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GSE39669
Mus musculus
12 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Inborn errors of lipid metabolism illustrate the importance of proper milk fat oxidation in newborn mammals. In the liver, a remarkable lipid catabolic competence is present at birth; however, it is unclear how this critical trait is acquired and regulated. In this work, we found that the genes required for milk lipid catabolism are already transcribed before birth in the term fetus (E19.5) and controlled by the peroxisome-proliferator activated receptor alpha (PPAR) in mouse liver. The developmental activity of PPAR strongly regulates fatty acid oxidation genes. Two days after birth (P2), during milk suckling, PPAR-null mice develop a congenital steatosis and milk protein oxidation is de-repressed to fuel an alternative energy pathway that maintains glucose homeostasis and postnatal growth. Our results demonstrate for the first time, the developmental role of PPAR in regulating the metabolic ability to use maternal milk as fuel in the early days of life.
Publication Title
Glucocorticoid receptor-PPARα axis in fetal mouse liver prepares neonates for milk lipid catabolism.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Inborn errors of lipid metabolism illustrate the importance of proper milk fat oxidation in newborn mammals. In the liver, a remarkable lipid catabolic competence is present at birth; however, it is unclear how this critical trait is acquired and regulated. In this work, we found that the genes required for milk lipid catabolism are already transcribed before birth in the term fetus (E19.5) and controlled by the peroxisome-proliferator activated receptor alpha (PPAR) in mouse liver. The developmental activity of PPAR strongly regulates fatty acid oxidation genes. Two days after birth (P2), during milk suckling, PPAR-null mice develop a congenital steatosis and milk protein oxidation is de-repressed to fuel an alternative energy pathway that maintains glucose homeostasis and postnatal growth. Our results demonstrate for the first time, the developmental role of PPAR in regulating the metabolic ability to use maternal milk as fuel in the early days of life.
Publication Title
Glucocorticoid receptor-PPARα axis in fetal mouse liver prepares neonates for milk lipid catabolism.
Sample Metadata Fields
Sex, Specimen part
View Samples- Pseudomonas aeruginosa
- 414 Downloadable Samples
Illumina HiSeq 2500
Description
Purpose : The goal of this study was to use RNA Seq to explore the correlation of gene expression of a collection of clinical P. aeruginosa isolates to various phenotypes, such as antimicrobial resistance, biofilm formation or virulence Methods : mRNA profiles were generated for Pseudomonas aerugionsa clinical samples derived from various geographical locations by deep sequencing. The removal of ribosomal RNA was performed using the Ribo-Zero Bacteria Kit (Illumina) and cDNA libraries were generated with the ScriptSeq v2 Kit (Illumina) . The samples were sequenced in single end mode on an Illumina HiSeq 2500 device and mRNA reads were trimmed and mapped to the NC_008463.1 (PA14) reference genome from NCBI using Stampy pipeline with defaut settings. Overall design: mRNA profiles from Pseudomonas aeruginosa derived from liquid LB cultures grown to an OD600 = 2 and deep sequenced using Illumina HiSeq 2500.
Publication Title
Predicting antimicrobial resistance in Pseudomonas aeruginosa with machine learning-enabled molecular diagnostics.
Sample Metadata Fields
Disease, Subject
View Samples- Homo sapiens
- 10 Downloadable Samples
- Affymetrix Clariom S Human array (clariomshuman)
Description
Tanning is a skin protection mechanism against UV radiation. Pigment production initiates hours after exposure, and the mechanism controlling this delay was unknown. Here we reveal a skin UV-protection timer, governed by damped oscillatory dynamics of the melanocyte master regulator, MITF, which after UV exposure, synchronizes regulatory programs, first cell survival and later pigmentation. Remarkably, the same amount of UV dosage resulted in higher pigmentation of human skin when given every-other day compared to daily exposure. Daily UV exposure appears to perturb MITF dynamics, thus re-ordering the survival and pigmentation programs. This demonstrates that the skin is more sensitive to frequency than quantity of UV exposure. Mathematical modeling identified a double negative regulatory loop involving HIF1a and microRNA-148a that regulates MITF dynamics. Our study suggests evolutionary leverage of the UV-protection timer, as it evolved to induce maximum protection with minimum damage for the reduction of skin cancer risk.
