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accession-icon GSE6918
The distinct response of gd T cells to the Nod2 agonist muramyl dipeptide
  • organism-icon Bos taurus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Bovine Genome Array (bovine)

Description

We have begun to approach gd T cells more as prospective innate cells than as conventional T cells. Recent results indicated that purified gd T cells are primed directly in response to pathogen associated molecular patterns (PAMPs) to better respond to secondary signals and increase expression of chemokine and activation-related genes. In microarray and real time PCR analyses of RNA derived from bovine and human gd T cells, transcripts encoding Nod2 were repeatedly amplified. Nod2 is the intracellular receptor for muramyl dipeptide (MDP), a subunit of PGN, functions in regulating innate activities, and was thought to be expressed primarily in APCs. Given our repeated detection of Nod2 transcripts in gd T cells, the specific direct response of gd T cells to MDP was analyzed by microarray, real time PCR, proteome array and in a functional priming assay. The results indicate a subtle activation in response to MDP akin to priming, and suggest a unique mechanism for differential gene expression.

Publication Title

The distinct response of gammadelta T cells to the Nod2 agonist muramyl dipeptide.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP061367
Transcriptome differences in the rumen of beef steers with variation in feed intake and gain
  • organism-icon Bos taurus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

RNA sequencing (RNA-Seq) was performed on rumen papillae from 16 steers with variation in gain and feed intake. Overall design: Sixteen rumen papillae samples were sequenced by Cofactor Genomics (St.Louis, MO).

Publication Title

Transcriptome differences in the rumen of beef steers with variation in feed intake and gain.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE21368
Myocardial expression data from ketogenic diet-fed mice
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Specific pathogen free wild-type C57Bl/6 male mice fed ketogenic diet (Bio-Serv AIN-76-A) for 4 weeks

Publication Title

Adaptation of myocardial substrate metabolism to a ketogenic nutrient environment.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP045305
mRNA sequencing of small intestinal tissue of germfree mice
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

With this study we wanted to evaluate the impact of murine norovirus infection of germfree mice and to compare it to germfree mice which have received fecal transplants of conventional mice. Overall design: whole small intestinal tissue analysis of 3 germfree, 3 germfree mice infected with murine norovirus and 3 conventionalized germfree mice

Publication Title

An enteric virus can replace the beneficial function of commensal bacteria.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE53231
Expression data from 18h-fasted WT versus KLF15-null mice: heart
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

We used microarray analysis to identify differences in gene expression levels in heart following an 18h (overnight) fast in WT control and KLF15-null mice

Publication Title

Kruppel-like factor 15 is a critical regulator of cardiac lipid metabolism.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE73261
Differential gene expression in the spleen among crossbred beef steers with divergent gain and feed intake phenotypes.
  • organism-icon Bos taurus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Bovine Gene 1.1 ST Array (bovgene11st)

Description

Steer spleen transcriptome

Publication Title

Profile of the Spleen Transcriptome in Beef Steers with Variation in Gain and Feed Intake.

