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GSE67022
Rattus norvegicus
40 Downloadable Samples
Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
Our strategy was to manipulate mTOR signaling in vivo, then characterize the transcriptome and translating mRNA in liver tissue. In adult rats, we used the non-proliferative growth model of refeeding after a period of fasting, and the proliferative model of liver regeneration following partial hepatectomy. We also studied livers from pre-term fetal rats (embryonic day 19-20) in which fetal hepatocytes are asynchronously proliferating. All three models employed rapamycin to inhibit mTOR signaling.
Publication Title
Profiling of the fetal and adult rat liver transcriptome and translatome reveals discordant regulation by the mechanistic target of rapamycin (mTOR).
Sample Metadata Fields
Specimen part, Time
View Samples- Rattus norvegicus
- 12 Downloadable Samples
Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Rapamycin response in tumorigenic and non-tumorigenic hepatic cell lines.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 10 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
MicroRNA profiling in mucosal biopsies of eosinophilic esophagitis patients pre and post treatment with steroids and relationship with mRNA targets.
Sample Metadata Fields
Specimen part, Disease
View Samples- Rattus norvegicus
- 14 Downloadable Samples
- Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
We previously identified the mTOR pathway as critical to progenitor cell proliferation in a model of liver injury, we investigated the temporal activation of mTOR signaling in a rat model of hepatic carcinogenesis. The model employed chemical carcinogens and partial hepatectomy to induce progenitor marker-positive HCC. Rats were administered the mTOR inhibitor rapamycin for a three week period and liver harvested one month following cessation of rapamycin treatment. Short-term rapamycin treatment resulted in a significant reduction of focal lesion burden. Microarray analysis was performed to characterize the gene expression signature of persistent focal lesions in the rapamcyin and placebo treated animals. This analysis revealed a persistent effect of short-term mTORC1 inhibition on gene expression that resulted in a genetic signature reminiscent of normal liver.
Publication Title
Persistent effect of mTOR inhibition on preneoplastic foci progression and gene expression in a rat model of hepatocellular carcinoma.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples- Rattus norvegicus
- 12 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
Two rat hepatic cell lines, WB-F344 and WB311, were characterized for the effect of rapamycin on gene expression. The WB311 cell line, which is tumorigenic and resistant to the growth inhibitory effects of rapamycin, was originally derived from the WB-F344 parental hepatic epithelial cell line. The goal of this experiment was to identify genes that responded to rapamycin in the sensitive cells but not the resistant cells, thereby providing insight into the mechanism of rapamycin resistance.
Publication Title
Rapamycin response in tumorigenic and non-tumorigenic hepatic cell lines.
Sample Metadata Fields
No sample metadata fields
View Samples- Rattus norvegicus
- 12 Downloadable Samples
- Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
The present study was designed to test the hypothesis that limited growth of the fetal liver in the model of maternal fasting is independent of well-characterized signaling mechanisms that are known to regulate somatic growth in adult animals.
Publication Title
Regulation of fetal liver growth in a model of diet restriction in the pregnant rat.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Sus scrofa
- 11 Downloadable Samples
- Porcine Gene 1.0 ST Array (porgene10st)
Description
Mesenchymal stem cell-derived extracellular vesicles (EVs) have been shown to promote angiogenesis in the ischemic myocardium. This study examines the difference in vascular density, myocardial perfusion, molecular signaling, and gene expression between normal diet (ND) and high fat diet (HFD) groups at baseline and following intra-myocardial injection of EVs
Publication Title
Effects of High Fat Versus Normal Diet on Extracellular Vesicle-Induced Angiogenesis in a Swine Model of Chronic Myocardial Ischemia.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples- Homo sapiens
- 10 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Eosinophlic esophagitis (EoE) is increasely recognized as an antigen-drived disorder. The goal of this study is to reveal the gene expression changes in EoE before and after a successful glucocorticoid steroid treatment.
Publication Title
MicroRNA profiling in mucosal biopsies of eosinophilic esophagitis patients pre and post treatment with steroids and relationship with mRNA targets.
Sample Metadata Fields
Specimen part, Disease
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
To assess the potential of PP6 as a therapeutic target in liver disorders, we attenuated expression of the PP6 catalytic subunit in HepG2 cells using lentiviral-transduced shRNA. Two PP6 knock-down (PP6KD) cell lines 18.5 and 19.5, (90% reduction of PP6-C protein content) were studied in depth.
Publication Title
Adaptation of HepG2 cells to a steady-state reduction in the content of protein phosphatase 6 (PP6) catalytic subunit.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Transcriptome Array 2.0 (hta20)
Description
microRNAs are small (22-24 nucleotide), non-coding RNA transcripts that play a role in RNA silencing and post transcriptional regulation of gene expression. They have been implicated to have profound roles in many cancers. The role of microRNAs in chondrosarcoma progression is not well understood. Our lab has identified miR-181a to be up-regulated in chondrosarcoma. miR-181a modulates CXCR4 signaling by targeting RGS-16, leading to increased levels of VEGF and MMP-1, major factors in tumor invasion. In an effort to identify other targets of miR-181a apart from RGS-16, we carried out a gene array to compare gene expression between untreated/control CS-1(chondrosarcoma cell line) cells and CS-1 cells transduced with a lenti virus expression construct with anti-miR-181a sequence.
Publication Title
No associated publication
Sample Metadata Fields
Cell line, Treatment
View Samples