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accession-icon GSE12730
Mouse gestational protein restriction: Newborn offspring liver and hindleg muscle
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Gestational protein restriction is a model for low birth size. We hypothesized that taurine supplementation would protect against changes in newborn liver and muscle caused by a maternal low protein diet.

Publication Title

Gestational protein restriction in mice has pronounced effects on gene expression in newborn offspring's liver and skeletal muscle; protective effect of taurine.

Alternate Accession IDs

E-GEOD-12730

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE3216
Gene regulatory networks along the small intestinal crypt-villus axis
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Genes encoding transcription factors function as hubs in gene regulatory networks because they encode DNA-binding proteins, which bind to promoters that carry their binding sites. In the present work we have studied gene regulatory networks defined by genes with transcripts belonging to different mRNA abundance classes in the small intestinal epithelial cell. The focus is the rewiring that occurs in transcription factor hubs in these networks during the differentiation of the small intestinal epithelial cell while it migrates along the crypt-villus axis and during its development from a fetal endodermal cell to a mature adult villus epithelial cell.

Publication Title

Metabolome, transcriptome, and bioinformatic cis-element analyses point to HNF-4 as a central regulator of gene expression during enterocyte differentiation.

Alternate Accession IDs

E-GEOD-3216

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE96670
Tamoxifen response and resistance in invasive lobular breast cancer
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integrated molecular analysis of Tamoxifen-resistant invasive lobular breast cancer cells identifies MAPK and GRM/mGluR signaling as therapeutic vulnerabilities.

Alternate Accession IDs

E-GEOD-96670

Sample Metadata Fields

Treatment

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accession-icon GSE96570
Integrated Molecular Analysis of Tamoxifen-Resistant Invasive Lobular Breast Cancer Cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Invasive lobular breast cancer (ILC) is an understudied malignancy with distinct clinical, pathological, and molecular features that distinguish it from the more common invasive ductal carcinoma (IDC). Mounting evidence suggests that estrogen receptor-alpha positive (ER+) ILC has a poor response to Tamoxifen (TAM), but the mechanistic drivers of this are undefined. In the current work, we comprehensively characterize the SUM44/LCCTam ILC model system through integrated analysis of gene expression, copy number, and mutation, with the goal of identifying actionable alterations relevant to clinical ILC that can be co-targeted along with ER to improve treatment outcomes. We show that TAM has several distinct effects on the transcriptome of LCCTam cells, that this resistant cell model has acquired copy number alterations and mutations that impinge on MAPK and metabotropic glutamate receptor (GRM/mGluR) signaling networks, and that pharmacological inhibition of either improves or restores the growth-inhibitory actions of endocrine therapy.

Publication Title

Integrated molecular analysis of Tamoxifen-resistant invasive lobular breast cancer cells identifies MAPK and GRM/mGluR signaling as therapeutic vulnerabilities.

Alternate Accession IDs

E-GEOD-96570

Sample Metadata Fields

Treatment

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accession-icon GSE46871
Hippocampal gene expression profiling of a model of Alzheimer`s Disease upon treatment with the ACE inhibitor captopril
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Extracellular senile plaques of amyloid beta (Abeta) are a pathological hallmark in brain of patients with Alzheimer`s Disease (AD). Abeta is generated by the amyloidogenic processing of the amyloid precursor protein (APP). Concomitant to Abeta load, AD brain is characterized by an increase in protein level and activity of the angiotensin-converting enzyme (ACE). ACE inhibitors are a widely used class of drugs with established benefits for patients with cardiovascular disease. However, the role of ACE and ACE inhibition in the development of Abeta plaques and the process of AD-related neurodegeneration is not clear since ACE was reported to degrade Abeta. To investigate the effect of ACE inhibition on AD-related pathomechanisms, we used Tg2576 mice with neuron-specific expression of APPSwe as AD model. From 12 months of age, substantial Abeta plaque load accumulates in the hippocampus of Tg2576 mice as a brain region, which is highly vulnerable to AD-related neurodegeneration. The effect of central ACE inhibition was studied by treatment of 12 month-old Tg2576 mice for six months with the brain penetrating ACE inhibitor captopril. At an age of 18 months, hippocampal gene expression profiling was performed of captopril-treated Tg2576 mice relative to untreated 18 month-old Tg2576 controls with high Abeta plaque load. As an additional control, we used 12 month-old Tg2576 mice with low Abeta plaque load. Whole genome microarray gene expression profiling revealed gene expression changes induced by the brain-penetrating ACE inhibitor captopril, which could reflect the neuro-regenerative potential of central ACE inhibition.

Publication Title

ACE inhibition with captopril retards the development of signs of neurodegeneration in an animal model of Alzheimer's disease.

Alternate Accession IDs

E-GEOD-46871

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE23844
Analysis of Notch signaling on Xenopus epidermis
  • organism-icon Xenopus laevis
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome Array (xenopuslaevis)

Description

Analysis of epithelial explants injected with the intracellular domain of Notch (ICD) to block the formation of multi-ciliate and proton secreting cells or with dominant negative human Mastermind (HMM) to induce the formation of ectopic multi-ciliate and proton secreting cells. Results show which genes are up or down-regulated when HMM is compared to ICD.

