refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 136 results
Sort by

Filters

Technology

Platform

accession-icon GSE63023
Expression data from heart muscle of cardiac-specific caspase-3 and -7 knockout and wild type newborn and young mice
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Caspases, proteolytic enzymes involved in cell death could play a role independent of cell death in the developing heart

Publication Title

Executioner Caspase-3 and 7 Deficiency Reduces Myocyte Number in the Developing Mouse Heart.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon SRP050448
Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

RNA sequencing of wild-type or Interferon Alpha receptor 1 Knockout MEF cells treated with DMSO or the Caspase Inhibitor Q-VD-OPh. The mechanism by which cells undergo death determines whether dying cells trigger inflammatory responses or remain immunologically silent. Mitochondria play a central role in the induction of cell death, as well as in immune signaling pathways. Here, we identify of a mechanism by which mitochondria and downstream pro-apoptotic caspases regulate the activation of antiviral immunity. In the absence of active caspases, mitochondrial outer membrane permeabilization by Bax and Bak results in the expression of type I interferons (IFNs). This induction is mediated by mitochondrial DNA-dependent activation of the cGAS/STING pathway and results in the establishment of a potent state of viral resistance. Our results show that mitochondria have the capacity to simultaneously expose a cell-intrinsic inducer of the IFN response, and to inactivate this response in a caspase-dependent manner. This mechanism provides a dual control, which determines whether mitochondria initiate an immunologically silent or a pro-inflammatory type of cell death. In order to determine whether the pharmacological inhibition of caspases could activate the type I interferon response, we treated WT MEFs with the caspase inhibitor Q-VD-OPH. The inhibitor induced an increased expression of ISGs, which was dependent on type I IFN receptor (IFNAR1) signaling. Overall design: RNA was extracted from duplicate samples and libraries generated for sequencing using the directional RNA-Seq library prep at the Yale Center for Genome Analysis. Libraries were sequenced using a Hiseq2500 sequencer to generate 76bp single-end reads. Duplicate samples were analyzed for each condition.

Publication Title

Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE36009
Gene expression data from Wild Type and Nlrp10 deficient dendritic cells treated with or without LPS
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Nlrp10-deficient mice have a profound defect in helper T cell-driven immune responses. T cell priming is impaired due to a defect in the emigration of a dendritic cells from inflamed tissue and antigen transport to draining lymph nodes. DC chemotaxis to CCR7-dependent and independent ligands is intact in the absence of Nlrp10.

Publication Title

NLRP10 is a NOD-like receptor essential to initiate adaptive immunity by dendritic cells.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE64028
Expression data from healthy human PB B cell subsets
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Human PB B cell subsets are functionally distinct and may derive from different developmental pathways, reflected by their differential gene expression profiles.

Publication Title

Functional capacities of human IgM memory B cells in early inflammatory responses and secondary germinal center reactions.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP074175
mRNA expression profile of dop-1 mutants to wild- type animals during adulthood (L4+48 hours) using RNA-seq
  • organism-icon Caenorhabditis elegans
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Developmentally synchronized animals were obtained by hypochlorite treatment of gravid adults to release embryos. Synchronized embryos were hatched on NGM plates and grown at 20°C until 48 h after the L4 stage of development. Fluorodeoxyuridine was used to prevent the development of second-generation embryos once animals reached fertile adulthood. For each RNA-seq experiment, populations for odIs77[Pcol-19::UbG76V-GFP] and dop-1(vs100); [Pcol- 19::UbG76V-GFP] were grown simultaneously under the same conditions. Total RNA was isolated from animals using trizol (Invitrogen) combined with Bead Beater lysis in 3 biological replicates, and an mRNA library (single-end, 50-bp reads) was prepared for each sample/replicate using Illumina Truseq with PolyA selection. Overall design: Examination of mRNA levels in adults dop-1 mutants and wild-type animals.

Publication Title

Dopamine signaling promotes the xenobiotic stress response and protein homeostasis.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE28573
Gene expression data from teratomas formed by C57BL/6 (B6) ES and EiPS cells in B6 mice
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Embryonic fibroblast from C57BL/6 (B6) mice were reprogrammed to EiPS without exogenous DNA integration using an single episomal vector. The EiPS cells and B6 ES cells were then transplanted into B6 mice to form teratomas.

