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accession-icon SRP079916
Ebola virus glycoprotein variant with increased infectivity for human cells dominated the 2013-2016 outbreak
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

The unprecedented magnitude of the 2013-2016 Makona Ebola virus (M-EBOV) epidemic likely resulted from multiple epidemiologic factors that set it apart from previous outbreaks. Nonetheless, genetic adaptations that distinguish M-EBOV from previous isolates may also have contributed to the scale of the epidemic. Of particular interest is a M-EBOV glycoprotein (GP) variant, GP-A82V, that was first detected at the inflection point of the 2013-2016 outbreak - when the number of cases increased exponentially - and which completely supplanted the earlier M-EBOV sequence. We found that, as compared with the earlier strain, GP-A82V increased the ability of M-EBOV to fuse with and infect cells of primate origin, including human blood dendritic cells, without altering innate immune signaling in target cells. Residue 82 is located at the NPC1-binding site on M-EBOV GP and the increased infectivity of GP-A82V was restricted to cells from species in which the NPC1 orthologue bears primate-defining residues at the critical interface. We utilized HIV-derived lentiviral vectors pseudotyped with founder and A82V containing M-EBOV GPs to explore the potential that this modification alters how human monocyte-derived dendritic cells (MDDCs) respond to EBOV GP stimulation. Overall design: We generated stocks of lentiviral vector bearing one the following three M-EBOV GPs: founder, A82V, and A82V/T230A. These viral stocks were used to challenge MDDCs from two healthy, anonymous human donors. Stimulated MDDCs were harvested at 1, 2, 4, and 6 hours after viral addition. Gene expression in M-EBOV GP challenged MDDCs was compared to a unstimulated control.

Publication Title

Ebola Virus Glycoprotein with Increased Infectivity Dominated the 2013-2016 Epidemic.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP067350
A Functionally Conserved Gene Regulatory Network Module Governing Olfactory Neuron Diversity
  • organism-icon Drosophila melanogaster
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Sensory neuron diversity is required for organisms to decipher complex environmental cues. In Drosophila, olfactory environment is detected by 50 different olfactory receptor neuron (ORN) classes that are clustered in combinations within distinct sensilla subtypes. Each sensilla subtype houses stereotypically clustered 1-4 ORN identities that arise through asymmetric divisions from a single multipotent sensory organ precursor (SOP). How each class of SOPs acquires a unique differentiation potential that accounts for ORN diversity is unknown. Previously, we reported a critical component of SOP diversification program, Rotund (Rn), which functions to increase ORN diversity by generating novel developmental trajectories from existing precursors within each independent sensilla type lineages. Here, we show that Rn, along with BarH1/H2, Bric-à-brac (Bab), Apterous (Ap) and Dachshund (Dac), constitute a functionally conserved transcription factor (TF) network, previously shown to pattern the segmentation of the leg, that patterns the developing olfactory tissue. Precursors with diverse ORN differentiation potentials are selected from concentric rings defined by unique combinations of these TFs along the proximodistal axis of the developing antennal disc. The combinatorial code that demarcates each precursor field is set up by cross-regulatory interactions among different factors within the network. Modifications of this network lead to predictable changes in the diversity of sensilla subtypes and ORN pools. In light of our data, we propose a molecular map that defines Overall design: Time-course RNAseq across 4 developmental stages, inlcuding flies mutant for rotund gene (rn), heterozygotes and wildtype

Publication Title

Comparative analysis of behavioral and transcriptional variation underlying CO<sub>2</sub> sensory neuron function and development in Drosophila.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE45417
Expression data from knockdown of ZXDC1/2 in PMA-treated U937
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

ZXDC1 augments the expression of various markers of monocyte/macrophage differentiation when over-expressed in the U937 cell line treated with the phorbol ester PMA. Likewise, knockdown of ZXDC1 restricts the induced expression of these markers. We sought to identify specfic gene targets of ZXDC1 during the process of monocyte/macrophage differentiation in U937 by performing gene expression profiling in cells exhibiting reduced expression of ZXDC1 compared to controls.

Publication Title

The zinc finger transcription factor ZXDC activates CCL2 gene expression by opposing BCL6-mediated repression.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE105826
Targeting CDK6 and BCL2 exploits the "MYB Addiction" of Ph+ acute lymphoblastic leukemia
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Transcriptome analysis of two Ph+ acute lymphoblastic leukemia cell lines after doxycycline induced silencing of MYB.

Publication Title

Targeting CDK6 and BCL2 Exploits the "MYB Addiction" of Ph&lt;sup&gt;+&lt;/sup&gt; Acute Lymphoblastic Leukemia.

