refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 66 results
Sort by

Filters

Technology

Platform

accession-icon GSE70958
Molecular function of Lhx1 in early mouse development
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Lhx1 functions together with Otx2, Foxa2, and Ldb1 to govern anterior mesendoderm, node, and midline development.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE70956
Molecular function of Lhx1 in early mouse development (BeadChip)
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Expression profiling of wild-type and Lhx1 null mouse definitive endoderm cultures using Illumina whole genome mouse V2 arrays.

Publication Title

Lhx1 functions together with Otx2, Foxa2, and Ldb1 to govern anterior mesendoderm, node, and midline development.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP113307
Loss of Apela peptide in mice causes low penetrance embryonic lethality and defects in early mesodermal derivatives
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Apela (also referred to as Elabela, Ende and Toddler) is a small signaling peptide that activates the G protein-coupled receptor Aplnr. We used CRISPR/Cas9 to generate a null, reporter-expressing allele, in order to study the role of Apela in the developing mouse embryo. We found that loss of Apela results in low penetrance cardiovascular defects that manifest after the onset of circulation. Targeted Apela null alleles exhibited different transcriptional activity depending on the presence or absence of a Neomycin selection cassette. These are referred to as Apela KO NEO-IN and Apela KO NEO-OUT strains, respectively. Despite subtle phenotypic characteristics that were unique to the NEO-OUT mutants, both Apela null strains shared the same variable expressivity of cardiovascular defects and the same penetrance of embryonic lethality. To investigate the earliest regulatory events leading to physical abnormalities in Apela mutants, we performed RNA-Seq on whole stage-matched and morphologically normal E7.5 embryos (3 wild-type, 6 Apela KO NEO-IN, and 6 Apela KO NEO-OUT individuals). We chose this stage because Apela is initially expressed in the embryo at late gastrulation, shortly after the emergence of extraembryonic mesoderm progenitors. Since modification of the Apela locus may influence the expression of neighboring genes, we examined the expression of upstream and downstream sequences and found no significant difference in their expression. Downregulated genes of interest included several mitochondrial genes, Ceacam2, Ulk4, and Mov10l1. Upregulated genes included the vascular endothelial growth factor Vegfc. Principal component analysis identified outliers (KO1 and KO9), both of which expressed lower levels of mesoderm markers. KO9 was further characterized by aberrant upregulation of erythroid and myeloid markers. This finding was confirmed in our study by qRT-PCR analysis of additional Apela null individuals. Overall design: 15 individual embryos were analyzed at E7.5. Embryos were stage-matched according to morphological landmarks. Control samples were wild-type (n=3), and Apela KO samples were null embryos from the NEO-IN (n=6, ‘KO1-6’) and NEO-OUT (n=6, ‘KO7-12) mutant strains. Whole embryos (including embryonic and extraembryonic tissues) were used for the analysis. Apela KO samples were isolated from homozygous KO intercrosses and therefore did not require genotyping.

Publication Title

Loss of Apela Peptide in Mice Causes Low Penetrance Embryonic Lethality and Defects in Early Mesodermal Derivatives.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP171152
The emergent landscape of the mouse gut endoderm at single-cell resolution
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

To comprehensively delineate the ontogeny of an organ system, we generated 112,217 single- cell transcriptomes representing all endoderm populations within the mouse embryo until midgestation. We employed graph-based approaches to model differentiating cells for spatio- temporal characterization of developmental trajectories. Our analysis reveals the detailed architecture of the emergence of the first (primitive or extra-embryonic) endodermal population and pluripotent epiblast. We uncover an unappreciated relationship between descendants of these lineages, before the onset of gastrulation, suggesting that mixing of extra-embryonic and embryonic endoderm cells occurs more than once during mammalian development. We map the trajectories of endoderm cells as they acquire embryonic versus extra-embryonic fates, and their spatial convergence within the gut endoderm; revealing them to be globally similar but retaining aspects of their lineage history. We observe the regionalized localization of cells along the forming gut tube, reflecting their extra-embryonic or embryonic origin, and their coordinate patterning into organ-specific territories along the anterior-posterior axis. Overall design: Total RNA was extracted from bulk tissue and dissociated cells of 13ss (~E8.75) gut tubes, from bulk tissue from anterior, anterior-midgut, midgut-posterior and posterior sections of 13ss gut tubes, as well as from extra-embryonic visceral endoderm and embryonic visceral endoderm of E7.5 embryos (see also table in section: Bulk RNA processing). The Trizol method (Invitrogen) was used for RNA extraction.

Publication Title

The emergent landscape of the mouse gut endoderm at single-cell resolution.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE80259
Acute dietary fat intake initiates alterations in energy metabolism and insulin resistance
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

BACKGROUND. Dietary intake of saturated fat is a likely contributor to nonalcoholic fatty liver disease (NAFLD) and insulin resistance, but the mechanisms that initiate these abnormalities in humans remain unclear. We examined the effects of a single oral saturated fat load on insulin sensitivity, hepatic glucose metabolism, and lipid metabolism in humans. Similarly, initiating mechanisms were examined after an equivalent challenge in mice.

