF knockdown
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Thousands of enhancers are characterized in the human genome, yet few have been shown important in cancer. Inhibiting oncokinases, such as EGFR, ALK, HER2, and BRAF, is a mainstay of current cancer therapy but is hindered by innate drug resistance mediated by upregulation of the HGF receptor, MET. The mechanisms mediating such genomic responses to targeted therapy are unknown. Here, we identify lineage-specific MET enhancers for multiple common tumor types, including a melanoma lineage-specific MET enhancer that displays inducible chromatin looping and MET gene induction upon BRAF inhibition. Epigenomic analysis demonstrated that the melanocyte-specific transcription factor, MITF, mediates this enhancer function. Targeted genomic deletion (<7bp) of the MITF motif within the MET enhancer suppressed inducible chromatin looping and innate drug resistance, while maintaining MITF-dependent, inhibitor-induced melanoma cell differentiation. Epigenomic analysis can thus guide functional disruption of regulatory DNA to decouple pro- and anti-oncogenic functions of tumor lineage-enriched transcription factors mediating innate resistance to oncokinase therapy.

Publication Title

Enhancer-targeted genome editing selectively blocks innate resistance to oncokinase inhibition.

Sample Metadata Fields

Cell line

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accession-icon SRP144647
Transcriptomes from naïve CD4+ T-cells from infants and children with and without food allergy [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 110 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Here we studied the epigenetic regulation of the naïve CD4+ T-cell activation response among children with IgE-mediated food allergy. Using integrated DNA methylation and transcriptomic profiling, we found that food allergy in infancy is associated with dysregulation of T-cell activation genes. Reduced expression of cell cycle related targets of the E2F and MYC transcription factor networks, and remodeling of DNA methylation at metabolic (RPTOR, PIK3D, MAPK1, FOXO1) and inflammatory genes (IL1R, IL18RAP, CD82) were associated with poorer T-lymphoproliferative responses in infancy after polyclonal activation of the T-cell receptor. Overall design: mRNA sequencing of naïve CD4+ T-cells under two conditions (anti-CD3+CD28 activated, or quiescent) at two ages (baseline (12months) and followup (2 or 4 years)) in allergic and non-allergic children.

Publication Title

Epigenetic dysregulation of naive CD4+ T-cell activation genes in childhood food allergy.

Sample Metadata Fields

Sex, Subject

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accession-icon SRP159156
Differential gene expression analysis in BRD4-PROTAC treated diffuse large B-cell lymphoma cell lines
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We identified differential gene expression after treatment with BRD4-PROTAC ARV771 in two ABC-like diffuse large B-cella lymphoma cell lines. We have identified cluster of gene expression regulated after BRD4 inhibition which are criticaly important for DLBCL malignancy. Overall design: Two ABC-DLBCL cell lines were used to identify the changes in gene expression profile after BRD4-PROTAC (ARV771) treatment.

Publication Title

Targetable genetic alterations of <i>TCF4</i> (<i>E2-2</i>) drive immunoglobulin expression in diffuse large B cell lymphoma.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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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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