Sample Metadata Fields

Specimen part

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accession-icon GSE6451
A genomic screen for activators of the antioxidant response element
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The antioxidant response element (ARE) is a cis-acting regulatory enhancer element found in the 5 flanking region of many phase II detoxification enzymes. Upregulation of ARE-dependent target genes is known to have neuroprotective effects; yet, the mechanism of activation is largely unknown. By screening an arrayed collection of approximately 15,000 full-length expression cDNAs in the human neuroblastoma cell line IMR-32 with an ARE-luciferase reporter, we have identified several cDNAs not previously associated with ARE activation. A subset of cDNAs, including sequestosome 1 (SQSTM1) and dipeptidylpeptidase III (DPP3), activated the ARE in primary mouse-derived cortical neurons. Overexpression of SQSTM1 and DPP3 in IMR-32 cells stimulated NRF2 nuclear translocation and led to increased levels of NAD(P)H:quinone oxidoreductase 1 (NQO1), a protein which is transcriptionally regulated by the ARE. When transfected into IMR-32 neuroblastoma cells that were depleted of transcription factor NRF2 by RNA interference, SQSTM1 and DPP3 were unable to activate the ARE or induce NQO1 expression, indicating that the ARE activation upon ectopic expression of these cDNAs is mediated by NRF2. Studies with pharmacological inhibitors indicated that 1-phosphatidylinositol 3-kinase (PI3K) and protein kinase C (PKC) signaling are also essential for activity. Lastly, overexpression of these cDNAs conferred partial resistance to hydrogen peroxide induced toxicity, consistent with the induction of antioxidant and phase II detoxification enzymes which can protect from oxidative stress. This work and other such studies may provide mechanisms for activating the ARE in the absence of general oxidative stress, and a novel therapeutic approach to degenerative diseases and aging.

Publication Title

A genomic screen for activators of the antioxidant response element.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE16193
Interfering with Proximal TLR4 to NF-kappaB Signal Transduction in Human Monocytes
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Carbon monoxide (CO) is an endogenous messenger that suppresses inflammation, modulates apoptosis and promotes vascular remodeling. Here, microarrays were employed to globally characterize the CO (250 ppm) suppression of early (1 h) LPS-induced inflammation in human monocytic THP-1 cells. CO suppressed 79 of 101 immediate-early genes induced by LPS; 19% (15/79) were transcription factors and most others were cytokines, chemokines and immune response genes. The prototypic effects of CO on transcription and protein production occurred early but decreased rapidly. CO activated p38 MAPK, ERK1/2 and Akt and caused an early and transitory delay in LPS-induced JNK activation. However, selective inhibitors of these kinases failed to block CO suppression of LPS-induced IL-1beta, an inflammation marker. Of CO-suppressed genes, 81% (64/79) were found to have promoters with putative NF-kappaB binding sites. CO was subsequently shown to block LPS-induced phosphorylation and degradation of IkappaBalpha in human monocytes, thereby inhibiting NF-kappaB signal transduction. CO broadly suppresses the initial inflammatory response of human monocytes to LPS by reshaping proximal events in TLR4 signal transduction such as stress kinase responses and early NF-kappaB activation. These rapid, but transient effects of CO may have therapeutic applications in acute pulmonary and vascular injury.

Publication Title

Carbon monoxide blocks lipopolysaccharide-induced gene expression by interfering with proximal TLR4 to NF-kappaB signal transduction in human monocytes.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP149190
Transcriptional profile of monocytes in the colon in response to C. rodentium infection
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Transcriptional profile of monocytes in the colon in response to C. rodentium infection Overall design: Eight samples have been analyzed. All are from Cd11b+Ly6C+ inflammatory monocytes sorted from colonic tissue 9 days after C. rodentium infection from Atg16L1HM(4) and WT(4) mice.

Publication Title

Autophagy proteins suppress protective type I interferon signalling in response to the murine gut microbiota.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon GSE16625
5-azacytidine and entinostat treatment of patients with MDS, chronic myelomonocytic leukemia (CMMoL), and high risk AML
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Early epigenetic changes and DNA damage do not predict clinical response in an overlapping schedule of 5-azacytidine and entinostat in patients with myeloid malignancies. The patients with MDS, chronic myelomonocytic leukemia (CMMoL), and high risk AML were treated with sequential administration of methylation inhibitor drugs (5AC and entinostat). To study gene expresion regulation in treated patients, microarray analysis was done on RNA samples extracted from CD34+ cells from 18 patients before and 15 days after treatment using Affymetrix U133Plus2.0.

Publication Title

Early epigenetic changes and DNA damage do not predict clinical response in an overlapping schedule of 5-azacytidine and entinostat in patients with myeloid malignancies.

Sample Metadata Fields

Specimen part, Disease

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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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