Publication Title

Acute dietary fat intake initiates alterations in energy metabolism and insulin resistance.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

View Samples
accession-icon SRP139927
Transcriptomic analysis of myosin IIa-deficient B cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Myosin IIa-deficient follicular B cells have a hyperactivated phenotype. To identify what pathways are regulated by myosin IIa, we performed RNA-seq of coding RNA on flow cytometry sorted follicular B cells from CD23Cre+Myh9fl/fl and CD23Cre+Myh9wt/fl mice. Overall design: B220+AA4.1-CD23+CD21lo follicular B cells were sorted from 3 CD23Cre+Myh9fl/fl and 3 CD23Cre+Myh9wt/fl mice and mRNA was isolated and sequenced.

Publication Title

Myosin IIa Promotes Antibody Responses by Regulating B Cell Activation, Acquisition of Antigen, and Proliferation.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon SRP111009
cGAS surveillance of micronuclei links genome instability to innate immunity
  • organism-icon Mus musculus
  • sample-icon 140 Downloadable Samples
  • Technology Badge IconNextSeq 550

Description

DNA is strictly compartmentalised within the nucleus to prevent autoimmunity despite this cGAS, a cytosolic sensor of dsDNA, is activated in autoinflammatory disorders and by DNA damage. Precisely how cellular DNA gains access to the cytoplasm remains to be determined. Here, we report that cGAS localises to micronuclei arising from genome instability in a model of monogenic autoinflammation, after exogenous DNA damage and spontaneously in human cancer cells. These micronuclei occur after mis-segregation of DNA during cell division and consist of chromatin surrounded by their own nuclear membrane. Breakdown of the micronuclear envelope, a process associated with chromothripsis, leads to rapid accumulation of cGAS, providing a mechanism by which self-DNA becomes exposed to the cytosol. cGAS binds to and is activated by chromatin and consistent with a mitotic origin, micronuclei formation and the proinflammatory response following DNA-damage are cell-cycle dependent. Furthermore, by combining live-cell laser microdissection with single cell transcriptomics, we establish that induction of interferon stimulated gene expression occurs in micronucleated cells. We therefore conclude that micronuclei represent an important source of immunostimulatory DNA. As micronuclei formed from lagging chromosomes also activate this pathway, cGAS recognition of micronuclei may act as a cell-intrinsic immune surveillance mechanism detecting a range of neoplasia-inducing processes. Overall design: RNA-seq of 35 individual mouse embryonic fibroblasts 48 h after 1 Gy irradiation: 21 test (with micronuclei) and 14 controls (without micronuclei).

Publication Title

cGAS surveillance of micronuclei links genome instability to innate immunity.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

View Samples
accession-icon SRP062444
Nef +/- infection and RNA transcriptome in different cell lines
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Identification of the counterpart protein of Nef during HIV infection

Publication Title

HIV-1 Nef promotes infection by excluding SERINC5 from virion incorporation.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP056835
Novel Observations from Next Generation RNA Sequencing of Highly Purified Human Adult and Fetal Islet Cell Subsets
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Understanding distinct gene expression patterns of normal adult and developing fetal human pancreatic a and b cells is crucial for developing stem cell therapies, islet regeneration strategies, and therapies designed to increase b cell function in patients with diabetes (type 1 or 2). Toward that end, we have developed methods to highly purify a, b, and d cells from human fetal and adult pancreata by intracellular staining for the cell-specific hormone content, sorting the sub-populations by flow cytometry and, using next generation RNA sequencing, we report on the detailed transcriptomes of fetal and adult a and b cells. We observed that human islet composition was not influenced by age, gender, or body mass index and transcripts for inflammatory gene products were noted in fetal b cells. In addition, within highly purified adult glucagon-expressing a cells, we observed surprisingly high insulin mRNA expression, but not insulin protein expression. This transcriptome analysis from highly purified islet a and b cell subsets from fetal and adult pancreata offers clear implications for strategies that seek to increase insulin expression in type 1 and type 2 diabetes. Overall design: RNA-sequencing of highly purified human adult and fetal islet cell subset was performed using our newly developed method. Using this data, we can study and compare the detailed transcriptome or alpha and beta cells during development.

Publication Title

Novel Observations From Next-Generation RNA Sequencing of Highly Purified Human Adult and Fetal Islet Cell Subsets.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP185707
Transcriptomic analysis of the effect of histone H4 K31R mutation in U2OS cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

To explore the genome-wide gene expression changes induced by the K31R mutation in the histone H4 protein, we performed RNA-sequencing analysis in U2OS cells expressing either wildtype H4 or K31R mutant H4. We found that the lysine (K) to arginine (R) mutation mainly affected oxidative phosphorylation, mtiochondria dysfunction and et al, but not DNA damage signaling pathways. Overall design: Total RNAs were extracted from 3 wild-type (WT) H4 and 3 K31R mutant H4 expressing U2OS cells and profiled by RNA-sequencing.

Publication Title

UFL1 promotes histone H4 ufmylation and ATM activation.

Sample Metadata Fields

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