Publication Title

Specification of ion transport cells in the Xenopus larval skin.

Alternate Accession IDs

E-GEOD-23844

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP040244
Drosophila melanogaster Transcriptome or Gene expression
  • organism-icon Drosophila melanogaster
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina HiSeq 2000

Description

RNA-seq from a cross between an isofemale line and the reference genotype for the purpose of measuring allele specific expression

Publication Title

Estimates of allele-specific expression in Drosophila with a single genome sequence and RNA-seq data.

Alternate Accession IDs

None

Sample Metadata Fields

Sex, Specimen part, Cell line

View Samples
accession-icon GSE19275
Muscle gene expression patterns in pigs with divergent phenotypes for fatness traits
  • organism-icon Sus scrofa
  • sample-icon 67 Downloadable Samples
  • Technology Badge Icon Affymetrix Porcine Genome Array (porcine)

Description

Background: Marketing products with added-value characteristics is a current trend in livestock production systems. Regarding meat, selection for intramuscular fat and muscular fatty acid composition is a way to improve the palatability and juiciness of meat while assuring a healthy fat content. This represents selecting animal with a different muscular metabolic profile with respect to the extended selection of lean animals. Results: The present study has analysed the muscular gene expression profiles of 68 commercial Duroc pigs belonging to two groups with extreme phenotypes for traits strongly related with lipid deposition and composition. This has allowed us to compare the physiological and metabolic implications of selecting for each of these extreme groups. Rather than upregulation of a single pathway, the main differences lied on the transcriptional levels of genes related with lipogenesis and lipolysis, revealing the existence of a cycle where triacylglycerols are continuously synthesized and degraded. Most strikingly, several genes which enhanced fatty acid -oxidation and favoured insulin signalling and glucose uptake were upregulated in the fattest animals, indicating that the events leading to peripheral insulin resistance in humans with increased levels of intramuscular fat and obesity do not take place in these pigs. Moreover, neither was detected the well-characterised low-grade inflammatory state observed in overweighed humans. Conclusion: As a whole, our data suggest that selection for increasing intramuscular fat content in pigs would lead to a shift but not a disruption of the metabolic homeostasis of muscle cells. Future studies on the post-translational changes affecting protein activity or expression as well as information about protein location within the cell would be needed to fully understand how lipid deposition affects muscle physiology in pigs.

Publication Title

Muscle transcriptomic profiles in pigs with divergent phenotypes for fatness traits.

Alternate Accession IDs

E-GEOD-19275

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE42771
Microarray gene expression profiling of kinase-dependent and kinase-independent effects of GRK2
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The ubiquitously expressed G-protein-coupled receptor kinase 2 (GRK2, ADRBK1) is an indispensable kinase involved in growth, differentiation and development. Exaggerated GRK2 activity plays a major pathophysiological role in the development of cardiovascular diseases such as heart failure and hypertension. GRK2 exerts its functions by kinase-dependent and kinase-independent effects. To assess the differential impact of GRK2 on cellular signalling we established HEK cell clones with over-expression of comparable protein levels of GRK2 or the kinase-deficient GRK2-K220R mutant, respectively. HEK cells were either cultured in vitro or expanded in vivo, in immunodeficient NOD.Scid mice to discriminate between in vitro and in vivo effects of GRK2. Whole genome microarray gene expression profiling was performed of cultured HEK cells and of NOD.Scid mouse-expanded HEK clones. As an additional control, cells were re-cultured in vitro after expansion in NOD.Scid mice.

Publication Title

Inhibition of G-protein-coupled receptor kinase 2 (GRK2) triggers the growth-promoting mitogen-activated protein kinase (MAPK) pathway.

Alternate Accession IDs

E-GEOD-42771

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE28031
Microarray gene expression profiling of heart failure induced in apolipoprotein E-deficient mice by treatment with rosiglitazone
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The anti-diabetic drug and agonist of the peroxisome proliferator-activated receptor gamma (Pparg), rosiglitazone, was recently withdrawn in many countries because the drug use was associated with an increased risk of heart failure. To investigate underlying pathomechanisms, we chose 6-month-old apolipoprotein E (apoE)-deficient mice, which are prone to atherosclerosis and insulin resistance, and thereby mimic the risk profile of patients with cardiovascular disease. After 8 weeks of rosiglitazone treatment (30 mg/kg/day), echocardiography and histology analyses demonstrated that rosiglitazone had induced heart failure with cardiac dilation. Concomitantly, cardiac lipid overload and lipid-induced cardiomyocyte death developed. The microarray gene expression study of heart tissue from rosiglitazone-treated apoE-deficient mice relative to untreated apoE-deficient mice and non-transgenic B6 mice identified cardiac Pparg-dependent lipid metabolism genes in rosiglitazone-treated mice, which seem to trigger a major heart failure promoting pathway.

Publication Title

Inhibition of G-protein-coupled Receptor Kinase 2 Prevents the Dysfunctional Cardiac Substrate Metabolism in Fatty Acid Synthase Transgenic Mice.

Alternate Accession IDs

E-GEOD-28031

Sample Metadata Fields

Age, Specimen part, Treatment

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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