This SuperSeries is composed of the SubSeries listed below.
Drosophila larvae fed palm fruit juice (PFJ) delay pupation via expression regulation of hormetic stress response genes linked to ageing and longevity.
Age, Specimen part, Treatment
View SamplesPFJ (4 ml for a final concentration of 19,000 mg gallic acid equivalent (GAE) per kg diet or 0.86 mg GAE per kcal diet) was supplemented to larvae of fruit flies (Drosophila melanogaster) given a semi-purified diet to observe for possible effects on energy metabolism and lifespan. Larvae were used five days since the egg stage for gene expression studies. Results from the microarray data analysis carried out show that fruit fly larvae given PFJ had up-regulated transport and metabolic processes, while development and morphogenesis processes were down-regulated.
Drosophila larvae fed palm fruit juice (PFJ) delay pupation via expression regulation of hormetic stress response genes linked to ageing and longevity.
Age, Specimen part, Treatment
View SamplesPFJ (4 ml for a final concentration of 19,000 mg gallic acid equivalent (GAE) per kg diet or 0.86 mg GAE per kcal diet) was supplemented to larvae of fruit flies (Drosophila melanogaster) given a semi-purified diet to observe for possible effects on energy metabolism and lifespan. Fat bodies extracted from these larvae were used five days since the egg stage for gene expression studies. Results from the microarray data analysis carried out show that fruit fly larva fat bodies given PFJ had up-regulated heat shock protein genes, while cell cycle and growth genes were down-regulated.
Drosophila larvae fed palm fruit juice (PFJ) delay pupation via expression regulation of hormetic stress response genes linked to ageing and longevity.
Age, Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Telomerase regulates MYC-driven oncogenesis independent of its reverse transcriptase activity.
Specimen part, Treatment
View SamplesConstitutively active MYC and reactivated telomerase often co-exist in cancers. While the reactivation of telomerase is thought to be essential for replicative immortality, MYC, in conjunction with co-factors, confers several growth advantages to cancer cells. However, it is unclear which co-factors sustain elevated MYC activity in tumors . Here, we identify TERT, the catalytic subunit of telomerase, as a novel regulator of MYC stability in cancers. Binding of TERT to MYC stabilizes its levels on chromatin, contributing to either activation or repression of its target genes. Mechanistically, TERT regulates MYC ubiquitination and stability, and this effect of TERT is independent of its role on telomeres. Genetic inhibition and knocking out of TERT phenocopied the loss of MYC, resulting in reduced disease burden of early- and late-stage MYC-driven murine lymphomas. Conversly, the ectopic expression of TERT could substitute for reduced MYC in these functions. Finally we show that TERT null mice, unlike Terc null mice, show delayed onset of MYC induced lymphomagenesis. Accordingly, inhibiting TERT function in primary human leukemia cells blocked the expression of MYC targets, while Terc depletion had no effects . Based on our data, we conclude that the re-expression of TERT, a direct MYC target in tumors, provides a feed-forward mechanism to potentiate MYC-dependent oncogenesis.
Telomerase regulates MYC-driven oncogenesis independent of its reverse transcriptase activity.
Specimen part, Treatment
View SamplesHuman infection with Cryptococcus neoformans (Cn), a prevalent fungal pathogen, occurs by inhalation and deposition in the lung alveoli of infectious particles. The subsequent host pathogen interaction is multifactorial and can result either in eradication, latency or extra-pulmonary dissemination. Successful control of Cn infection is dependent on host macrophages as shown by numerous studies. However in vitro macrophages display little ability to kill Cn. Recently, we reported that ingestion of Cn by macrophages induces early cell cycle progression that is subsequently followed by mitotic arrest, an event that almost certainly reflects damage to the host cell. The goal of the present work was to understand macrophage pathways affected by Cn toxicity. Infection of J774.16 macrophage-like cell line macrophages by Cn in vitro was associated with changes in gene pattern expression. Concomitantly we observed depolarization of macrophage mitochondria and alterations in protein translation rate. Our results indicate that Cn infection impairs multiple host cellular functions. Therefore we conclude Cn intracellular residence in macrophages undermines the health of these critical phagocytic cells interfering with their ability to clear the fungal pathogen.
Macrophage mitochondrial and stress response to ingestion of Cryptococcus neoformans.
Specimen part, Cell line, Time
View SamplesObesity has emerged as a formidable health crisis due to its association with metabolic risk factors such as diabetes, dyslipidaemia and hypertension. Recent work has demonstrated the multifaceted roles of lncRNAs in regulating mouse adipose development, but its implication in human adipocytes remain largely unknown at least partially due to the lack of a comprehensive lncRNA catalog, particularly those specifically expressed in brown adipose tissue (BAT). In this study, we performed deep RNA-seq on adult subcutaneous, omental and fetal brown adipose tissues to de novo construct a catalog of 3,149 adipose active lncRNAs of which 1,351 are specifically detected in BAT. We further identified 318 lncRNAs conserved between human and mouse which, compared with non-conserved ones, are more broadly expressed in multiple cell types. One of these, lnc-dPRDM16, is transcribed divergently from Prdm16, tightly correlated with Prdm16 (R = 0.7) in both mouse and human, and co-expressed (R = 0.7) with protein-coding genes enriched in lipid and fatty acid catabolic processes. Loss of function of lnc-dPRDM16 led to a down-regulation of Prdm16 and an obvious reduction of adipogenesis in brown adipocyte culture. Together, our work has provided a comprehensive human adipose catalog built from diverse fat types, which when applied to our roadmap, identifies lnc-dPRDM16 as a promising modulator of adipose development for future clinical research. Overall design: Transcriptome profiling of BAT, OME and SUB samples
De novo reconstruction of human adipose transcriptome reveals conserved lncRNAs as regulators of brown adipogenesis.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Molecular pathways reflecting poor intrauterine growth are found in Wharton's jelly-derived mesenchymal stem cells.
Specimen part
View SamplesIn order to identify gene-expression patterns in mesenchymal stem cells associated with different birth weights and intrauterine growth parameters,
Molecular pathways reflecting poor intrauterine growth are found in Wharton's jelly-derived mesenchymal stem cells.
Specimen part
View SamplesIn order to identify gene-expression patterns in mesenchymal stem cells associated with different birth weights and intrauterine growth parameters,
Molecular pathways reflecting poor intrauterine growth are found in Wharton's jelly-derived mesenchymal stem cells.
Specimen part
View Samples