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accession-icon E-MEXP-231
Transcription profiling by array of human primary lung adenocarcinomas
  • organism-icon Homo sapiens
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Gene transcription in a set of 49 human primary lung adenocarcinomas and 9 normal lung tissue samples was examined using Affymetrix GeneChip technology. We aimed to investigate differential gene expression between the two tissue types. A total of 3,442 genes, called the set MAD, were found to be either up- or down-regulated by at least two fold between the two phenotypes. Genes assigned to a particular gene ontology term were found, in many cases, to be significantly unevenly distributed between the genes in and outside MAD. Terms that were overrepresented in MAD included functions directly implicated in cancer cell metabolism. Based on their functional roles and expression profiles, genes in MAD were grouped into likely co-regulated gene sets.

Publication Title

Conserved transcription factor binding sites of cancer markers derived from primary lung adenocarcinoma microarrays.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage

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accession-icon GSE9785
Expression data from Newborn mice infected with Shigella flexneri
  • organism-icon Mus musculus
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

In order to identify the developmental changes controlling the switch from disease susceptibility to resistance, we performed global gene expression analysis on non-infected and infected intestinal tissues taken from 4-day- and 7-day-old animals.

Publication Title

Maturation of paneth cells induces the refractory state of newborn mice to Shigella infection.

Sample Metadata Fields

Age

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accession-icon GSE84366
Gene expression of E13 fetal liver of common lymphoid progenitors Flt3+ a4b7+ compared to a4b7-HSAint, a4b7-HSAhi or a4b7-HSAlow
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We used whole genome transcriptome as gene discovery to further understand the rules of lineage restriction in the lymphoid compartment

Publication Title

Asynchronous lineage priming determines commitment to T cell and B cell lineages in fetal liver.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE37369
Caco-2 cell gene expression following co-culture with Lactobacillus casei and Bifidobacterium breve
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

To characterize how symbiotic bacteria affect the lolecular and cellular mechanisms of epithelial homeostasis, human colonic Caco-2 cells

Publication Title

Epithelial cell proliferation arrest induced by lactate and acetate from Lactobacillus casei and Bifidobacterium breve.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE6082
An injected bacterial effector targets chromatin access for NF-kB as a strategy to shape transcription of immune genes
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Phosphorylation of histone H3 at Serine 10 emerges as a mechanism increasing chromatin accessibility of the transcription factor NF-kB for a particular set of immune genes. Here we report that a bacterial pathogen uses this strategy to shape the transcriptional response of infected host cells. We identify the Shigella flexneri type III protein effector OspF as a Dual Specific Phosphatase. OspF dephosphorylates MAP kinases within the nucleus impairing histone H3 phosphorylation at Serine 10 in a gene-specific manner. Therefore, OspF reprograms the transcriptional response for inactivation of a subset of NF-kB responsive genes. This regulation leads to repression of polymorphonuclear leukocytes recruitment in infected tissues. Thus, pathogens have evolved the ability to precisely modulate host cell epigenetic information as a strategy to repress innate immunity.

Publication Title

An injected bacterial effector targets chromatin access for transcription factor NF-kappaB to alter transcription of host genes involved in immune responses.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE8636
Intestinal xenotransplants infected with Shigella
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

to analyse the transcriptomic response of human intestinal tissue engrafted in SCID mice to Shigella infection

Publication Title

Virulent Shigella flexneri subverts the host innate immune response through manipulation of antimicrobial peptide gene expression.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE52192
Transcriptional profiling of embryonic skeletal muscle stem/progenitor cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Muscle stem cells (MuSC) change molecular and functional properties during development. Using a transgenic Tg:Pax7-nGFP mice, we FACS-isolated MuSC from embryonic (E12.5) and foetal (E17.5) stages to understand the differences and similarities amongst the myogenic stem/progenitor populations.

Publication Title

Cell-autonomous Notch activity maintains the temporal specification potential of skeletal muscle stem cells.

Sample Metadata Fields

Specimen part

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accession-icon SRP094834
Homo sapiens Transcriptome or Gene expression
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

RNA-sequencing analysis of RBP2 overexpressing MCF7 cell lines. RBP2 (also known as JARID1A), a member of the JARID1 family of histone H3 lysine K4 demethylases, has been considered to have an oncogenic potential in several cancer including breast cancer. Results provide insight into the transcriptional regulation of RBP2 in estrogen receptor positve breast cancer.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Cell line

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accession-icon SRP076437
Raw sequence reads
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

HLA-I positive and negative subpopulations isolated from human clear cell sarcoma xenografts

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Disease

View Samples
accession-icon SRP125568
The FRA1–JUNB/AP-1 transcription complex, a downstream target of STAT3, induces Th17 differentiation and promotes experimental autoimmune arthritis
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Dysfunction of Th17 cells leads to chronic inflammatory disorders. STAT3 orchestrates the expression of proinflammatory cytokinesand pathogenic cell differentiation from IL-17-producing Th17 cells. However, the pathways mediated by STAT3 signaling are not fully understood. Here, we observed that FRA1 and JUNB are directly involved in STAT3 binding to sites in the promoters of Fosl1 and Junb. Promoter binding increased expression of IL-17 and the development of Th17 cells. Overexpression of Fra1 and Junb in mice resulted in susceptibility to collagen-induced arthritis (CIA) and an increase in Th17 cell numbers and inflammatory cytokine production. In patients with rheumatoid arthritis (RA), FRA1 and JUNB were colocalized with STAT3 in the inflamed synovium. These observations suggest that FRA1 and JUNB are associated closely with STAT3 activation, and that this activation leads to Th17 cell differentiation in autoimmune diseases and inflammation.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Cell line

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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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Developed by the Childhood Cancer Data Lab

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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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