Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30224423.fastq.gz | Fastqsanger.gz | |||
| SRR30224424.fastq.gz | Fastqsanger.gz | |||
| SRR30224425.fastq.gz | Fastqsanger.gz | |||
| SRR30224426.fastq.gz | Fastqsanger.gz | |||
| SRR30224427.fastq.gz | Fastqsanger.gz |
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Project description:Recent studies have reported that glycosphingolipids (GSL) might be involved in obesity induced insulin resistance. Those reports suggested that inhibition of GSL biosynthesis in animals ameliorated insulin sensitivity accompanied with improved glycemic control leading to decreased liver steatosis in obese mice. In addition, GSL depletion altered hepatic secretory function. In those studies, ubiquitously acting inhibitors for GSL-biosynthesis have been used to inhibit function of the enzyme Ugcg (UDP-glucose:ceramide glucosyltransferase), catalyzing the first step of the glucosylceramide based GSL-synthesis pathway. In the present study, a genetic approach for GSL deletion in hepatocytes was chosen to achieve full inhibition of GSL synthesis and to prevent possible adverse effects caused by Ugcg-inhibitors. Using the Cre/loxP system under control of the albumin promoter, GSL biosynthesis in hepatocytes and their release into the plasma could be effectively blocked. Deletion of GSL in hepatocytes did not change quantity of bile excretion through the biliary duct. Total bile salt content in bile-, feces- and plasma from mutant mice showed no difference as compared to control animals. Cholesterol concentration in liver-, bile-, feces- and plasma-samples remained unaffected. Lipoprotein concentration in plasma-samples in mutant animals reached similar levels as in their control littermates. No alteration in glucose tolerance after intraperitoneal application of glucose and insulin appeared in mutant animals. A preventive effect of GSL-deficiency on development of liver steatosis after high fat diet feeding could not be observed. Conclusion: The data suggest that GSL in hepatocytes are not essential for sterol, glucose and lipoprotein metabolism and do not prevent high fat diet-induced liver steatosis, indicating that Ugcg inhibitors exert their effect on hepatocytes either independently of GSL or mediated by other (liver) cell types. Comparison of wildtype mouse liver function versus Ugcg-deficient
2010-05-14 | E-GEOD-19316 | biostudies-arrayexpress
Project description:Recent studies have reported that glycosphingolipids (GSL) might be involved in obesity induced insulin resistance. Those reports suggested that inhibition of GSL biosynthesis in animals ameliorated insulin sensitivity accompanied with improved glycemic control leading to decreased liver steatosis in obese mice. In addition, GSL depletion altered hepatic secretory function. In those studies, ubiquitously acting inhibitors for GSL-biosynthesis have been used to inhibit function of the enzyme Ugcg (UDP-glucose:ceramide glucosyltransferase), catalyzing the first step of the glucosylceramide based GSL-synthesis pathway. In the present study, a genetic approach for GSL deletion in hepatocytes was chosen to achieve full inhibition of GSL synthesis and to prevent possible adverse effects caused by Ugcg-inhibitors. Using the Cre/loxP system under control of the albumin promoter, GSL biosynthesis in hepatocytes and their release into the plasma could be effectively blocked. Deletion of GSL in hepatocytes did not change quantity of bile excretion through the biliary duct. Total bile salt content in bile-, feces- and plasma from mutant mice showed no difference as compared to control animals. Cholesterol concentration in liver-, bile-, feces- and plasma-samples remained unaffected. Lipoprotein concentration in plasma-samples in mutant animals reached similar levels as in their control littermates. No alteration in glucose tolerance after intraperitoneal application of glucose and insulin appeared in mutant animals. A preventive effect of GSL-deficiency on development of liver steatosis after high fat diet feeding could not be observed. Conclusion: The data suggest that GSL in hepatocytes are not essential for sterol, glucose and lipoprotein metabolism and do not prevent high fat diet-induced liver steatosis, indicating that Ugcg inhibitors exert their effect on hepatocytes either independently of GSL or mediated by other (liver) cell types.
