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accession-icon GSE33024
Sequentially acting Sox transcription factors in neural lineage development
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Sequentially acting Sox transcription factors in neural lineage development.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE33061
Sequentially acting Sox transcription factors in neural lineage development [microarray]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

We report sequential binding but unique functions of different Sox transcription factors during distinct stages of neural differentiation

Publication Title

Sequentially acting Sox transcription factors in neural lineage development.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE143151
The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 12 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

The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition.

Sample Metadata Fields

Age, Specimen part, Cell line, Treatment

View Samples
accession-icon GSE143150
The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition [microarray]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Human Exon 1.0 ST Array (huex10st)

Description

Endothelial cells play an important role in maintenance of the vascular system and the repair after injury. Under pro-inflammatory conditions, endothelial cells can acquire a mesenchymal phenotype by a process named endothelial-to-mesenchymal transition (EndMT), which affects the functional properties of endothelial cells. Here, we investigated the epigenetic control of EndMT. We show that the histone demethylase JMJD2B is induced by EndMT promoting pro-inflammatory and hypoxic conditions. Silencing of JMJD2B reduced TGF-β2-induced expression of mesenchymal genes and prevented the alterations in endothelial morphology and impaired endothelial barrier function. Endothelial-specific deletion of JMJD2B in vivo confirmed a reduction of EndMT after myocardial infarction. EndMT did not affect global H3K9me3 levels but induced a site-specific reduction of repressive H3K9me3 marks at promoters of mesenchymal genes, such as Calponin (CNN1), and genes involved in TGF-β signaling, such as AKT Serine/Threonine Kinase 3 (AKT3) and sulfatase 1 (SULF1). Silencing of JMJD2B prevented the EndMT-induced reduction of H3K9me3 marks at these promotors and further repressed these EndMT-related genes. Our study reveals that endothelial identity and function is critically controlled by the histone demethylase JMJD2B, which is induced by EndMT-promoting pro-inflammatory and hypoxic conditions and support the acquirement of a mesenchymal phenotype.

Publication Title

The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition.

Sample Metadata Fields

Age, Cell line, Treatment

View Samples
accession-icon SRP212738
The Toll signaling pathway targets the insulin-like peptide Dilp6 to inhibit growth in Drosophila
  • organism-icon Drosophila melanogaster
  • sample-icon 64 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

To identify genes that mediate altered communication between fat body and peripheral tissues, we report the gene expression changes in Drosophila third instar larval fat bodies with or without constitutively-active Toll (Toll10b) to activate innate immune signaling, myristoylated Akt (myrAkt) to activate insulin signaling, or both transgenes to bypass the block from Toll signaling to the upstream part of the insulin signaling pathway Overall design: Comparison of RFP/GFP (Control), Toll10b/GFP (Toll10b), RFP/myrAkt (myrAkt), and Toll10b/myrAkt (Toll10b + myrAkt)

Publication Title

The Toll Signaling Pathway Targets the Insulin-like Peptide Dilp6 to Inhibit Growth in Drosophila.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE54775
Effect of choline kinase inhibitor hexadecyltrimethylammonium bromide on Plasmodium falciparum gene expression
  • organism-icon Plasmodium falciparum
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Plasmodium/Anopheles Genome Array (plasmodiumanopheles)

Description

Investigations on the fundamental of malaria parasite biology, such as invasion, growth cycle, metabolism and cell signalling have uncovered a number of potential antimalarial drug targets, including choline kinase, a key enzyme involved in the synthesis of phosphatidylcholine, an important component in parasite membrane compartment.

Publication Title

Effect of choline kinase inhibitor hexadecyltrimethylammonium bromide on Plasmodium falciparum gene expression.

Sample Metadata Fields

Treatment

View Samples
accession-icon SRP109169
Thiol-linked alkylation for the metabolic sequencing of RNA [SLAM-seq pulse/chase labeling in wildtype mES cells]
  • organism-icon Mus musculus
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Gene expression profiling by high-throughput sequencing reveals qualitative and quantitative changes in RNA species at steady-state but obscures the intracellular dynamics of RNA transcription, processing and decay. We developed thiol(SH)-linked alkylation for the metabolic sequencing of RNA (SLAM-seq), an orthogonal chemistry-based epitranscriptomics-sequencing technology that uncovers 4-thiouridine (s4U)-incorporation in RNA species at single-nucleotide resolution. In combination with well-established metabolic RNA labeling protocols and coupled to standard, low-input, high-throughput RNA sequencing methods, SLAM-seq enables rapid access to RNA polymerase II-dependent gene expression dynamics in the context of total RNA. When applied to mouse embryonic stem cells, SLAM-seq provides global and transcript-specific insights into pluripotency-associated gene expression. We validated the method by showing that the RNA-polymerase II-dependent transcriptional output scales with Oct4/Sox2/Nanog-defined enhancer activity; and provides quantitative and mechanistic evidence for transcript-specific RNA turnover mediated by post-transcriptional gene regulatory pathways initiated by microRNAs and N6-methyladenosine. SLAM-seq facilitates the dissection of fundamental mechanisms that control gene expression in an accessible, cost-effective, and scalable manner. Overall design: Wildtype mouse embryonic stem cells (mES cells) were subjected to s4U metabolic RNA labeling for 24 h (pulse, 100 µM s4U), followed by washout (chase) using non-thiol-containing uridine. Total RNA was prepared at various time points along the chase (0h, 0.5h, 1h, 3h, 6h, 12h, and 24h). Total RNA was then subjected to alkylation and mRNA 3' end sequencing library preparation (QuantSeq, Lexogen).

