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accession-icon SRP159106
The effect of genetic background on cognitive and pathological traits: AD-BXD [dataset 2]
  • organism-icon Mus musculus
  • sample-icon 88 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Cg.5XFAD females (MMRRC Stock No #34848-JAX) were bred to males from BXD strains. The resulting F1 progeny were monitored throughout their lifepan to evaluate the effect of genetic background on cognitive and pathological traits. Samples here come from various AD-BXD lines at either 6 or 14 months of age. An earlier dataset of similar design (plus Non-transgenic littermates) was deposited as GSE101144. Ntg littermates of mice sampled here will be deposited as a separate GEO series. Overall design: 88 AD samples. For final by-strain analysis, samples were averaged into strain/age/genotype/sex groups (For example, all D2 6mo 5XFAD males were averaged for final by-strain analysis)

Publication Title

Identification of Pre-symptomatic Gene Signatures That Predict Resilience to Cognitive Decline in the Genetically Diverse AD-BXD Model.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Subject

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accession-icon SRP111520
The effect of genetic background on cognitive and pathological traits: AD-BXD
  • organism-icon Mus musculus
  • sample-icon 108 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Female C57BL/6J mice hemizygous for the 5XFAD transgene (MMRRC Stock No #34848-JAX) were bred to males from BXD strains, which do not carry the 5XFAD transgene. The resulting F1 progeny were monitored throughout their lifespan to evaluate the effect of genetic background on cognitive and pathological traits. All of the mice were fear conditioned and sacrificed within 30 minutes of testing. On the sample records, the characteristics: age field provides the age at which fear conditioning, sacrifice, and tissue collection occurred. Samples here come from various AD-BXD lines and their non-transgenic (Ntg) littermate counterparts at either 6 or 14 months of age. Overall design: 133 samples, 64 Ntg and 69 AD. For final by-strain analysis, samples were averaged into strain/age/genotype/sex groups (For example, all D2 6mo 5XFAD males were averaged for final by-strain analysis)

Publication Title

Harnessing Genetic Complexity to Enhance Translatability of Alzheimer's Disease Mouse Models: A Path toward Precision Medicine.

Sample Metadata Fields

Sex, Age, Specimen part, Subject

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accession-icon SRP165993
The aryl hydrocarbon receptor pathway defines the time frame for restorative neurogenesis
  • organism-icon Danio rerio
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We compared transcriptomes of two ependymoglial populations isolated from adult zebrafish telencephalon. Overall design: Ependymoglial cells are acutely isolated from the adult zebrafish brains form 3 months old transgenic gfap:GFP animals. GFP is experssed in all ependymoglial cells and two populations are separated using GFP intensity in FACS.

Publication Title

The Aryl Hydrocarbon Receptor Pathway Defines the Time Frame for Restorative Neurogenesis.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP100979
HSF1-dependent and -independent regulation of the mammalian in vivo heat shock response and its impairment in Huntington's disease
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The heat shock response (HSR) is a mechanism to cope with proteotoxic stress by inducing the expression of molecular chaperones and other heat shock response genes. The HSR is evolutionarily well conserved and has been widely studied in bacteria, cell lines and lower eukaryotic model organisms. However, mechanistic insights into the HSR in higher eukaryotes, in particular in mammals, are limited. We have developed an in vivo heat shock protocol to analyze the HSR in mice and dissected heat shock factor 1 (HSF1)-dependent and -independent pathways. Whilst the induction of proteostasis-related genes was dependent on HSF1, the regulation of circadian function related genes, indicating that the circadian clock oscillators have been reset, was independent of its presence. Furthermore, we demonstrate that the in vivo HSR is impaired in mouse models of Huntington's disease but we were unable to corroborate the general repression of transcription after a heat shock found in lower eukaryotes. Overall design: RNA-Seq was performed on mRNA isolated from quadriceps femoris muscle of 24 mice. These mice were of wild type, R6/2, and Hsf1-/- genotypes. Two mice of each genotype were tested in four conditions: (1) heat shock, (2) control heat shock, (3) HSP90 inhibition (NVP-HSP990), and (4) HSP90 inhibition vehicle.

Publication Title

HSF1-dependent and -independent regulation of the mammalian in vivo heat shock response and its impairment in Huntington's disease mouse models.

Sample Metadata Fields

Age, Specimen part, Treatment, Subject

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accession-icon GSE30873
Effects of caspase-8 deletion in the intestinal epithelium
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Caspase-8 is a cystein protease involved in regulating apoptosis. The function of caspase-8 was studied in the intestinal epithelium, using mice with an intestinal epithelial cell specific deletion of caspase-8.

Publication Title

Caspase-8 regulates TNF-α-induced epithelial necroptosis and terminal ileitis.

