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Homo sapiens
40 Downloadable Samples
Illumina HumanHT-12 V4.0 expression beadchip
Description
Skeletal muscle adapts to resistance exercise (RE) performance acutely and chronically. An important regulatory step of muscle adaptation to RE is gene expression. Microarray analysis can be used as an exploratory method to investigate how genes and gene clusters are modulated acutely and chronically by RE. The purpose of the present study was to investigate the effect of training status in the basal (rested) and pre- to 24h post-RE on the global transcriptome in vastus lateralis muscle biopsies of young men. Muscle biopsies of nine young men who undertook RE training for 10-wks were collected pre and 24h post-RE at the first (W1) and last (W10) weeks of training and analysed using microarray. An unaccustomed RE bout (at W1) up-regulated muscle gene transcripts related to stress (e.g., heat shock proteins), damage and inflammation, structural remodelling, protein turnover and increased translational capacity. Trained muscles (at W10) became more efficient metabolically, as training favoured a more oxidative metabolism, refined response to stress, showed by genes suppression related to RE-induced stress and inflammation, and up-regulated genes indicating greater muscle contractile efficiency and contribution to promote muscle growth and development. These data highlight that chronic repetition of RE increases muscle efficiency and adapt muscles to respond more specifically and accurately to RE-induced stress.
Publication Title
Resistance training in young men induces muscle transcriptome-wide changes associated with muscle structure and metabolism refining the response to exercise-induced stress.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 54 Downloadable Samples
Illumina HiSeq 2500
Description
To investigate the relationship between histones, chaperone function, and cataracts, we performed RNA-seq, isothermal titration calorimetry (ITC), size-exclusion chromatography, and gel electrophoresis of histones. The RNA-seq of postnatal lenses from 2-day-old cryaa -R49C mice revealed increased histone gene expression, suggesting that a a-crystallin mutation regulates histones via a transcriptional mechanism . Overall design: RNA-seq studies on lenses of 2-day-old wild-type and 2-day-old cryaa-R49C heterozygous mutant and cryaa-R49C homozygous mutant knock-in mice; and 14-day old wild-type and 14-day-old cryab-R120G heterozygous mutant and cryab-R120G homozygous mutant knock-in mice
Publication Title
Probing the changes in gene expression due to α-crystallin mutations in mouse models of hereditary human cataract.
Sample Metadata Fields
Cell line, Subject
View Samples- Gallus gallus
- 48 Downloadable Samples
- Affymetrix Chicken Genome Array (chicken)
Description
Because refractive development is governed largely by the retina, we analyzed the retinal transcriptome in chicks wearing a spectacle lens, a well-established means to induce refractive errors, to identify gene expression alterations and to develop novel mechanistic hypotheses about refractive development.
Publication Title
Image defocus and altered retinal gene expression in chick: clues to the pathogenesis of ametropia.
Sample Metadata Fields
Specimen part
View Samples
GSE6543- Gallus gallus
- 22 Downloadable Samples
- Affymetrix Chicken Genome Array (chicken)
Description
One-day old white Leghorn chicks were housed in brooders with a 12 hr light:dark cycle, using General Electric chroma 50 fluorescent lighting with irradiance of approximately 50W/cm2 at chick eye level. They received Purina Chick Chow food and water ad libitum. At one week of age and at the onset of the light phase, the chicks were anesthetized with inhalation ether, and a unilateral translucent white plastic goggle was glued to the periorbital feathers to induce ipsilateral form-deprivation myopia, alternating between the left or right eye.
Publication Title
Form-deprivation myopia in chick induces limited changes in retinal gene expression.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 44 Downloadable Samples
- Illumina HiSeq 2000
Description
Purpose: In this study, we identify global transcriptome alterations following removal of individual or multiple miR-196 family members in mouse. Next generation sequencing-derived transcriptome profiling (RNA-seq) was performed. Methods: A GFP reporter cassette was engineered to replace the mature miR-196a1 and miR-196a2 miRNA genomic loci in mouse (creating a knockout). GFP positive cells from an extensive knock-out allellic series of the three individual miR-196 genes, as detailed below, were isolated from E9.5 mouse embryos by FACS. miR-196b knockout cells were not marked with a fluorescent reporter and an assumption of co-expression with miR-196a2 was made. mRNA profiles were generated by deep sequencing in a minimum of four biological replicates per genotype, using an Illumina HiSeq 2000 instrument. Read information was mapped to the mouse genome and processed as described. Conclusions: Our study represents the first detailed analysis of embryonic transcriptomes following loss of single and multiple miR-196 family members. We identify complex dysregulation of many Hox genes, in addition to key developmental signalling pathways involved in somitogenesis. Overall design: mRNA profiles of E9.5 mouse embryos with miR-196 loss-of-function were generated by deep sequencing, in a minimum of four biological replicates, using Illumina HiSeq 2000.
