Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Lipidomic characterization of Candida albicans in response to Aureobasidin treatment in vitro.

ABSTRACT: Candida albicans is an opportunistic yeast pathogen that causes a wide range of infections especially amongst immunocompromised patients. Aureobasidin A (AbA) has been shown to inhibit inositolphosphoryl ceramide synthase (IPCS), a key enzyme responsible for sphingolipid biosynthesis. There are limited studies exploring IPCS as a target molecule for antifungal treatment. It is hypothesized that the mechanism of AbA inhibition involves alteration of C. albicans phospholipid and sphingolipid profiles. The profiling of C. albicans phospholipid and sphingolipid upon exposure to 0.5-4 µg/ml of AbA were determined using Liquid chromatography-mass spectrometry (LC-MS).

ORGANISM(S): Candida Albicans

TISSUE(S): Yeast Cells

SUBMITTER: Nur Wahida Hamdan

PROVIDER: ST001982 | MetabolomicsWorkbench | Thu Sep 16 00:00:00 BST 2021

REPOSITORIES: MetabolomicsWorkbench

ACCESS DATA

Json Xml

Similar Datasets

in vitro differentiated Th0, Th17, and Tr1 cells

Project description:Gene expression profiling of in vitro differentiated murine Th cell subsets. Flow cytometrically sorted naive Th cells (CD4+ CD44- Foxp3-) were polyclonally stimulated in vitro for 3 days using 4 µg/ml plate-bound antibody to CD3 (145-2C11) and 2 µg/ml soluble antibody to CD28 (PV-1). Th0 cells were cultured in the absence of exogenous cytokines. Th17 cells were differentiated with 50 ng/ml IL-6 plus 0.5 ng/ml TGF-β. Tr-1 cells were differentiated with 100 ng/ml IL-27 plus 0.5 ng/ml TGF-β.

2014-03-20 | GSE56021 | GEO

Aging stress and ceramide dependent RNA sequencing expression profiling depends on ceramide synthase 6

Project description:The bioactive sphingolipid ceramide, generated by ceramide synthase, is an adaptive stress effector induced in response to various stress stimuli such as aging. In fact, ceramide synthase (CerS) was first discovered in yeast as a longevity assurance gene (LAG1), as the reduced ceramide generation consequent to LAG1 deletion increased longevity. There are six homologues of mammalian LAG1/ceramide synthases (CerS1-6) that generate ceramides with different fatty acid chain lengths with distinct functions and hydrophobicity. Ceramide can be metabolized by sphingosine kinase 1 or 2 for the generation of pro-survival sphingosine 1-phosphate (S1P), which enhances immune cell egress to the blood stream, activating immune function. Ceramide is known to induce mitophagy and cell death. Here we investigated the role of this sphingolipid pathway in immune function, specifically T cell functions, via high throughput expression profiling.

2021-01-01 | GSE148498 | GEO

Cardiac lipidomic profiling and mechanistic exploration by transcriptome in murine model of dilated cardiomyopathy

Project description:Dilated cardiomyopathy (DCM) and heart failure are associated with mitochondrial dysfunction and dysregulated lipid metabolism. Recent studies have implicated a pivotal role of Hippo pathway activation in the development of DCM with profound metabolic remodelling. However, alterations in the cardiac lipid profile and responsible molecular mechanisms, including upregulated galectin-3, remain unclear in the setting of DCM. Mice with DCM induced by Hippo pathway activation (Mst1 gene overexpression alone or with galectin-3 gene deletion) were studied by lipidomic profiling, transcriptomic profiling and immunoblotting for mRNA and protein expression. Profound alterations in cardiac lipid classes were observed, notably elevated sphingolipids, reduced triacylglycerol (TG) and ether lipids, alterations in phospholipid species, elevated lysophosphatidylcholine, and a profound reduction in mitochondria-specific cardiolipin and coenzyme Q10. Relative to adult mice with advanced DCM, reduced TG content was evident but sphingolipid accumulation was absent in young mice at early phase of DCM. Mechanistically, the lipidomic profile in DCM heart was in consistent with dysregulated expression of specific gene sets for biosynthesis of ceramides or TG, TG storage/hydrolysis, mitochondrial lipid metabolism, peroxisome biogenesis, and suppressed PPAR-alpha signaling. Furthermore, galectin-3 gene deletion resulted in changes in some lipid classes and numerous lipid species in settings of healthy and DCM. Multiple alterations in cardiac lipids were identified by lipidomics in a mouse model of DCM due to activation of the Hippo pathway. By employing transcriptome and galectin-3 gene deletion, we revealed underlying mechanisms for lipid abnormalities involving upregulated galectin-3, downregulated expression of specific gene sets of lipid metabolism, and attenuated PPAR-alpha signaling.