2010-02-04 | GSE19316 | GEO
Project description:Sulfur-deficiency-induced repressor proteins optimize glucosinolate biosynthesis in plants Glucosinolates (GSLs) in the plant order of the Brassicales are sulfur-rich secondary metabolites harboring anti-pathogenic and anti-herbivory plant-protective functions as well as possessing medicinal properties such as carcinopreventive and antibiotic activities. Plants repress GSL biosynthesis upon sulfur deficiency (–S), hence, field performance and medicinal quality are impaired by inadequate sulfate supply. The molecular mechanism linking –S to GSL biosynthesis has remained understudied. We report here the identification of the –S marker genes Sulfur deficiency induced1 and Sulfur deficiency induced2 (SDI1, SDI2) acting as major repressors controlling GSL biosynthesis in Arabidopsis under –S condition. SDI1 and SDI2 expression negatively correlated with GSL biosynthesis in both transcript and metabolite levels. Principal component analysis of transcriptome data indicated that SDI1 regulates aliphatic GSL biosynthesis as part of –S-response. SDI1 was localized to the nucleus and interacted with MYB28, a major transcription factor promoting aliphatic GSL biosynthesis, in both yeast and plant cells. SDI1 inhibited transcription of aliphatic GSL biosynthetic genes through maintaining the DNA-binding composition in a form of a SDI1-MYB28 complex, leading to down-regulate GSL biosynthesis and prioritize sulfate usage for primary metabolites under sulfur-deprived conditions.
2016-10-07 | GSE81347 | GEO
Project description:This study demonstrates that distinct composition of histone modifications between aliphatic and indolic GSL pathway genes contribute to the two phase activation of two different groups of GSL pathway genes in stress condition of Arabidopsis.
2024-01-31 | GSE239725 | GEO
Project description:In this study, we found that a light signaling factor, Long Hypocotyl 5 (HY5) is closely involved in the regulation of GSLs contents in light condition. In addition, HY5 was shown to physically interact with a histone deacetylase HDA9 and bind to proximal promoter region of MYB29 and IMD1 to suppress aliphatic GSL biosynthetic process. These results demonstrate that HY5 acts to suppress GSL accumulation at daytime, thus properly modulating the GSL contents on a daily basis of Arabidopsis plant.
2024-06-12 | GSE250418 | GEO
Project description:Glucose is essential for T cell proliferation and function, yet the metabolic fates of glucose critical for T cell responses in vivo remain poorly defined. Here, we identify glycosphingolipid (GSL) biosynthesis as an essential arm of glucose metabolism that fuels CD8+ T cell expansion and cytotoxic function in vivo. Using stable isotope tracing, we show that CD8+ effector T (Teff) cells in vivo use glucose to synthesize uridine diphosphate-glucose (UDP-Glc), a common precursor for glycogen, glycan, and GSL biosynthesis. Blocking GSL production–by targeting the enzymes UDP-Glc pyrophosphorylase 2 (UGP2) or UDP-Glc ceramide glucosyltransferase (UGCG)–blunts CD8+ T cell expansion and cytotoxic activity without impacting glucose-dependent energy production. Mechanistically, we show that glucose-dependent GSL biosynthesis (via UGCG) maintains lipid integrity at the plasma membrane and is required for lipid raft aggregation following T cell receptor (TCR) stimulation. CD8+ T cells lacking UGCG display poor cytotoxic function and reduced tumor control in vivo. Together, our data highlight GSL biosynthesis as an essential metabolic fate for glucose–independent of energy production–required to maintain membrane lipid homeostasis and CD8+ T cell cytotoxic function in vivo.
2025-08-07 | GSE295573 | GEO
Project description:Idiomarina loihiensis GSL 199 Genome sequencing
| PRJNA196939 | ENA
Project description:GM1-ganglioside, an abundant GSL in neuronal membranes, is integral to ER-PM junctions where it interacts with synaptic proteins/receptors and regulates Ca2+ signaling.
2024-03-19 | PXD042994 | Pride