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GSE19696
Bos taurus
18 Downloadable Samples
Affymetrix Bovine Genome Array (bovine)
Description
Selenium (Se) is an essential nutrient for beef cattle health and commercial production. The molecular mechanisms responsible for the physiological responses of the animal to dietary Se supplementation, however, have not been evaluated. Furthermore, the potential effect of two chemical forms (organic vs. inorganic) of Se on gene expression by Se-sufficient cattle has not been evaluated.
Publication Title
Dietary supplementation of selenium in inorganic and organic forms differentially and commonly alters blood and liver selenium concentrations and liver gene expression profiles of growing beef heifers.
Sample Metadata Fields
Specimen part
View Samples- Bos taurus
- 13 Downloadable Samples
- Bovine Gene 1.0 ST Array (bovgene10st)
Description
In many parts of the US, selenium (Se)-deficient soils dictate the necessity of supplementing this trace mineral directly to the diet of cattle, with the form of Se supplied known to affect tissue-level gene expression profiles and presumably function. Because a deficiency of Se will reduce fertility, including reduced biosynthesis of testosterone by the testis and an increased frequency of abnormalities in mature spermatozoa, we hypothesized that the form of Se supplemented to cows during gestation would affect the transcriptome of the neonatal bull calf testis. Microarray analysis using the Bovine gene 1.0 ST array (GeneChip; Affymetrix, Inc., Santa Clara, CA) was conducted to determine whether gestational form of supplemental Se affected gene expression profiles in the testis. GeneChip transcript annotations were last updated in January 2013 using the annotation update release 33 from the NetAffx annotation database.
Publication Title
Gestational form of Selenium in Free-Choice Mineral Mixes Affects Transcriptome Profiles of the Neonatal Calf Testis, Including those of Steroidogenic and Spermatogenic Pathways.
Sample Metadata Fields
Specimen part
View Samples- Rattus norvegicus
- 18 Downloadable Samples
IlluminaHiSeq2500
Description
Heart failure remains a major unmet clinical need and current therapies targeting neurohomonal and hemodynamic regulation have limited efficacy. We report that pharmacological activation of the transcriptional repressor REV-ERBa prevents expression of a pathological gene program and cardiomyocyte hypertrophy. In vivo, REV-ERBa agonism prevents development and halts progression of heart failure in mouse models. Thus, modulation of gene networks by targeting REV-ERBa represents a novel approach to heart failure therapy. Overall design: We performed RNAseq on NRVM at baseline and after PE stimulation (4 hr and 48 hr) in the presence or absence of SR9009 (SR or Veh were given 24 hr prior to PE).
Publication Title
REV-ERBα ameliorates heart failure through transcription repression.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Cells respond heterogeneously to DNA damage. We engineered genetic circuits to detect differential responses in a population that persist for many days post-stimulus.
Publication Title
Synthetic memory circuits for tracking human cell fate.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 80 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Patients with metastatic colorectal cancer were enrolled for treatment with cetuximab monotherapy. Transcriptional profiling was conducted on RNA from pre-treatment metastatic site biopsies to identify genes whose expression correlates with best clinical responses.
Publication Title
Expression of epiregulin and amphiregulin and K-ras mutation status predict disease control in metastatic colorectal cancer patients treated with cetuximab.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Baseline gene expression of adipose stem cell derived iPSCs generated by lentiviral Yamanaka 4 factors. We used microarrays to analyze the global gene expression of hACS derived iPSCs with KMOS and KMOS+miR-302.
Publication Title
MicroRNA-302 increases reprogramming efficiency via repression of NR2F2.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Little is known about the function of induced pluripotent stem cell-derived endothelial cells (iPSC-ECs) generated from diabetics, as this could potentially limit subsequent therapeutic use in this patient population.
Publication Title
Pravastatin reverses obesity-induced dysfunction of induced pluripotent stem cell-derived endothelial cells via a nitric oxide-dependent mechanism.
Sample Metadata Fields
Age, Specimen part
View Samples- Sus scrofa
- 16 Downloadable Samples
- Affymetrix Porcine Genome Array (porcine)
Description
Caesarean-delivered preterm pigs were fed 3 d of parenteral nutrition followed by 2 d of enteral formula feeding. Antibiotics (n=11) or control saline (n=13) were given twice daily from birth to tissue collection at d 5. NEC-lesions and intestinal structure, function, microbiology and immunity markers were recorded.
Publication Title
Antibiotics modulate intestinal immunity and prevent necrotizing enterocolitis in preterm neonatal piglets.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 8 Downloadable Samples
- IlluminaHiSeq2000
Description
We investigated the ALDH2*2 genetic polymorphism and its underlying mechanisms for the first time in a human model system of induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) generated from individuals carrying the most common heterozygous form of the ALDH2*2 genotype. We showed that the ALDH2*2 mutation confers elevated levels of reactive oxygen species (ROS) and toxic aldehydes such as 4HNE, thereby inducing cell cycle arrest and activation of apoptotic signaling pathways, especially during ischemic injury. ALDH2 exerts control of cell survival decisions via modulation of oxidative stress levels. This regulatory circuitry was found to be dysfunctional in the loss-of-function ALDH2*2 genotype, causing upregulation of apoptosis in cardiomyocytes following ischemic insult. These results reveal a novel function of the metabolic enzyme ALDH2 in modulation of cell survival decisions. Overall design: Molecular mechanism of increased ischemic damage in cardiomyocytes of ALDH2*2 genotype.
Publication Title
Characterization of the molecular mechanisms underlying increased ischemic damage in the aldehyde dehydrogenase 2 genetic polymorphism using a human induced pluripotent stem cell model system.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 12 Downloadable Samples
- IlluminaHiSeq2000
Description
Doxorubicin (Adriamycin) is an anthracycline chemotherapy agent effective in treating a wide range of malignancies1 with a well-established dose-response cardiotoxic side-effect that can lead to heart failure2-4. Even at relatively low cumulative doses of 200–250 mg/m2, the risk of cardiotoxicity is estimated at 7.8% to 8.8%4,5. Doxorubicin-induced cardiotoxicity (DIC) can range from asymptomatic reductions in left ventricular ejection fraction (LVEF) to highly symptomatic heart failure6,7. At present, it is not possible to predict which patients will be affected by DIC or adequately protect patients who are at risk for suffering this devastating side-effect8. Here we demonstrate that patient-specific human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) can recapitulate individual patients’ predilection to DIC at the single cell level. hiPSC-CMs derived from breast cancer patients who suffered clinical DIC are consistently more sensitive to doxorubicin toxicity, demonstrating decreased cell viability, mitochondrial/metabolic function, calcium handling, and antioxidant pathway gene expression, along with increased reactive oxygen species (ROS) production compared to hiPSC-CMs from patients who did not experience DIC. Together, our data indicate that hiPSC-CMs are a suitable platform for identifying and verifying the genetic basis and molecular mechanisms of DIC. Overall design: Comparision of the effect of 1uM doxorubicin for 24 h on gene expression in hiPSC-CM derived from 6 patients
Publication Title
Human induced pluripotent stem cell-derived cardiomyocytes recapitulate the predilection of breast cancer patients to doxorubicin-induced cardiotoxicity.
Sample Metadata Fields
No sample metadata fields
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