Sample Metadata Fields

Cell line

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accession-icon GSE40752
Transcriptional analysis of whole blood, primary fibroblasts, and PBMCs upon TNF-alpha or IL-1beta stimulation from HOIL-1-deficient patients
  • organism-icon Homo sapiens
  • sample-icon 68 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Immunodeficiency, autoinflammation and amylopectinosis in humans with inherited HOIL-1 and LUBAC deficiency.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject, Time

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accession-icon GSE40560
Transcriptome analysis in primary fibroblasts from HOIL-1-deficient patients upon TNF- or IL-1 stimulation
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

HOIL-1 deficient disease is a new early onset fatal autosomal recessive human disorder charaterized by chronic auto-inflammation, recurrent invasive bacterial infections and progressive muscular amylopectinosis. We studied the effect of TNF- and IL-1 on transcriptional changes of primary fibroblasts from HOIL-1-, MYD88- and NEMO-deficient patients.

Publication Title

Immunodeficiency, autoinflammation and amylopectinosis in humans with inherited HOIL-1 and LUBAC deficiency.

Sample Metadata Fields

Disease, Disease stage, Subject, Time

View Samples
accession-icon GSE40561
Transcriptional analysis of whole blood in patients with auto-inflammatory disorders
  • organism-icon Homo sapiens
  • sample-icon 51 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

HOIL1 deficient disease is a new early onset fatal autosomal recessive human disorder charaterized by chronic auto-inflammation, recurrent invasive bacterial infections and progressive muscular amylopectinosis. We studied the transcriptional profiles of whole blood from one HOIL dificient patient and other auto-inflammatory patients, including CINCA, Muckle-Wells syndrome and MVK deficiency.

Publication Title

Immunodeficiency, autoinflammation and amylopectinosis in humans with inherited HOIL-1 and LUBAC deficiency.

Sample Metadata Fields

Specimen part

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accession-icon GSE40838
Transcriptome analysis in peripheral blood mononuclear cells (PBMC) from HOIL-1-deficient patients upon TNF- or IL-1 stimulation
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

HOIL-1 deficient disease is a new early onset fatal autosomal recessive human disorder charaterized by chronic auto-inflammation, recurrent invasive bacterial infections and progressive muscular amylopectinosis. We studied the effect of TNF- and IL-1 on transcriptional changes of PBMCs from HOIL-1- and MYD88-deficient patients.

Publication Title

Immunodeficiency, autoinflammation and amylopectinosis in humans with inherited HOIL-1 and LUBAC deficiency.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject, Time

View Samples
accession-icon SRP020490
Single-cell RNA-Seq reveals dynamic, random monoallelic gene expression in mammalian cells
  • organism-icon Mus musculus
  • sample-icon 293 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

In the diploid genome, genes come in two copies, which can have different DNA sequence and where one is maternal and one is paternal. In a particular cell, a gene could potentially be expressed from both copies (biallelic expression) or only one (monoallelic). We performed RNA-Sequencing on individual cells, from zygote to the cells of the late blastocyst, and also individual cells from the adult liver. Using first generation crosses between two distantly related mouse strains, CAST/Ei and C57BL/6, we determined the expression separately from the maternal and paternal alleles. We found that half of the genes were expressed by only one allele, randomly so that some cells would express the paternal allele, some the maternal and a few cell both alleles. We also observed the spread of the progressive inactivation of the paternal X chromosome. Overall design: First generation mouse strain crosses were used to study monoallelic expression on the single cell level

Publication Title

Single-cell RNA-seq reveals dynamic, random monoallelic gene expression in mammalian cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP049815
RNA-seq analysis of differences in gene expression between dorsal and ventral MEC
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Neural circuits in the medial entorhinal cortex (MEC) encode an animal’s position and orientation in space. Within the MEC spatial representations, including grid and directional firing fields, have a laminar and dorsoventral organization that corresponds to a similar topography of neuronal connectivity and cellular properties. Yet, in part due to the challenges of integrating anatomical data at the resolution of cortical layers and borders, we know little about the molecular components underlying this organization. To address this we develop a new computational pipeline for high-throughput analysis and comparison of in situ hybridization (ISH) images at laminar resolution. We apply this pipeline to ISH data for over 16,000 genes in the Allen Brain Atlas and validate our analysis with RNA sequencing of MEC tissue from adult mice. We find that differential gene expression delineates the borders of the MEC with neighboring brain structures and reveals its laminar and dorsoventral organization. Our analysis identifies ion channel-, cell adhesion- and synapse-related genes as candidates for functional differentiation of MEC layers and for encoding of spatial information at different scales along the dorsoventral axis of the MEC. Our results support the hypothesis that differences in gene expression contribute to functional specialization of superficial layers of the MEC and dorsoventral organization of the scale of spatial representations. Overall design: Examination of dorsal and ventral regions from 4 replicate samples each containing pooled data from 3-4 mice

Publication Title

Laminar and dorsoventral molecular organization of the medial entorhinal cortex revealed by large-scale anatomical analysis of gene expression.

Sample Metadata Fields

No sample metadata fields

View Samples
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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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