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GSE27648
Zea mays
14 Downloadable Samples
Affymetrix Maize Genome Array (maize)
Description
Seed germination is a critical developmental process in plant propagation. Knowledge of the gene expression patterns in this critical process is important in order to understand the main biochemical reactions involved in successful germination, specially for economically relevant plants such as Maize.
Publication Title
Expression profile of maize (Zea mays L.) embryonic axes during germination: translational regulation of ribosomal protein mRNAs.
Sample Metadata Fields
Treatment, Time
View Samples- Arabidopsis thaliana
- 6 Downloadable Samples
Illumina HiSeq 2500, Illumina HiSeq 2000
Description
We report the role of LSM1-7 complex in the Arabidopsis tolerance to abiotic stresses. LSM1-7 controls gene expression reprogramming at the post-transcriptional level by promoting the decapping of mRNA. This function is selectively achieve over selected stress-induced transcripts depending on stress nature. Overall design: Comparison of transcriptomes from Col-0 and lsm1a lsm1b plants exposed to low temperatures, drought or high salt conditions
Publication Title
The LSM1-7 Complex Differentially Regulates Arabidopsis Tolerance to Abiotic Stress Conditions by Promoting Selective mRNA Decapping.
Sample Metadata Fields
Specimen part, Subject
View Samples- Arabidopsis thaliana
- 4 Downloadable Samples
- Illumina HiSeq 2000
Description
We report the role of SmE1 protein in the control of Arabidopsis development and tolerance to abiotic stresses. SmE1 controls gene expression reprogramming at the post-transcriptional level by promoting the splicing of pre-mRNA. This function is selectively achieve over selected transcripts depending on the stimulus nature. Overall design: Transcriptomic profiling through RNAseq of Col-0 and sme1-1 plants under control conditions or exposed to low temperatures (4ºC, 24h)
Publication Title
Arabidopsis SME1 Regulates Plant Development and Response to Abiotic Stress by Determining Spliceosome Activity Specificity.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 9 Downloadable Samples
- Illumina HiSeq 2500
Description
Heart failure (HF) is a major health and economic burden in developed countries. It has been proposed that the pathogenesis of HF may involve the action of mitochondria. Here we evaluate three different models of HF: tachycardiomyopathy, HF with preserved left ventricular (LV) ejection fraction, and LV myocardial ischemia and hypertrophy. Regardless of whether LVEF is preserved or reduced, our results indicate that the three models share common molecular features: an increase in mitochondrial ROS, followed by ultrastructural alterations in the mitochondrial cristae and loss of mitochondrial integrity that lead to cardiomyocyte death. We show that the ablation of the mitochondrial protease OMA1 averts cardiomyocyte death in all three experimental HF models, and thus, plays a direct role in cardiomyocyte protection. This finding identifies OMA1 as a potential target for preventing the progression of myocardial damage in HF associated to a variety of etiologies. Overall design: Transcriptome analysis of 12-week-old wild type mice versus OMA1 KO mice under control (non-treated) or treated with Isoproterenol chronically (implanted minipumps) for 7 days in heart tissue. The nuclear genetic background for both genotypes is C57BL/6JOlaHsd.
Publication Title
Ablation of the stress protease OMA1 protects against heart failure in mice.
Sample Metadata Fields
Sex, Age, Specimen part, Treatment, Subject
View Samples- Danio rerio
- 6 Downloadable Samples
- IlluminaHiSeq2500
Description
Cardiomyopathies-associated metabolic pathologies (e.g. T2D and insulin resistance) are a leading cause of mortality. It is known that the association between the pathologies works in both directions, where heart failure can lead to metabolic derangements such as insulin resistance. This intricate crosstalk exemplifies the importance of a fine coordination between one of the most energy demanding organs and an equilibrated carbohydrate metabolism. In this light, to assist in the understanding of the role of insulin regulated glucose transporters and the development of cardiomyopathies, we set out to study GLUT12. GLUT12 is a novel insulin regulated GLUT expressed in the main insulin sensitive tissues such as cardiac and skeletal muscle and adipose tissue. This study investigates the role of GLUT12 in heart failure and diabetes by developing a model for glut12 deficiency in zebrafish. Overall design: 6 samples in total were analyzed. 3 replicates from control samples (injected with contol MO) and 3 replicates from glut12 morphant samples (injected with glut12 splice MO). In each sample 10 embryos were pooled.
Publication Title
GLUT12 deficiency during early development results in heart failure and a diabetic phenotype in zebrafish.
Sample Metadata Fields
No sample metadata fields
View Samples- Caenorhabditis elegans
- 11 Downloadable Samples
- Affymetrix C. elegans Gene 1.1 ST Array
Description
Effects of betalains in C. elegans gene expression is studied, as our previous results showed a lifespan extension effect produced by theses molecules
Publication Title
Betalain health-promoting effects after ingestion in Caenorhabditis elegans are mediated by DAF-16/FOXO and SKN-1/Nrf2 transcription factors.
Sample Metadata Fields
Age, Specimen part, Treatment
View Samples- Rattus norvegicus
- 2 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
Two major subsets of rat natural killer (NK) cells can be distinguished based on their expression of either the Ly49s3 or the NKR-P1B lectin-like receptor. Ly49s3+ NK cells, but not NKR-P1B+ NK cells, express a wide range of Ly49 receptors.
Publication Title
Two complementary rat NK cell subsets, Ly49s3+ and NKR-P1B+, differ in phenotypic characteristics and responsiveness to cytokines.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 29 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Survival transcriptome in the coenzyme Q10 deficiency syndrome is acquired by epigenetic modifications: a modelling study for human coenzyme Q10 deficiencies.
Sample Metadata Fields
Sex, Age, Specimen part, Treatment, Subject
View Samples- Homo sapiens
- 15 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Coenzyme Q10 deficiency syndrome includes a clinically heterogeneous group of mitochondrial diseases characterized by low content of CoQ10 in tissues. The only currently available treatment is supplementation with CoQ10, which improves the clinical phenotype in some patients but does not reverse established damage. We analyzed the transcriptome profiles of fibroblasts from different patients irrespective of the genetic origin of the disease. These cells showed a survival genetic profile apt at maintaining growth and undifferentiated phenotype, promoting anti-apoptotic pathways, and favoring bioenergetics supported by glycolysis and low lipid metabolism. WE conclude that the mitochondrial dysfunction caused byCoQ10 deficiency induces a stable survival adaptation of somatic cells from patients.
Publication Title
Survival transcriptome in the coenzyme Q10 deficiency syndrome is acquired by epigenetic modifications: a modelling study for human coenzyme Q10 deficiencies.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples- Homo sapiens
- 14 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Coenzyme Q10 deficiency syndrome includes a clinically heterogeneous group of mitochondrial diseases characterized by low content of CoQ10 in tissues. The only currently available treatment is supplementation with CoQ10, which improves the clinical phenotype in some patients but does not reverse established damage.
Publication Title
Survival transcriptome in the coenzyme Q10 deficiency syndrome is acquired by epigenetic modifications: a modelling study for human coenzyme Q10 deficiencies.
Sample Metadata Fields
Sex, Age, Treatment, Subject
View Samples