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accession-icon GSE10741
Toll-like Receptor 3-induced Suppression via Binding of Suppressors of Cytokine Signaling 3 to Tyrosine Kinase 2
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

The Suppressor of cytokine signaling (SOCS) family of negative regulatory proteins are upregulated in response to several cytokines and pathogen-associated molecular patterns (PAMPs), and suppress cellular signaling responses by binding receptor phosphotyrosine residues. Exposure of bone marrow-derived dendritic cells (BMDCs) to 1D8 cells, a murine model of ovarian carcinoma, suppresses their ability to express CD40 and stimulate antigen specific responses in response to PAMPs, and in particular to poly I: C with the upregulated SOCS3 transcript and protein levels. The ectopic expression of SOCS3 in both the macrophage cell line RAW264.7 and BMDCs decreased signaling in response to both poly I:C and IFN. Further, knockdown of SOCS3 transcripts significantly enhanced the responses of RAW264.7 and BMDCs to both poly I: C and IFN. Immunoprecipitation and pull-down studies demonstrate that SOCS3 binds to the IFN receptor TYK2. Since poly I: C triggers autocrine IFN signaling, binding of SOCS3 to TYK2 may thereby suppress the activation of BMDCs by polyI:C and IFN. Thus, elevated levels of SOCS3 in tumor-associated DCs may potentially resist the signals induced by TLR3 ligands and type I interferon to decrease DC activation via binding with IFN receptor TyK2.

Publication Title

No associated publication

Alternate Accession IDs

E-GEOD-10741

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE89215
Expression data from control and demylination zebrafish at 10dpf
  • organism-icon Danio rerio
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

Zebrafish is ideal model organism to study myelination and demyelination. We could use this model to screen demylination relative genes and provide a new idea for clinic therapy.

Publication Title

Down-regulation of interleukin 7 receptor (IL-7R) contributes to central nervous system demyelination.

Alternate Accession IDs

E-GEOD-89215

Sample Metadata Fields

Specimen part

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accession-icon GSE111111
Expression data from Germ-Free (GF) and L.NK2-colonized mice intestinal epithelial cells and Peyer's patches cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Lactobacillus NK2 (L.NK2) is a commensal microbe, isolated from the mouse intestinal feces in our lab. To examine the potential role of L. NK2 in the gut immunity, we monocolonized GF mice with L.NK2. And, we conducted a microarray experiment to compare the transcriptomes of GF and L.NK2-colonized mice intestines under the same experimental condition

Publication Title

No associated publication

Alternate Accession IDs

E-GEOD-111111

Sample Metadata Fields

Specimen part

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accession-icon GSE104558
Expression data from mouse MDSC with interference or overexpression of lncMDSC
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Myeloid-derived suppressor cells (MDSCs) have emerged as major regulators of immune responses in cancer and other pathological conditions. At the epigenetic level, lncRNA play an important role in cell differentiation and function. We identify a novel long non-coding RNA (lncRNA) termed as lnc-mdsc in MDSCs, which may tightly control the development of MDSCs.

Publication Title

No associated publication

Alternate Accession IDs

E-GEOD-104558

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE104571
Expression data from mouse MDSC with interference of lncMDSC
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

Myeloid-derived suppressor cells (MDSCs) have emerged as major regulators of immune responses in cancer and other pathological conditions. At the epigenetic level, lncRNA play an important role in cell differentiation and function. We identify a novel long non-coding RNA (lncRNA) termed as lnc-mdsc in MDSCs, which may tightly control the development of MDSCs.

Publication Title

No associated publication

Alternate Accession IDs

E-GEOD-104571

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE14929
Myocardial expression data from gnotobiotic wild-type and Ppara-/- mice
  • organism-icon Mus musculus
  • sample-icon 38 Downloadable Samples
  • Technology Badge Icon

Description

Germ free (GF) and conventionalized (CONV-D) wild-type C57Bl/6 male mice in the CARB-fed, 24h fasted, and 30d trained states; plus GF and CONV-D CARB-fed Ppara-/- mice. CARB-fed indicates a standard polysaccharide-rich mouse chow diet.

Publication Title

No associated publication

Alternate Accession IDs

E-GEOD-14929

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE64750
Lung expression data from highly pathogenic H5N1 virus infected and uninfected mice
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon

Description

Susceptible and Resistant mouse strain, e.g. DBA/2J and C57BL/6J respectively, were inoculated with a highly pathogenic H5N1 influenza A virus (A/Hong Kong/213/2003) for 72 hours.

Publication Title

Host genetic variation affects resistance to infection with a highly pathogenic H5N1 influenza A virus in mice.

Alternate Accession IDs

E-GEOD-64750

Sample Metadata Fields

Sex

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accession-icon GSE43716
Microarray to find CHOP/ATF5 dependent genes in response to proteasome inhibition
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

CHOP induces activating transcription factor 5 (ATF5) to trigger apoptosis in response to perturbations in protein homeostasis.

Alternate Accession IDs

E-GEOD-43716

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE54581
Selective mRNA translation during eIF2 phosphorylation induces expression of IBTKalpha
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon

Description

Disruption of protein folding in the endoplasmic reticulum triggers the Unfolded Protein Response (UPR), a transcriptional and translational control network designed to restore protein homeostasis. Central to the UPR is PERK phosphorylation of the alpha subunit of eIF2 (eIF2~P), which represses global translation coincident with preferential translation of mRNAs, such as ATF4 and CHOP, that serve to implement the UPR transcriptional regulation. In this study, we used sucrose gradient ultracentrifugation and a genome-wide microarray approach to measure changes in mRNA translation during ER stress. Our analysis suggests that translational efficiencies vary across a broad range during ER stress, with the majority of transcripts being either repressed or resistant to eIF2~P, while a notable cohort of key regulators are subject to preferential translation. From this latter group, we identify IBTKa as being subject to both translation and transcriptional induction during eIF2~P in both cell lines and a mouse model of ER stress. Translational regulation of IBTKalpha mRNA involves the stress-induced relief of two inhibitory uORFs in the 5'-leader of the transcript. Depletion of IBTKalpha by shRNA reduced viability of cultured cells coincident with increased caspase 3/7 cleavage, suggesting that IBTKalpha is a key regulator in determining cell fate during the UPR.

Publication Title

Selective mRNA translation during eIF2 phosphorylation induces expression of IBTKα.

Alternate Accession IDs

E-GEOD-54581

Sample Metadata Fields

Specimen part

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accession-icon GSE10964
Virus-Induced Airway Disease in Mice (C57BL/6J, d21/d49)
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon

Description

Analysis of gene expression in lungs of C57BL/6J mice that develop chronic airway disease phenotypes after a single Sendai virus infection, compared with mice treated with UV-inactivated virus.

Publication Title

Persistent activation of an innate immune response translates respiratory viral infection into chronic lung disease.

Alternate Accession IDs

E-GEOD-10964

Sample Metadata Fields

Sex, Time

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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