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accession-icon GSE17925
Gene expression from TCDD treated C57BL6/J and human Aryl hydrocarbon Receptor expressing primary mouse hepatocytes
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The human and mouse aryl hydrocarbon receptor (hAHR and mAHRb) share limited (58%) transactivation domain sequence identity. Compared to the mAHRb allele, the hAHR displays 10-fold lower relative affinity for prototypical ligands such as 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD). However, in previous studies we have demonstrated that the hAHR can display a higher relative ligand binding affinity than the mAHRb for specific AHR ligands such as indirubin. Each receptor has also been shown to differentially recruit LXXLL co-activator-motif proteins and to utilize different TAD subdomains in gene transactivation. Using hepatocytes isolated from C57BL6/J mice (Ahrb/b) and AHRTtr transgenic mice which express hAHR protein specifically in hepatocytes, we investigated whether the hAHR and mAHRb differentially regulate genes. Microarray and quantitative-PCR analysis of Ahrb/b and AHRTtr primary-mouse hepatocytes treated with 10 nM TCDD revealed that a number of established AHR target genes such as Cyp1a1 and Cyp1b1 are significantly induced by both receptors. Remarkably, of the 1752 genes induced by mAHRb and 1186 genes induced by hAHR, only 265 genes (<10%) were significantly activated by both receptors in response to TCDD. Conversely of the 1100 and 779 genes significantly repressed in mAHRb and hAHR hepatocytes respectively, only 462 (<25%) genes were significantly repressed by both receptors in response to TCDD treatment. Genes identified as differentially expressed are known to be involved in a number of biological pathways, including cell proliferation and inflammatory response which suggests that compared to the mAHRb, the hAHR may play contrasting roles in TCDD-induced toxicity and endogenous AHR-mediated gene regulation.

Publication Title

Differential gene regulation by the human and mouse aryl hydrocarbon receptor.

Alternate Accession IDs

E-GEOD-17925

Sample Metadata Fields

Specimen part

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accession-icon GSE82137
Molecular impact of electronic cigarette aerosol exposure in human bronchial epithelium
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Analysis of primary human bronchial epithelial cells grown in air liquid interface, exposed in vitro to whole tobacco cigarette smoke (48 puffs, 48 minutes) and electronic cigarette aerosol (400 puffs, 200 minutes). Electronic cigarette exposures included two flavors (menthol, tobacco) both with, and without nicotine.

Publication Title

Molecular Impact of Electronic Cigarette Aerosol Exposure in Human Bronchial Epithelium.

Alternate Accession IDs

E-GEOD-82137

Sample Metadata Fields

Specimen part

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accession-icon GSE49029
Transcriptome partitioning for mRNA translation in hypoxia
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Protein synthesis belongs to the most energy consuming processes in the cell. Lowering oxygen tension below normal (hypoxia) causes a rapid inhibition of global mRNA translation due to the decreased availability of energy. Interestingly, subsets of mRNAs pursue active translation under such circumstances. In human fibrosarcoma cells (HT1080) exposed to prolonged hypoxia (36 h, 1% oxygen) we observed that transcripts are either increasingly or decreasingly associated with ribosomes localized at the endoplasmic reticulum (ER). In a global setting it turned out that only 31% of transcripts showing elevated total-RNA levels were also increasingly present at the ER in hypoxia. These genes, regulated by its expression as well as its ER-localization, belong to the gene ontologys hypoxia response, glycolysis and HIF-1 transcription factor network supporting the view of active mRNA translation at the ER during hypoxia. Interestingly, a large group of RNAs was found to be unchanged at the expression level, but translocate to the ER in hypoxia. Among these are transcripts encoding translation factors and >180 ncRNAs. In summary, we provide evidence that protein synthesis is favoured at the ER and, thus, partitioning of the transcriptome between cytoplasmic and ER associated ribosomes mediates adaptation of gene expression in hypoxia.

Publication Title

Hypoxia-induced gene expression results from selective mRNA partitioning to the endoplasmic reticulum.

Alternate Accession IDs

E-GEOD-49029

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE25763
Comparative expression profiling identifies differential roles for Myogenin and p38 MAPK signaling in myogenesis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Mitogen activated protein kinase (MAPK) signaling regulates differentiation of many cell types. During myogenesis in particular, p38a MAPK (MAPK14) phosphorylates multiple transcriptional regulators to modulate muscle-specific gene expression. Among the p38a MAPK modulated genes is the muscle-specific transcriptional regulator Myogenin (Myog) that is also essential to complete the muscle differentiation program, and while it is known that both p38a MAPK and Myog are critically required for myogenesis, the individual contribution of each of these proteins is poorly defined. Here we show that Myog expression (in the absence of p38a MAPK signaling) is sufficient to establish expression of many late markers of muscle differentiation and to mediate cell migration. However, Myog expression alone did not led to the formation of multinucleated muscle cells, highlighting a critical role for p38a MAPK in myoblast fusion. Using comparative microarray analysis we identified p38a MAPK-dependent genes that are not regulated by Myog

Publication Title

Comparative expression profiling identifies differential roles for Myogenin and p38α MAPK signaling in myogenesis.