Sample Metadata Fields

Specimen part

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accession-icon SRP043967
The CNS-Heart Axis is a Source of Cardiac Dysfunction in Mouse Models of Huntington’s Disease
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: Transcriptome profiling (RNA-seq) to microarray to evaluate transcriptional changes in the heart of HD mouse models Methods: Heart mRNA profiles of 4-weeks-old wild-type (WT) and R6/2 transgenic; 15-weeks-old WT and R6/2 transgenic mice; 8-month-old WT and HdhQ150 knock-in mice; 22-month-old WT and HdhQ150 knock-in mice were generated by deep sequencing, in triplicate, using Illumina Hi-seq 2000. Conclusions: Our study showed that there is no major transcriptional deregulation in the heart of mouse models of HD. Overall design: Heart mRNA profiles of 4-weeks-old wild-type (WT) and R6/2 transgenic; 15-weeks-old WT and R6/2 transgenic mice; 8-month-old WT and HdhQ150 knock-in mice; 22-month-old WT and HdhQ150 knock-in mice were generated by deep sequencing, in triplicate, using Illumina Hi-seq 2000.

Publication Title

Dysfunction of the CNS-heart axis in mouse models of Huntington's disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon E-TABM-585
Transcription profiling by array of human lung cancer cells after treatment with dasatinib, imatinib, nilotinib or PD0325901
  • organism-icon Homo sapiens
  • sample-icon 111 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Human Genome U133A Array (hthgu133a)

Description

Cell Line: This experiment was designed to measure the transcriptional responses to four kinase inhibitors across a five-logarithm dose range. The A549 human lung cancer cell line was treated with dasatinib, imatinib or nilotinib (4 hours and 20 hours) or PD0325901 (4 hours). Treatments used a 12-point dose range (30 uM with 3-fold dilutions down to 0.17 nM; 0.5% DMSO vehicle for all treatments). Experimental design prevented row or column handling effects being confounded with dose effect.

Publication Title

Transcriptional profiling of the dose response: a more powerful approach for characterizing drug activities.

Sample Metadata Fields

Disease, Cell line, Compound, Time

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accession-icon GSE57417
Role of Blimp-1 in programing Th effector cells into IL-10 producers
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Gene expression profiling on IL-10-secreting and non-secreting murine Th1 cells, stimulated in the presence or absence of the Notch ligand Delta-like 4 (Dll4), was performed to identify transcription factors co-expressed with IL-10.

Publication Title

Role of Blimp-1 in programing Th effector cells into IL-10 producers.

Sample Metadata Fields

Specimen part

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accession-icon GSE43338
Gene expression profiling of colitis-associated and sporadic colorectal tumors in mice
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

To uncover molecular mechanisms specifically involved in the pathogenesis of colitis-associated colon cancer (CAC), we studied tumorigenesis in experimental models of CAC and sporadic CRC that mimic characteristics of human CRC. Using comparative whole genome expression profiling, we observed differential expression of epiregulin (Ereg) in mouse models of colitis-associated, but not sporadic colorectal cancer. Similarly, highly significant upregulation of Ereg expression was found in cohorts of patients with colitis-associated cancer in inflammatory bowel disease but not in sporadic colorectal cancer. Furthermore, tumor-associated fibroblasts were identified as major source of Ereg in colitis-associated neoplasias. Functional studies showed that Ereg-deficient mice, although more prone to colitis, are strongly protected from colitis-associated tumors, and data from serial endoscopic studies revealed that Ereg promotes growth rather than initiation of tumors.

Publication Title

Tumor fibroblast-derived epiregulin promotes growth of colitis-associated neoplasms through ERK.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE21477
Gene Expression Changes in Primary Human Nasal Epithelial Cells exposed to Formaldehyde in vitro
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Using various exposure conditions, we studied the induction of DNA-protein crosslinks (DPX) by formaldehyde (FA) and their removal in primary human nasal epithelial cells (HNEC). DPX were indirectly measured by the alkaline comet assay as the reduction of gamma ray induced DNA migration. DPX are the most relevant primary DNA alterations induced by FA and the comet assay is a very sensitive method for the detection of FA-induced DPX. In parallel experiments, we investigated changes in gene expression by using a full genome human microarray. After a single treatment with FA (50 to 200 M), concentration and time-dependent changes in gene expression were seen under conditions that also induced genotoxicity. Repeated treatments with low FA concentrations (20 and 50 M) did not lead to a significant induction of DPX but repeated treatments with 50 M FA changed the expression of more than 100 genes. Interestingly, the expression of genes involved in the main pathway for FA detoxification and the repair of DPX were not specifically enhanced. A high degree of overlap was seen among the pattern of gene changes induced by FA in HNEC in comparison to recently published array studies for nasal epithelial cells from rats exposed to FA in vivo. Our results suggest that HNEC are a suited in vitro model for the characterization of FA-induced toxicity and the relationship between genotoxic and other cytotoxic effects.

Publication Title

Gene expression changes in primary human nasal epithelial cells exposed to formaldehyde in vitro.

Sample Metadata Fields

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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