Publication Title
Independent regulation of vertebral number and vertebral identity by microRNA-196 paralogs.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Transcriptome Array 2.0 (hta20)
Description
Novel strategies are needed to modulate -cell differentiation and function as potential -cell replacement or restorative therapies for diabetes. We previously demonstrated that small molecules based on the isoxazole scaffold drive neuroendocrine phenotypes. The nature of the effects of isoxazole compounds on cells was incompletely defined. We find that isoxazole largely induced genes that support neuroendocrine and -cell phenotypes, and suppressed a set of genes important for proliferation. Isoxazole alters -cell metabolites and protects glucose-responsive signaling pathways under lipotoxic conditions. Finally, we show that isoxazole improves glycemia in a mouse model of -cell regeneration. Isoxazole is a prime candidate for altering cell fate in different contexts.
Publication Title
Isoxazole Alters Metabolites and Gene Expression, Decreasing Proliferation and Promoting a Neuroendocrine Phenotype in β-Cells.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
microRNA are aberrantly expressed in acute myeloid leukemia (AML), and clinically may have diagnostic, prognostic, and therapeutic value. We identify one such microRNA, miR-196b, is essential for MLL-AF9 leukemia initiation and maintenance. To discover how miR-196b contributes to leukemogenesis, we utilized multiple unbiased approaches that identified and functionally screened miR-196b target activity in AML. Our studies resolved how conflicting networks of miRNA-regulated targets are integrated during leukemogenesis. This work uncovered two miR-196b direct targets, the cell cycle regulator Cdkn1b (p27Kip1) and Polycomb group member Phc2, that independently cooperate with MLL-AF9 to promote leukemogenesis by regulating stem cell transcriptional programs. Finally, we found that therapeutic disruption of miR-196b direct targeting of Cdkn1b suppresses leukemogenesis.
Publication Title
miR-196b target screen reveals mechanisms maintaining leukemia stemness with therapeutic potential.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 10 Downloadable Samples
- Illumina HiSeq 2500
Description
microRNA are aberrantly expressed in acute myeloid leukemia (AML), and clinically may have diagnostic, prognostic, and therapeutic value. We identify one such microRNA, miR-196b, is essential for MLL-AF9 leukemia initiation and maintenance. To discover how miR-196b contributes to leukemogenesis, we utilized multiple unbiased approaches that identified and functionally screened miR-196b target activity in AML. Our studies resolved how conflicting networks of miRNA-regulated targets are integrated during leukemogenesis. This work uncovered two miR-196b direct targets, the cell cycle regulator Cdkn1b (p27Kip1) and Polycomb group member Phc2, that independently cooperate with MLL-AF9 to promote leukemogenesis by regulating stem cell transcriptional programs. Finally, we found that therapeutic disruption of miR-196b direct targeting of Cdkn1b suppresses leukemogenesis. Overall design: To identify the gene expression changes assoicated with knockdown of Cdkn1b and knockdown of Phc2 in murine MLL-AF9 leukemia cells.
Publication Title
miR-196b target screen reveals mechanisms maintaining leukemia stemness with therapeutic potential.
Sample Metadata Fields
Specimen part, Subject
View Samples- Rattus norvegicus
- 8 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
Pharmacological and gene ablation studies have demonstrated a crucial role of the cardiac natriuretic peptides (NP) hormones ANF and BNP in the maintenance of cardiovascular homeostasis. In addition, hypertension and chronic congestive heart failure are clinical entities that may be regarded as states of relative NP deficiency. Hence the study of the function of the endocrine heart is highly relevant.
Publication Title
Transcriptional analysis of the mammalian heart with special reference to its endocrine function.
Sample Metadata Fields
Sex, Specimen part
View Samples- Rattus norvegicus
- 24 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Ras dexamethasone-induced protein 1 is a modulator of hormone secretion in the volume overloaded heart.
Sample Metadata Fields
No sample metadata fields
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