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Sortilin Deficiency Reduces Ductular Reaction, Hepatocyte Apoptosis, and Liver Fibrosis in Cholestatic-Induced Liver Injury
2017, American Journal of PathologyCitation Excerpt :In addition, liver extracts of Sortilin−/− mice after BDL showed reduced expression of IL-6, TNF-α, and interferon-γ, particularly 3 and 7 days after BDL (Supplemental Figure S2). Serum levels of hepatic enzymes are increased 2 days after BDL, which is the starting point for development of chronic injury and repair process from 7 to 14 days.34 Indeed, serum levels of aspartate aminotransferase, alkaline phosphatase, and total serum bile acids, but not alanine aminotransferase, were significantly lower in Sortilin−/− mice 3 days after BDL, as compared to WT mice (Figure 3A), indicating reduced hepatocellular and cholestatic damage.
Sortilin deficiency improves the metabolic phenotype and reduces hepatic steatosis of mice subjected to diet-induced obesity
2015, Journal of HepatologyCitation Excerpt :Blots were incubated with antibodies to pAkt (dilution 1:1000, Cell Signaling Technology, Danvers, MA) and Akt1/2 (dilution 1:1000), fatty acid synthase (FAS) (dilution 1:1000) or β-actin (dilution 1:5000) (Santa Cruz Biotechnology, Santa Cruz, CA), then incubated with horseradish peroxidase-conjugated secondary antibodies and subjected to chemiluminescent detection. aSMase activity from liver and adipose tissue extracts was assessed as described [18–19]. Briefly, liver or adipose tissue was homogenated in sodium acetate buffer (50 mM sodium acetate, pH 4.5) with protease inhibitor (Sigma).
Intracellular trafficking of sphingolipids: Relationship to biosynthesis
2006, Biochimica et Biophysica Acta - BiomembranesCitation Excerpt :Initial experiments using C6-NBD-ceramide demonstrated that this lipid was internalized by a non-energy-dependent mechanism, and subsequently accumulated in the Golgi apparatus [15,16] where it was metabolized to C6-NBD-sphingomyelin (C6-NBD-SM) and C6-NBD-glucosylceramide (C6-NBD-GlcCer) [17]), suggesting that the Golgi apparatus was the major site of ceramide metabolism rather than the other intracellular sites which had been proposed earlier. Based on this work, it was later shown by biochemical studies, using short-acyl chain radioactive ceramides [18], that the Golgi apparatus is indeed the site of ceramide metabolism to SM [19,20] and GlcCer [21,22], and taken together with the demonstration that ceramide is synthesized in the endoplasmic reticulum (ER) [23,24], lead to the concept that SL synthesis is compartmentalized between the ER and the Golgi apparatus [25]. This being the case, ceramide would need to be transported between the ER, its site of synthesis, and the Golgi apparatus, its site of further metabolism.
Synthesis and biological evaluation of novel PDMP analogues
2006, Bioorganic and Medicinal ChemistryThe role of de novo ceramide synthesis in the mechanism of action of the tricyclic xanthate D609
2004, Journal of Lipid ResearchComparison of the metabolism of L-erythro- and L-threo-sphinganines and ceramides in cultured cells and in subcellular fractions
2001, Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids