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accession-icon SRP189743
scRNA sequencing of 2 leukemia patients in remission after T cell therapy
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

peripheral blood samples of two leukemia patients in remission were profiled by single cell RNA sequencing approximately 1 year after receiving WT1 specific transgenic T cell therapy, at a time when patients were in clinical remission Overall design: single cell RNA sequencing of peripheral blood mononuclear cells

Publication Title

T cell receptor gene therapy targeting WT1 prevents acute myeloid leukemia relapse post-transplant.

Sample Metadata Fields

Specimen part, Disease, Subject

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

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accession-icon GSE51524
LNCaP prostate cancer cell lines overexpressing wild-type or GARRPR-mutant Bag-1L
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The BF-3 pocket of the androgen receptor (AR) has been identified as an allosteric modulator of the transactivation function of the AR. We now demonstrate that a duplicated GARRPR motif at the N-terminus of the cochaperone Bag-1L functions through this BF-3 domain. Amino acid exchanges in these two motifs impair binding of Bag-1L to the AR but increase the androgen-dependent activation of a subset of AR-target genes. We have therefore identified GARRPR as a novel BF-3 regulatory sequence important for fine-tuning the activity of the receptor.

Publication Title

Coregulator control of androgen receptor action by a novel nuclear receptor-binding motif.

Sample Metadata Fields

Specimen part, Treatment

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 GSE146108
VEGF-B Signaling Impairs Endothelial Glucose Transcytosis via an LDLR-dependent Decrease in Membrane Cholesterol Loading [HBMEC]
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Regulation of endothelial nutrient transport is poorly understood. Vascular endothelial growth factor (VEGF)-B signaling in endothelial cells promotes uptake and transcytosis of fatty acids (FA) from the bloodstream to the underlying tissue, advancing pathological lipid accumulation and lipotoxicity in diabetic complications. Here we demonstrate a VEGF-B dependent obstruction of endothelial glucose transport attributed to plasma membrane lipid alterations affecting glucose transporter 1 function, which was independent of FA uptake. Specifically, VEGF-B signaling impaired recycling of low-density lipoprotein receptor to the plasma membrane, leading to reduced cholesterol uptake and membrane cholesterol loading, decreasing endothelial glucose uptake capacity. Inhibiting VEGF-B in vivo was accordingly linked to reconstitution of membrane cholesterol and induction of glucose uptake, of particular relevance for conditions inferring insulin resistance and diabetic complications. In summary, our study reveals a novel mechanism of action for VEGF-B in endothelial nutrient uptake and highlights the impact of membrane cholesterol for the regulation of endothelial glucose transport.

Publication Title

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

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE146107
VEGF-B Signaling Impairs Endothelial Glucose Transcytosis via an LDLR-dependent Decrease in Membrane Cholesterol Loading [mouse heart]
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Regulation of endothelial nutrient transport is poorly understood. Vascular endothelial growth factor (VEGF)-B signaling in endothelial cells promotes uptake and transcytosis of fatty acids (FA) from the bloodstream to the underlying tissue, advancing pathological lipid accumulation and lipotoxicity in diabetic complications. Here we demonstrate a VEGF-B dependent obstruction of endothelial glucose transport attributed to plasma membrane lipid alterations affecting glucose transporter 1 function, which was independent of FA uptake. Specifically, VEGF-B signaling impaired recycling of low-density lipoprotein receptor to the plasma membrane, leading to reduced cholesterol uptake and membrane cholesterol loading, decreasing endothelial glucose uptake capacity. Inhibiting VEGF-B in vivo was accordingly linked to reconstitution of membrane cholesterol and induction of glucose uptake, of particular relevance for conditions inferring insulin resistance and diabetic complications. In summary, our study reveals a novel mechanism of action for VEGF-B in endothelial nutrient uptake and highlights the impact of membrane cholesterol for the regulation of endothelial glucose transport.

Publication Title

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

Sample Metadata Fields

Age, Specimen part

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

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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

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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

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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