Publication Title

Quantification of experimentally induced nucleotide conversions in high-throughput sequencing datasets.

Sample Metadata Fields

Specimen part, Treatment, Subject

View Samples
accession-icon GSE146109
VEGF-B Signaling Impairs Endothelial Glucose Transcytosis via an LDLR-dependent Decrease in Membrane Cholesterol Loading
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st), Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

VEGF-B signaling impairs endothelial glucose transcytosis by decreasing membrane cholesterol content.

Sample Metadata Fields

Age, Specimen part, Cell line, Treatment

View Samples
accession-icon SRP109094
Thiol-linked alkylation for the metabolic sequencing of RNA [Transcriptional inhibition by Actinomycin D]
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Gene expression profiling by high-throughput sequencing reveals qualitative and quantitative changes in RNA species at steady-state but obscures the intracellular dynamics of RNA transcription, processing and decay. We developed thiol(SH)-linked alkylation for the metabolic sequencing of RNA (SLAM-seq), an orthogonal chemistry-based epitranscriptomics-sequencing technology that uncovers 4-thiouridine (s4U)-incorporation in RNA species at single-nucleotide resolution. In combination with well-established metabolic RNA labeling protocols and coupled to standard, low-input, high-throughput RNA sequencing methods, SLAM-seq enables rapid access to RNA polymerase II-dependent gene expression dynamics in the context of total RNA. When applied to mouse embryonic stem cells, SLAM-seq provides global and transcript-specific insights into pluripotency-associated gene expression. We validated the method by showing that the RNA-polymerase II-dependent transcriptional output scales with Oct4/Sox2/Nanog-defined enhancer activity; and provides quantitative and mechanistic evidence for transcript-specific RNA turnover mediated by post-transcriptional gene regulatory pathways initiated by microRNAs and N6-methyladenosine. SLAM-seq facilitates the dissection of fundamental mechanisms that control gene expression in an accessible, cost-effective, and scalable manner. Overall design: 5 µg/ml Actinomycin D was added to wildtype mouse embryonic stem (mES) cells and total RNA was prepared at various time points after addition of Actinomycin D (0h, 0.25h, 0.5h, 1h, 3h and 10h). Total RNA was subjected to mRNA 3' end library preparation (QuantSeq, Lexogen) and high througput sequencing.

Publication Title

Quantification of experimentally induced nucleotide conversions in high-throughput sequencing datasets.

Sample Metadata Fields

Specimen part, Treatment, Subject

View Samples
accession-icon SRP109172
Thiol-linked alkylation for the metabolic sequencing of RNA [SLAM-seq in wildtype and Xpo5 knockout mES cells]
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Gene expression profiling by high-throughput sequencing reveals qualitative and quantitative changes in RNA species at steady-state but obscures the intracellular dynamics of RNA transcription, processing and decay. We developed thiol(SH)-linked alkylation for the metabolic sequencing of RNA (SLAM-seq), an orthogonal chemistry-based epitranscriptomics-sequencing technology that uncovers 4-thiouridine (s4U)-incorporation in RNA species at single-nucleotide resolution. In combination with well-established metabolic RNA labeling protocols and coupled to standard, low-input, high-throughput RNA sequencing methods, SLAM-seq enables rapid access to RNA polymerase II-dependent gene expression dynamics in the context of total RNA. When applied to mouse embryonic stem cells, SLAM-seq provides global and transcript-specific insights into pluripotency-associated gene expression. We validated the method by showing that the RNA-polymerase II-dependent transcriptional output scales with Oct4/Sox2/Nanog-defined enhancer activity; and provides quantitative and mechanistic evidence for transcript-specific RNA turnover mediated by post-transcriptional gene regulatory pathways initiated by microRNAs and N6-methyladenosine. SLAM-seq facilitates the dissection of fundamental mechanisms that control gene expression in an accessible, cost-effective, and scalable manner. Overall design: Wildtype (wt) mouse embryonic stem (mES) cells, clonal mES cells that had been transfected with non-targeting control guide RNAs (ctr), or Exportin-5 depleted (Xpo5KO) mES cells were subjected to 3h and 12h s4U-pulse labeling followed by total RNA extraction, alkylation, mRNA 3' end library preparation (QuantSeq, Lexogen) and high throughput sequencing.

Publication Title

Quantification of experimentally induced nucleotide conversions in high-throughput sequencing datasets.

Sample Metadata Fields

Specimen part, Treatment, 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

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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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