Publication Title

Immunogenicity of induced pluripotent stem cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP059663
LECT2 effect on the bone marrow cells of mice
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

Hematopoietic stem cell (HSC) is under dynamic controlled in the bone marrow to differentiate into cells of all lineages that constitute the blood. The bone marrow niches form a specific microenvironment to maintain and regulate HSC. However, the mechanisms that the effect of cytokines from blood on HSC function still remain largely unknown. Leukocyte chemotactic factor 2 (LECT2), a liver-derived cytokine, is involved in many immune dysfunctions, such as sepsis, cancer and diabetes. Here we showed that LECT2 affected the gene expression of bone marrow cells in mice. Especially, we found that LECT2 treatment for 3 and 5 days led to the down-regulation of cytokines such as, TNF, IL-6, IL-1ß, CXCL10, CCL4, CCL3 et al. Moreover, the functions and mechanisms for LECT2 regulated HSC in bone marrow is still needed further investigation. Overall design: Recombinant LECT2 was subcutaneously injected at a dose of 300 µg/kg body weight (once a day for 0, 3, or 5 days) in mice. The bone marrow cells were flushed out from femur, tibia, pelvis, and humerous in PBS.

Publication Title

LECT2 drives haematopoietic stem cell expansion and mobilization via regulating the macrophages and osteolineage cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP083945
NCR- and Dal80-sensitive genes in Saccharomyces cerevisiae
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

GATA transcription factors are highly conserved among eukaryotes and play roles in transcription of genes implicated in cancer progression and hematopoiesis. However, although their consensus binding sites have been well defined in vitro, the in vivo selectivity for recognition by GATA factors remains poorly characterized. Using ChIP-Seq, we identified the Dal80 GATA factor targets in yeast. Our data reveal Dal80 binding to a large set of promoters, sometimes independently of GATA sites, correlating with nitrogen- and/or Dal80-sensitive gene expression. Strikingly, Dal80 was also detected across the body of promoter-bound genes, correlating with high expression. Mechanistic single-gene experiments showed that Dal80 spreading across gene bodies requires active transcription. Consistently, Dal80 co-immunoprecipitated with the initiating and post-initiation forms of RNA Polymerase II. Our work suggests that GATA factors could play dual, synergistic roles during transcription initiation and post-initiation steps, promoting efficient remodeling of the gene expression program in response to environmental changes. Overall design: Strand-specific total RNA-Seq analysis in wild-type (WT) and dal80-delta (dal80) cells grown in glutamine- and/or proline-containing medium.

Publication Title

Transcription-dependent spreading of the Dal80 yeast GATA factor across the body of highly expressed genes.

Sample Metadata Fields

Subject

View Samples
accession-icon GSE65352
Gene expression of livers from Lpcat3fl/fl and Lpcat3fl/fl Albumin-Cre mice on chow diet
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The total abundance of phosphatidylcholine (PC) is known to influence lipoprotein production. However, the role of specific phospholipid species in lipid transport has been difficult to assess due to an inability to selectively manipulate membrane composition in vivo. Here we show that the LXR-regulated phospholipid remodeling enzyme lysophosphatidylcholine acyltransferase 3 (Lpcat3) is a critical determinant of membrane phospholipid composition and lipoprotein production. Mice lacking Lpcat3 in the liver show defects in lipoprotein production.

Publication Title

Lpcat3-dependent production of arachidonoyl phospholipids is a key determinant of triglyceride secretion.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE65353
Gene expression of livers from Lpcat3fl/fl and Lpcat3fl/fl Albumin-Cre mice on a western diet
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The total abundance of phosphatidylcholine (PC) is known to influence lipoprotein production. However, the role of specific phospholipid species in lipid transport has been difficult to assess due to an inability to selectively manipulate membrane composition in vivo. Here we show that the LXR-regulated phospholipid remodeling enzyme lysophosphatidylcholine acyltransferase 3 (Lpcat3) is a critical determinant of membrane phospholipid composition and lipoprotein production. Mice lacking Lpcat3 in the liver show defects in lipoprotein production.

Publication Title

Lpcat3-dependent production of arachidonoyl phospholipids is a key determinant of triglyceride secretion.

Sample Metadata Fields

Sex, 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

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