Publication Title
UV-Protection Timer Controls Linkage between Stress and Pigmentation Skin Protection Systems.
Sample Metadata Fields
Time
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
Heparan sulfate (HS), a long linear polysaccharide, is implicated in various steps of tumorigenesis, including angiogenesis. We successfully interfered with HS biosynthesis using a peracetylated 4-deoxy analog of the HS constituent GlcNAc and studied the compounds metabolic fate and its effect on angiogenesis. The 4-deoxy analog was activated intracellularly into UDP-4-deoxy-GlcNAc and HS expression was inhibited up to ~96% (IC50 = 16 M). HS chain size was reduced, without detectable incorporation of the 4-deoxy analog, likely due to reduced levels of UDP-GlcNAc and/or inhibition of glycosyltransferase activity. Comprehensive gene expression analysis revealed reduced expression of genes regulated by HS binding growth factors as FGF-2 and VEGF. Cellular binding and signaling of these angiogenic factors was inhibited. Micro-injection in zebrafish embryos strongly reduced HS biosynthesis, and angiogenesis was inhibited in both zebrafish and chicken model systems. All these data identify 4-deoxy-GlcNAc as a potent inhibitor of HS synthesis which hampers pro-angiogenic signaling and neo-vessel formation.
Publication Title
Interfering with UDP-GlcNAc metabolism and heparan sulfate expression using a sugar analogue reduces angiogenesis.
Sample Metadata Fields
Cell line, Treatment
View Samples- Mus musculus
- 112 Downloadable Samples
- Illumina HiSeq 4000
Description
Sensitivity to different pain modalities has a genetic basis that remains largely unknown. The use of closely related inbred mouse strains can facilitate gene mapping of nociceptive behaviors in preclinical pain models. We previously reported enhanced sensitivity to acute thermal nociception in C57BL/6J (B6J) versus C57BL/6N (B6N) substrains. Here, we expanded on pain phenotypes and observed an increase in inflammatory nociceptive behaviors induced by hindpaw formalin injections in B6J versus B6N mice (Charles River Laboratories). No strain differences were observed in mechanical or thermal hypersensitivity or in paw diameter following the Complete Freund s Adjuvant (CFA) model of inflammatory pain, indicating specificity in the inflammatory nociceptive stimulus. In the chronic nerve constriction injury (CCI), a model of neuropathic pain, no strain differences were observed in baseline mechanical threshold or in mechanical hypersensitivity up to one month post-CCI. We replicated the enhanced thermal nociception in B6J mice in the 52.5 C hot plate test relative to B6N mice from The Jackson Laboratory. Using a B6J x B6N-F2 cross (N=164), we mapped a major QTL underlying hot plate sensitivity to chromosome 7 that peaked at 26 Mb (LOD = 3.81, 8.74 Mb-36.50 Mb) that was more pronounced in males. Genes containing expression QTLs (eQTLs) associated with the peak nociceptive marker that have been implicated in pain and inflammation include Ryr1, Cyp2a5, Pou2f2, Clip3, Sirt2, Actn4, and Ltbp4 (FDR < 0.05). Future studies involving positional cloning and gene editing will determine the quantitative trait gene(s) and potential pleiotropy of this locus across other pain modalities. RNA-seq data and genotype information from striatum punches of F2 C57BL/6J (B6J) cross C57BL/NJ (B6NJ) oxycodone-treated mice. Genotypes are given relative to B6J allele, eg 0 = homozygous B6J. Overall design: C57BL/6J (B6J) and C57BL/NJ (B6NJ) mice were purchased from JAX at 7 weeks of age and were habituated in the vivarium one week prior to experimental testing that occurred next door. B6J females were crossed to B6NJ males to generate B6J x B6NJ-F1 mice and B6J x B6NJ F1 offspring were intercrossed to generate B6J x B6NJ F2 mice. Mice were 50-100 days old at the time of testing. F2 mice recieved four daily oxycodone injections (20 mg/kg, i.p.). Ninety SNP markers spaced approximately 30 Mb (approximately 15 cM) apart were genotyped using a custom-designed Fluidigm array.