2022-09-22 | GSE213707 | GEO

Transcriptional suppression of sphingolipid catabolism controls pathogen resistance in C. elegans [ChIP-Seq]

Project description:Sphingolipids are required for diverse biological functions and are degraded by specific catabolic enzymes. However, the mechanisms that regulate sphingolipid catabolism are not known. Here we characterize a transcriptional axis that regulates sphingolipid breakdown to control resistance against bacterial infection. From an RNAi screen for transcriptional regulators of pathogen resistance in the nematode C. elegans, we identified the nuclear hormone receptor nhr-66, a ligand-gated transcription factor homologous to human hepatocyte nuclear factor 4. Tandem chromatin immunoprecipitation-sequencing (ChIP-seq) and RNA sequencing (RNA-seq) experiments revealed that NHR-66 is a transcriptional repressor, which directly targets sphingolipid catabolism genes. Transcriptional de-repression of two sphingolipid catabolic enzymes in nhr-66 loss-of-function mutants drives the breakdown of sphingolipids, which enhances host susceptibility to infection with the bacterial pathogen Pseudomonas aeruginosa. These data define transcriptional control of sphingolipid catabolism in the regulation of cellular sphingolipids, a process that is necessary for pathogen resistance.

2023-09-08 | GSE240426 | GEO

Transcriptional suppression of sphingolipid catabolism controls pathogen resistance in C. elegans [RNA-Seq]

2023-09-08 | GSE240425 | GEO

Gene expression comparison of L. reuteri ATCC PTA 6475 and cyclopropane-fatty-acyl-phospholipid synthase mutant

Project description:Gene expression comparison of L. reuteri ATCC PTA 6475 and cyclopropane-fatty-acyl-phospholipid synthase mutant in MRS medium in anaerobic condition at 37C

2011-01-15 | GSE24413 | GEO

Transcriptome analysis of gene expression in sec59-1∆ yeast cells

Project description:Microarray data revealed that, 1880 genes were up regulated and 1430 genes were down regulated among that 3310 genes, 92 lipidomic genes were up regulated and 17 genes were down regulated in sec59-1∆. In sec59-1∆ cells, phospholipid, neutral lipid, sphingolipid and fatty acid metabolism genes were up regulated. N-Glycosylation defect affected various organelle functions such as mitochondria, peroxisome, vacuole and ER. Finally we can conclude from the microarray data, N-glycosylation plays a crucial role in regulating the lipidome homeostasis Microarray data revealed that, 1880 genes were up regulated and 1430 genes were down regulated among that 3310 genes, 92 lipidomic genes were up regulated and 17 genes were down regulated in sec59-1∆. In sec59-1∆ cells, phospholipid, neutral lipid, sphingolipid and fatty acid metabolism genes were up regulated. N-Glycosylation defect affected various organelle functions such as mitochondria, peroxisome, vacuole and ER. Finally we can conclude from the microarray data, N-glycosylation plays a crucial role in regulating the lipidome homeostasis

2018-01-15 | GSE70809 | GEO

Gene expression comparison of L. reuteri ATCC PTA 6475 and cyclopropane-fatty-acyl-phospholipid synthase mutant

Project description:Gene expression comparison of L. reuteri ATCC PTA 6475 and cyclopropane-fatty-acyl-phospholipid synthase mutant in MRS medium in anaerobic condition at 37C Include 3 biological replicate and dye-swap for each comparison. Reference time point = L. reuteri ATCC PTA 6475

2011-01-15 | E-GEOD-24413 | biostudies-arrayexpress

Transcriptomic profiling of vegfc(hy-/-);vegfd(-/-) mutant hearts reveals that vegfc/d signaling and lymphatics vasculature play a role in cardiac metabolism [fresh tissue]

Project description:Recent studies have suggested that promoting lymphangiogenesis enhances cardiac repair following injury, but it is unknown whether lymphangiogenesis is required for cardiac regeneration. Here, we describe the anatomical distribution, regulation and function of the cardiac lymphatic network in a highly regenerative zebrafish model system using transgenic reporter lines and loss-of-function approaches.To understand the transcriptional profile of the model, we performed RNA-seq on cardiac ventricles from control and mutant (vegfc(hy-/-);vegfd(-/-)) ventricles. Overall, vegfc(hy-/-;vegfd-/-) mutant ventricles were characterized by an up-regulation of pathways related to sphingolipid and phospholipid metabolism, translation, protein maturation and nonsense mediated decay compared to control hearts. Our findings suggest that lymphatics vasculature play a role in lipid transport and when lymphatic function is compromised in vegfch(y-/-;vegfd-/-) mutant, there are consequences to sphingolipid and phospholipid metabolism. Vegfc(hy-/-;vegfd-/-) mutant ventricles were not characterized by an enrichment of genes pathways implicated in pathological hypertrophy. This finding suggests that the absence of cardiac lymphatics induced a physiological rather than pathological cardiac hypertrophy.

2019-09-03 | GSE133130 | GEO