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accession-icon GSE99580
A Systems Genetics Approach to Fracture Healing
  • organism-icon Mus musculus
  • sample-icon 239 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Phosphate is essential for healthy bone growth and plays an essential role in fracture repair. Although phosphate deficiency has been shown to impair fracture healing, the mechanisms involved in impaired healing are unknown. More recently, studies have shown that the effect of phosphate deficiency on the repair process varied based on the genetic strain of mice, which is not characterized.

Publication Title

Hypophosphatemia Regulates Molecular Mechanisms of Circadian Rhythm.

Sample Metadata Fields

Sex, Specimen part, Time

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accession-icon GSE19941
Control of LPS induced gene expression in bone marrow derived macrophages by the p50/p105 subunit of NF-kB and IL-10
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Bone marrow-derived macrophages were produced from mice lacking IL-10 alone (IL10-def) or mice lacking both IL-10 and the p50/p105 subunit of NF-kB (p50/IL10), and left unstimulated, stimulated with LPS (1 ng/ml) or stimulated with LPS and IL-10 (0.3 ng/ml).

Publication Title

NF-κB1 inhibits TLR-induced IFN-β production in macrophages through TPL-2-dependent ERK activation.

Sample Metadata Fields

Specimen part

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accession-icon GSE52474
Late Multiple Organ Surge in Interferon-regulated Target Genes Characterizes Staphylococcal Enterotoxin B Lethality
  • organism-icon Mus musculus
  • sample-icon 154 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Bacterial superantigens are virulence factors that cause toxic shock syndrome. Here, the genome-wide, temporal response of mice to lethal intranasal staphylococcal enterotoxin B (SEB) was investigated in six tissues (PBMC, lung, spleen, kidney, heart, Liver).The earliest responses and largest number of affected genes occurred in tissues (PBMCs, spleen and lung) with the highest content of both T-cells and monocyte/macrophages, the direct cellular targets of SEB. In contrast, the response of liver, kidney and heart was delayed and involved fewer genes, but revealed a dominant genetic program that was seen in all 6 tissues. Many of the 85 uniquely annotated transcripts participating in this shared genomic response have not been previously linked to SEB. Global gene-expression changes measured serially across multiple organs identified new candidate mechanisms of SEB-induced death.

Publication Title

Late multiple organ surge in interferon-regulated target genes characterizes staphylococcal enterotoxin B lethality.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP067494
In vivo analysis of astrocyte ribosome-associated mRNA after traumatic spinal cord injury
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Analysis of gene expression by astrocytes or non-astrocyte cells in spinal cord injury (SCI) lesions may lead to the identification of molecules that impact on axon regrowth. We conducted genome-wide RNA sequencing of (i) immunoprecipitated astrocyte-specific ribosome-associated RNA (ramRNA) from WT or STAT3-CKO astrocytes, and (ii) the non-precipitated (flow-through) RNA deriving from non-astrocyte cells in the same tissue samples 14 days following SCI. DOI: 10.1038/nature17623 Overall design: Young adult female mGFAP-Cre-RiboTag or mGFAP-Cre-RiboTag-STAT3-LoxP mice underwent severe crush SCI at thoracic level 10. 14 days following SCI, the central 3mm of the SCI lesion was extracted, homogenized and (i) astrocyte-specific ribosome-associated RNA (ramRNA) precipitated via a hemagglutinin (HA) tag targeted to either WT (n=4) or STAT3-CKO (n=3) astrocytes, and (ii) the non-precipitated (flow-through) RNA deriving from non-astrocyte cells in the same tissue samples. Sex and age-matched mGFAP-Cre-RiboTag mice served as uninjured controls (n=4).

Publication Title

Astrocyte scar formation aids central nervous system axon regeneration.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE27000
Peripheral blood transcriptome responses to Salmonella Typhimurium in pigs differing in Salmonella shedding phenotypes
  • organism-icon Sus scrofa
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Porcine Genome Array (porcine)

Description

Salmonella species infect many vertebrate species, and pigs colonized with Salmonella enterica serovar Typhimurium (ST) are usually asymptomatic, making detection of these Salmonella-carrier pigs difficult. The variable fecal shedding of this gram-negative bacteria in such pigs is an important cause of foodborne illness and zoonotic disease. To investigate gene pathways and biomarkers associated with the variance in Salmonella shedding following experimental inoculation, we have initiated the first analysis of the whole blood transcriptional response induced by Salmonella. A population of pigs (n=40) was inoculated with ST and the peripheral blood and feces were collected between 2 and 20 days post-inoculation. Two groups of pigs with either low shedding (LS) or persistent shedding (PS) phenotypes were identified. The global transcriptional changes in response to ST inoculation were identified by Affymetrix Genechip?analysis of peripheral blood RNA at day 0 and day 2 post-inoculation.

