Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1213749 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32062273.fastq.gz | Fastqsanger.gz | |||
| SRR32062274.fastq.gz | Fastqsanger.gz | |||
| SRR32062275.fastq.gz | Fastqsanger.gz | |||
| SRR32062276.fastq.gz | Fastqsanger.gz | |||
| SRR32062277.fastq.gz | Fastqsanger.gz |
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2007-08-31 | GSE8332 | GEO
Project description:Apo2L/TRAIL stimulates cancer-cell death through the proapoptotic receptors DR4 and DR5, but the determinants of tumor susceptibility to this ligand are not fully defined. mRNA expression of the peptidyl O-glycosyl transferase GALNT14 correlated with Apo2L/TRAIL sensitivity in pancreatic carcinoma, non-small cell lung carcinoma and melanoma cell lines (P < 0.00009; n=83), and up to 30% of samples from various human malignancies displayed GALNT14 overexpression. RNA interference of GALNT14 reduced cellular Apo2L/TRAIL sensitivity, whereas overexpression increased responsiveness. Biochemical analysis of DR5 identified several ectodomain O-GalNAc-Gal-Sialic acid structures. Sequence comparison predicted conserved extracellular DR4 and DR5 O-glycosylation sites; progressive mutation of the DR5 sites attenuated apoptosis signaling. O-glycosylation promoted ligand-stimulated clustering of DR4 and DR5, which mediated recruitment and activation of the apoptosis-initiating protease caspase-8. These results uncover a novel link between death receptor O-glycosylation and apoptosis signaling, providing potential predictive biomarkers for Apo2L/TRAIL-based cancer therapy. Experiment Overall Design: Gene expression for untreated cell lines analyzed. Some cell lines have one replicate profile, some two (Samples with 2 CEL files). Normalized data for replicates was averaged. Analysis involved a regularized t-test to identify genes with expression differences between Apo2L sensitive and resistant lines.
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Project description:GPR31 signaling induced dendrite protrusion of lysozyme-expressing dendritic cells (LysoDCs) into basolateral pockets of M cells. To investigate the effect of GPR31 signaling on LysoDC function during infection, we analyzed the gene expression profile of LysoDCs from WT and Gpr31b-deficient mice at 2 days after L. monocytogenes infection.
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Project description:We here report that GPR31 is specifically expressed in cDC1 in human intestinal mononuclear phagocytes. Since GPR31 has been previously reported to be activated by PA, LA, and 12-HETE, RNA-seq was performed to analyze the transcriptional changes in human ileal cDC1 under the stimulation of PA, LA, or 12-HETE.
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Project description:The S. cerevisiae ISR1 gene encodes a putative kinase with no ascribed function. Here, we show that Isr1 acts as a negative regulator of the highly conserved hexosamine biosynthesis pathway (HBP), which converts glucose into uridine diphosphate N-acetylglucosamine (UDP-GlcNAc), the carbohydrate precursor to protein glycosylation, GPI-anchor formation and chitin biosynthesis. Overexpression of Isr1 is lethal and, at lower levels, causes sensitivity to tunicamycin and resistance to calcofluor white, implying impaired protein glycosylation and reduced chitin deposition. GFA1 is the first enzyme in the HBP and is conserved from bacteria and yeast to humans. Isr1 lethality is rescued by overexpression of GFA1 or exogenous glucosamine, which bypasses GFA1's essential function. Gfa1 is phosphorylated in an ISR1-dependent fashion and mutation of Isr1-dependent sites ameliorates the lethality associated with Isr1 overexpression. Isr1 contains a phosphodegron that is phosphorylated by Pho85 and subsequently ubiquitinated by the SCF -Cdc4 complex, largely confining Isr1 protein levels to the time of bud emergence. Mutation of this phosphodegron stabilizes Isr1 and recapitulates the overexpression phenotypes. As Pho85 is a cell cycle and nutrient responsive kinase, this tight regulation of Isr1 may serve to dynamically regulate flux through the HBP and modulate how the cell’s energy resources are converted into structural carbohydrates in response to changing cellular needs.
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Project description:Secondary metabolites play a key role in coordinating ecology and defense strategies of plants. Diversity of these metabolites arise by conjugation of core structures with diverse chemical moieties, such as sugars in glycosylation. Active pools of phytohormones, including those involved in plant stress response are regulated by glycosylation. While, much is known about glycosylation enzymes, we know little about their regulation or coordination with other biological processes. We characterized the flavonoid pathway transcription factor, TRANSPARENT TESTA 8 (TT8) in Arabidopsis thaliana, using an integrative 'omics strategy to provide a systems level understanding of the cellular machinery used to generate metabolite diversity by glycosylation. Metabolomics analysis of loss-of-function and inducible overexpression lines of TT8 showed that it coordinates glycosylation of not only flavonoids, but also nucleotides, thus, implicating TT8 in regulating pools of activated sugars. Transcriptome and promoter network analyses revealed that TT8 regulome included sugar transporters, sugar binding and sequestration proteins, and carbohydrate active enzymes. Interestingly, TT8 also affects brassinosteroid and jasmonic acid biosynthesis by directly binding to the promoters of key genes of these two pathways. This combined effect on metabolites glycosylation and stress hormones by TT8 overexpression lead to significant increase in tolerance towards multiple abiotic and biotic stresses. Conversely, loss of TT8 leads to increased sensitivity to these stresses. Thus, TT8 is an integrator of secondary metabolism and stress response.
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