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GSE107630
Mus musculus
9 Downloadable Samples
Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
The peroxisome proliferator-activated receptor-coactivator-11 (PGC-11) regulates genes involved in energy metabolism. Increasing adipose tissue energy expenditure through PGC-11 activation has been suggested to be beneficial for systemic metabolism. Pharmacological PGC-11 activators could be valuable tools in the fight against obesity and metabolic disease. Finding such compounds has been challenging partly because PGC-11 is a transcriptional coactivator with no known ligand-binding activities. Importantly, PGC-11 activation is regulated by several mechanisms but protein stabilization is a limiting step as the protein has a short half-life under unstimulated conditions.
Publication Title
Small molecule PGC-1α1 protein stabilizers induce adipocyte Ucp1 expression and uncoupled mitochondrial respiration.
Sample Metadata Fields
Specimen part
View Samples- Arabidopsis thaliana
- 4 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
7d-old WT ler seedlings were submitted to 12h of non-stress (air) or hypoxia-stress treatment under low light conditions (45 uM m-2 s-2), and Total and Large Polysome RNA from both treatments were extracted and hybridized against Affymetrix genome chips. Values were used to evaluate changes in transcript abundance and transcript association with large polysomal complexes.
Publication Title
Genome-wide analysis of transcript abundance and translation in Arabidopsis seedlings subjected to oxygen deprivation.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 16 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Forkhead BoxO (FoxO) transcription factors expressed in adult skeletal muscle promote muscle atrophy during various catabolic conditions. We have identified the genome wide target genes and biological networks regulated by FoxO in skeletal muscle during Colon-26 (C-26) cancer cachexia.
Publication Title
Genome-wide identification of FoxO-dependent gene networks in skeletal muscle during C26 cancer cachexia.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Treatment
View Samples- Saccharomyces cerevisiae
- 14 Downloadable Samples
- Affymetrix Yeast Genome 2.0 Array (yeast2)
Description
Arsenic metalloid is a double-edge sword. On the one hand it is a very toxic and powerful carcinogen, and on the other it has been successfully used in the treatment of acute promyelocytic leukemia. In order to prevent the deleterious effects caused by arsenic compounds, almost all living organisms have developed mechanisms to eliminate it. In this study genome-wide response of S. cerevisiae to arsenic shows that this metal interferes with genes involved in the iron homeostasis including those encoding proteins that function in iron uptake, incorporation into FeS clusters, and more. In addition our data indicate that Yap1 transcriptionally controls the iron homeostasis regulator AFT2 as well as its direct target, MRS4. Most importantly in response to arsenate exposure Yap1 strongly regulates the expression of several genes involved in the Fe-S proteins biosynthesis, namely NBP35 and YFH1. Interestingly mRNA levels encoding Fet3, Ferro-O2-oxidoreductase required for high-affinity iron uptake, are drastically destabilized upon arsenic exposure. Such destabilization is due to the 5 to 3 exonuclease Xrn1 localized in the P Bodies. Moreover FET3 mRNA decay is not mediated by Cth2 and is independent on the formation of ROS responsible for the toxic effects of arsenic compounds. Strikingly, in presence of arsenate fet3 mutant shows resistance over the wild-type which leads us to suggest that Fet3 has a role in arsenic toxicity. Unexpectedly arsenic treatment seems to activate the non-reductive iron uptake in order to maintain the cellular iron homeostasis. Furthermore our genetic, biochemical, and physiological analysis demonstrate that aft1 mutant is sensitive to arsenic compounds and such phenotype is reversible upon addition of iron. We also show that arsenic exposure induces iron deficiency in aft1 mutant. In conclusion this work shows for the first time that arsenic, a chemotherapy drug used to treat a specific type of acute promyelocytic leukemia (APL), disrupts iron homeostasis and our results suggest that this disruption is independent on ROS generation. Finally we provide preliminary data confirming that such disruption also takes place in mammalian cells, an observation that can be very relevant in term of clinical applications.
Publication Title
Arsenic stress elicits cytosolic Ca(2+) bursts and Crz1 activation in Saccharomyces cerevisiae.
Sample Metadata Fields
Time
View Samples- Homo sapiens
- 6 Downloadable Samples
IlluminaHiSeq2000
Description
PBRM1 is a component of the PBAF chromatin remodelling complex and has been observed to be deregulated in a significant proportion of patients with clear-cell Renal Cell Carcinoma (ccRCC). This study employs RNA-Seq to identify differentially expressed genes in cellular models of ccRCC by expressing PBRM1 in PBRM1-deficient Caki2 cells. Overall design: Using lentiviral mediated mechanism, stable Caki-2 cell line expressing PBRM1 was developed (Caki2-PBRM1). Empty vector inserted in Caki2 cells served as control (Caki2-Ø)
Publication Title
PBRM1 Regulates the Expression of Genes Involved in Metabolism and Cell Adhesion in Renal Clear Cell Carcinoma.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Neuroinflammation is a key phenomenon in the pathogenesis of many neurodegenerative diseases. Understanding the mechanisms by which brain inflammation is engaged and delineating the key players in the immune response and their contribution to brain pathology is of great importance for the identification of novel therapeutic targets for these devastating diseases. Gaucher disease, the most common lysosomal storage disease, is caused by mutations in the GBA1 gene and is a significant risk factor for Parkinson?s disease; in some forms of Gaucher disease, neuroinflammation is observed. An unbiased gene profile analysis was performed on a severely affected brain area of a neurological form of a Gaucher disease mouse at a pre-symptomatic stage; the mouse used for this study, the Gbaflox/flox; nestin-Cre mouse, was engineered such that GBA1 deficiency is restricted to cells of neuronal lineage, i.e., neurons and macroglia. The 10 most up-regulated genes in the ventral posteromedial/posterolateral region of the thalamus were inflammatory genes, with the gene expression signature significantly enriched in interferon signaling genes. Our results imply that the type I interferon response is involved in the development of nGD pathology, and support the notion that interferon signaling pathways play a vital role in the sterile inflammation that often occurs during chronic neurodegenerative diseases in which neuroinflammation is present.