Publication Title
C57BL/6 substrain differences in inflammatory and neuropathic nociception and genetic mapping of a major quantitative trait locus underlying acute thermal nociception.
Sample Metadata Fields
Sex, Age, Subject
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
To further analyze the effect of WWOX on metastasis formation, we studied the differential expression of mRNAs using Affymetrix genechip in WWOX- sufficient and deficient metastatic cells.
Publication Title
Pleiotropic tumor suppressor functions of WWOX antagonize metastasis.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
- NextSeq 500
Description
We performed a 3' RACE of a novel HIV RNA TAR-gag in order to determine the sequence of the RNA at the 3' end. Our data had shown that TAR-gag was potentially a noncoding RNA and our hypothesis was that TAR-gag ended somewhere prior to the end of the gag region of the HIV genome. The 3' RACE experiment showed that TAR-gag actually consists of four different RNA clusters, the longest of which ends at 615 bases from the transcription start site; this is in the middle of the p17 region of the gag gene. In addition, we sequenced all host RNAs in the EVs. Overall design: RNA from J1.1 and U1 exosomes was isolated and converted to cDNA. Sequencing libraries of the cDNA were made and a 3' RACE was perforemed to determine how long TAR-gag RNA is. Please note that the clustering analysis (published in PMID 28536264) was done only on the unfragmented samples (i.e. *-U samples).
Publication Title
An Omics Approach to Extracellular Vesicles from HIV-1 Infected Cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Introduction: Mechanisms that contribute to the pathogenesis of liver damage caused by hepatitis C virus (HCV) are not fully understood. Our previous work on liver biopsies from chronic HCV patients has shown modulation of the expression of certain cell cycle proteins indicating HCV-induced modifications of cell cycle events. We therefore hypothesize that HCV infection disrupts normal regulation of cell cycle that contributes to disease progression. Objective: To identify molecular disruptions during the course of HCV-associated disease progression, using liver biopsy specimens of chronic hepatitis C patients. Methods: Liver biopsy samples classified on histological basis as early (fibrosis stage 0-1) or advanced (fibrosis stage 3-4) disease stage were studied using oligonucleotide array ( HG U133 Plus 2.0, Affymetrix GeneChip System). For comparison, liver specimens from patients with non-viral hepatitis were also analyzed by microarray. Expression data was analyzed using Genespring (GX 7.2) and Ingenuity Pathway analysis (3.0). The differential expression of selected cell cycle genes (cyclin D2, KPNA2, HERC5 and Bcl-2) identified after microarray analysis was confirmed by quantitative real-time RT-PCR. Results: Microarray analysis revealed two-fold or greater transcriptional change in 792 genes of the total 38,500 known human genes in HCV-advance disease stage (HCV-A) as compared to HCV-early disease stage (HCV-E). Most of the genes have a defined role in immune response, extracellular matrix and cell cycle and apoptosis.
Publication Title
Gene profiling of early and advanced liver disease in chronic hepatitis C patients.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 23 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We have performed gene expression microarray analysis to profile transcriptomic signatures affected by EtOH in human dental pulp stem cells
Publication Title
Genome-wide transcriptomic alterations induced by ethanol treatment in human dental pulp stem cells (DPSCs).
Sample Metadata Fields
Specimen part
View Samples