Alternate Accession IDs

E-GEOD-25763

Sample Metadata Fields

Cell line

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accession-icon GSE28359
Aryl hydrocarbon receptor antagonists promote the expansion of human hematopoietic stem cells
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Although practiced clinically for more than 40 years, the use of hematopoietic stem cell (HSC) transplants remains limited by the ability to expand these cells ex vivo. An unbiased screen with primary human HSCs identified a purine derivative, StemRegenin 1 (SR1), that promotes the ex vivo expansion of CD34+ cells. Culture of HSCs with SR1 led to a 50-fold increase in cells expressing CD34 and a 17-fold increase in cells that retain the ability to engraft immunodeficient mice. Mechanistic studies show that SR1 acts by antagonizing the aryl hydrocarbon receptor (AHR). The identification of SR1 and AHR modulation as a means to induce ex vivo HSC expansion should facilitate the clinical use of HSC therapy.

Publication Title

Aryl hydrocarbon receptor antagonists promote the expansion of human hematopoietic stem cells.

Alternate Accession IDs

E-GEOD-28359

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE61993
Expression data from human keratinocytes stimulated with streptococcal M1 protein
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

We used microarray analysis to investigate if keratinocytes excert an immuno-inflammatory response towards streptococcal M1 protein.

Publication Title

Vigilant keratinocytes trigger pathogen-associated molecular pattern signaling in response to streptococcal M1 protein.

Alternate Accession IDs

E-GEOD-61993

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE10812
Expression data from thylakoidal ascorbate peroxidase overexpressor Arabidopsis thaliana (Col) rosette leaves
  • organism-icon Arabidopsis thaliana
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

We used the flu mutant of Arabidopsis and a transgenic line that overexpresses the thylakoid-bound ascorbate peroxidase (tAPX) to address the interactions between different reactive oxygen species (ROS) signaling pathways. The conditional flu mutant of Arabidopsis accumulates excess protochlorophyllide in the dark within chloroplast membranes that upon illumination acts as a photosensitizer and generates singlet oxygen (1O2). Immediately after the release of singlet oxygen rapid changes in nuclear gene expression occur. Distinct sets of genes were activated that were different from those induced by other reactive oxygen species, superoxide or hydrogen peroxide (H2O2), suggesting that different types of active oxygen species activate distinct signaling pathways. It was not known whether the pathways operate separately or interact with each other. We have addressed this problem by modulating noninvasively the level of H2O2 in plastids by means of a transgenic line that overexpresses the thylakoid-bound ascorbate peroxidase (tAPX, line 14/2 PMID: 15165186). In the flu mutant overexpressing tAPX, the expression of most of the nuclear genes that were rapidly activated after the release of 1O2 was significantly higher in flu plants overexpressing tAPX, whereas in wild-type plants, overexpression of tAPX had only a very minor impact on nuclear gene expression. The results suggest that H2O2 antagonizes the 1O2-mediated signaling of stress responses as seen in the flu mutant. This cross-talk between H2O2- and 1O2-dependent signaling pathways might contribute to the overall stability and robustness of wild-type plants exposed to adverse environmental stress conditions.

Publication Title

Cross-talk between singlet oxygen- and hydrogen peroxide-dependent signaling of stress responses in Arabidopsis thaliana.

Alternate Accession IDs

E-GEOD-10812

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP098696
Subpopulations of mouse beta cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Type 1 diabetes (T1D) is a chronic autoimmune disease that involves immune mediated destruction of ß cells. How ß cells respond to immune attack is unknown. We identified a population of ß cells during the progression of T1D in non-obese diabetic (NOD) mice that survives immune attack. This population develops from normal ß cells confronted with islet infiltrates. Pathways involving cell movement, growth and proliferation, immune responses, and cell death and survival are activated in these cells. There is reduced expression of ß cell identity genes and diabetes antigens and increased immune inhibitory markers and stemness genes. This new subpopulation is resistant to killing when diabetes is precipitated with cyclosphosphamide. Human ß cells show similar changes when cultured with immune cells. These changes may account for the chronicity of the disease and the long term survival of ß cells in some patients. Overall design: mRNA profiles of top and bottom beta cells were generated by RNA-seq. 4 samples were processed from each population of cells.

Publication Title

β Cells that Resist Immunological Attack Develop during Progression of Autoimmune Diabetes in NOD Mice.

Alternate Accession IDs

GSE94382

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE35592
Microarray analysis of wildtype and Klf3 KO E14.5 fetal liver cells (TER119- and TER119+)
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The aim of this experiment was to investigate the role of KLF3 in regulating gene expression at different stages throughout the erythroid maturation process.

Publication Title

The CACCC-binding protein KLF3/BKLF represses a subset of KLF1/EKLF target genes and is required for proper erythroid maturation in vivo.

Alternate Accession IDs

E-GEOD-35592

Sample Metadata Fields

Specimen part

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accession-icon GSE35594
Microarray analysis of wildtype and Klf1-/- E13.5 fetal liver
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The aim of this experiment was to investigate the role of KLF1 in the fetal liver

Publication Title

The CACCC-binding protein KLF3/BKLF represses a subset of KLF1/EKLF target genes and is required for proper erythroid maturation in vivo.

Alternate Accession IDs

E-GEOD-35594

Sample Metadata Fields

Specimen part

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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