Publication Title
Induction of the type I interferon response in neurological forms of Gaucher disease.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 24 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Great interest has been shown in understanding the pathology of Gaucher disease (GD) due to the recently-discovered genetic relationship with Parkinsons disease. For such studies, suitable animal models of GD are required. Chemical induction of GD by inhibition of acid -glucosidase (GCase) using the irreversible inhibitor, conduritol-B-epoxide (CBE), is particularly attractive, although few systematic studies examining the effect of CBE on development of symptoms associated with neurological forms of GD have been performed. We now demonstrate a correlation between the amount of CBE injected into mice and levels of accumulation of the GD substrates, glucosylceramide and glucosylsphingosine, and show that disease pathology, indicated by altered levels of pathological markers, depends on the dose of CBE and its time of injection. Gene array analysis shows a remarkable similarly in the gene expression profile of CBE-treated mice and a genetic GD mouse model, the Gbaflox/flox;nestin-Cre mouse, with 120 of the 144 genes up-regulated in CBE-treated mice also up regulated in Gbaflox/flox;nestin-Cre mice. Finally, we demonstrate that some aspects neuropathology and some behavioral abnormalities can be arrested upon cessation of CBE treatment during a specific time window. Together, our data demonstrate that injection of mice with CBE provides a rapid and relatively easy way to induce symptoms typical of neuronal forms of GD, which will prove particularly useful when examining the role of specific biochemical pathways in GD pathology, since CBE can be injected into mice defective in components of putative pathological pathways, alleviating the need for time consuming crossing of mice.
Publication Title
Identification of Modifier Genes in a Mouse Model of Gaucher Disease.
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 6 Downloadable Samples
- NextSeq 500
Description
To understand the the effect of antagomir-17 treatment on human endothelial cells derived from human umbilical cord blood (UCB) CD34+ hematopoietic stem cells, we have employed mRNA sequencing. The antagomiR-17 used in this study was purchased from Dharmacon and cell transfection was performed using Lipofectamine RNAiMAx from Life Technologies. Scramble antagomiR from Ambion was used as control. Cells were transfected with antagomiR-17 or scrambled antagomiR for 48 hours. After 48 h, the cells were collected, RNA was isolated and RNA samples were shipped to Exiqon Services, Denmark for mRNA sequencing. All sequencing experiments (RNA integrity measurements, library preparation and next generation sequencing) were conducted at Exiqon Services, Denmark. Overall design: CD34+ endothelial cells differentiated from umbilical cord blood hematopoietic stem cells (CD34+) were treated with 50 nM antagomiR-17 (Dharmacon) or scrambled antagomiR (Ambion) using Lipofectamine RNAiMAx (Life Technologies) for 48 h. Three replicates were used for each condition (i.e. antagomiR-17 and scramble antagomiR conditions).
Publication Title
Synthetic microparticles conjugated with VEGF<sub>165</sub> improve the survival of endothelial progenitor cells via microRNA-17 inhibition.
Sample Metadata Fields
No sample metadata fields
View Samples- Arabidopsis thaliana
- 12 Downloadable Samples
- Illumina HiSeq 2000
Description
The quintuple jaz mutant jazQ and the triple myc mutant mycT affect plant defense and growth. We used RNA-sequencing to query the transcriptomes of jazQ and mycT, as well as the combined jazQ mycT octuple mutatant, and examined how these mutations alter the expression of genes mis-regulated in jazQ. The data highlight how jasmonate signaling pathways are largely governed by MYC transcription factors, but also highlight some MYC-independent expression patterns. Overall design: Analysis of Col-0 (wildtype), jazQ, mycT, and jazQ mycT (four genotypes), with three biological replicates per genotype - 12 total samples. This series contains the re-use of 6 samples from GSE79012 (Col-0 and jazQ).
Publication Title
Regulation of growth-defense balance by the JASMONATE ZIM-DOMAIN (JAZ)-MYC transcriptional module.
Sample Metadata Fields
Age, Specimen part, Subject
View Samples- Mus musculus
- 8 Downloadable Samples
- NextSeq 500
Description
This study aimed to explore the role of NIPP1 in adult germline cell proliferation and differentiation, using a ubiquitous inducible NIPP1 knockout (TKO) mouse model. To gain unbiased insight into the molecular mechanism that underly the sertoli-only phenotype in TKO, we performed a comparative RNA sequencing profiling of control and TKO, in which NIPP1 was tamoxifin-induced depleted. Overall design: Two genotypes are compared after treatment with tamoxifen. The control genotype (UBC CRE-ERT2+/- Ppp1r8 fl/+) looses the floxed allele of PPP1R8 (aka NIPP1) as a consequence of the treatment with tamoxifen and becomes heterozygous for PPP1R8. The KO genotype (UBC CRE-ERT2+/- Ppp1r8 fl/-) also looses the floxed allele of PPP1R8 as a consequence of the tamoxifen treatment and becomes homozygous KO. For each genotype, 4 replicates are profiled.
Publication Title
The protein phosphatase 1 regulator NIPP1 is essential for mammalian spermatogenesis.
Sample Metadata Fields
Age, Specimen part, Subject
View Samples