Publication Title

Distinct peripheral blood RNA responses to Salmonella in pigs differing in Salmonella shedding levels: intersection of IFNG, TLR and miRNA pathways.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP149944
Transcription profile analysis of wild type and Irf9-/- bone marrow derived macrophages in response to type I and type II interferons
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Host defense by the innate immune system requires the establishment of antimicrobial states allowing cells to cope with microorganisms before the onset of the adaptive immune response. Interferons (IFN) are of vital importance in the establishment of cell-autonomous antimicrobial immunity. Speed is therefore an important attribute of the cellular response to IFN. With much of the antimicrobial response being installed de novo, this pertains foremost to gene expression, the rapid switch between resting-state and active-state transcription of host defense genes. Our results show how mRNA expression changes upon IFNb or IFNg treatment in wild typ and Irf9-/- bone marrow derived macrophages. Overall design: Methods: Bone marrow derived macrophage mRNA of wild-type (WT) and Irf9 knock out mice (IRF9-/-) untreated, as well as 2h IFNb and IFNg treated were generated by deep sequencing, in triplicate, using Illumina sequencing.

Publication Title

A molecular switch from STAT2-IRF9 to ISGF3 underlies interferon-induced gene transcription.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE89073
Expression data from WT and RGS5 KO mice treated with DOCA/salt
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

The activation of vascular smooth muscle cells (VSMCs) during hypertension-induced arterial remodeling processes relies on a change of the gene expression program, i.e., up-regulation of genes to induce migration, proliferation and matrix degradation/synthesis. At the same time, genes controlling the quiescent, contractile VSMC phenotype are down-regulated. We used microarrays to detail the global program of gene expression underlying hypertension-induced vascular remodeling in the presence and absence of regulator of G-protein signaling 5 (RGS5) and identified distinct classes of down-regulated genes during vascular remodeling when RGS5 was not present.

Publication Title

Hypertension-evoked RhoA activity in vascular smooth muscle cells requires RGS5.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon SRP188096
Transcription profile analysis of wild type and Irf9-/- mouse embryonic fibroblasts (MEF) in response to type I interferons
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Host defense by the innate immune system requires the establishment of antimicrobial states allowing cells to cope with microorganisms before the onset of the adaptive immune response. Interferons (IFN) are of vital importance in the establishment of cell-autonomous antimicrobial immunity. Speed is therefore an important attribute of the cellular response to IFN. With much of the antimicrobial response being installed de novo, this pertains foremost to gene expression, the rapid switch between resting-state and active-state transcription of host defense genes. Our results show how mRNA expression changes upon IFNb treatment in wild type and Irf9-/- mouse embryonic fibroblasts. Overall design: Methods: Mouse embryonic fibroblast (MEF) mRNA of wild-type (WT) and Irf9 knock out mice (IRF9-/-) untreated, as well as 2h IFNb treated were generated by deep sequencing, in triplicate, using Illumina sequencing.

Publication Title

A molecular switch from STAT2-IRF9 to ISGF3 underlies interferon-induced gene transcription.

Sample Metadata Fields

Subject

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accession-icon SRP188099
Transcription profile analysis of wild type and Irf9-/- human monocytic THP1 cells in response to type I interferons
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Host defense by the innate immune system requires the establishment of antimicrobial states allowing cells to cope with microorganisms before the onset of the adaptive immune response. Interferons (IFN) are of vital importance in the establishment of cell-autonomous antimicrobial immunity. Speed is therefore an important attribute of the cellular response to IFN. With much of the antimicrobial response being installed de novo, this pertains foremost to gene expression, the rapid switch between resting-state and active-state transcription of host defense genes. Our results show how mRNA expression changes upon IFNb treatment in wild type and Irf9-/- THP1 cells. Overall design: Methods: mRNA of untreated and IFNb treated wild-type (WT) and Irf9 knock out (IRF9-/-) human monocytic THP1 cells were analyzed by deep sequencing, in triplicate, using Illumina sequencing.

Publication Title

A molecular switch from STAT2-IRF9 to ISGF3 underlies interferon-induced gene transcription.

Sample Metadata Fields

Subject

View Samples
accession-icon GSE46515
Expression data from mouse model using targeted deletion of hepatic RICTOR (Albumin-Cre Rictor LoxP/LoxP)
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Recent work using mouse models has revealed that mTORC2, which unlike mTORC1 is not acutely sensitive to rapamycin, plays a key role in the regulation of organismal physiology. The substrates and pathways regulated by mTORC2 are at present relatively unknown

Publication Title

Hepatic signaling by the mechanistic target of rapamycin complex 2 (mTORC2).

Sample Metadata Fields

Sex, Specimen part, Treatment

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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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