| pubmed-article:20026359 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20026359 | lifeskim:mentions | umls-concept:C0023270 | lld:lifeskim |
| pubmed-article:20026359 | lifeskim:mentions | umls-concept:C0031676 | lld:lifeskim |
| pubmed-article:20026359 | lifeskim:mentions | umls-concept:C1158438 | lld:lifeskim |
| pubmed-article:20026359 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:20026359 | pubmed:dateCreated | 2010-2-1 | lld:pubmed |
| pubmed-article:20026359 | pubmed:abstractText | In many eukaryotes, phospholipids (PLs) and sphingolipids (SLs) are abundant membrane components and reservoirs for important signaling molecules. In Leishmania, the composition, metabolism, and function of PLs and SLs differ significantly from those in mammalian cells. Although only a handful of enzymes have been experimentally characterized, available data suggest many steps of PL/SL metabolism are critical for Leishmania viability and/or virulence, and could be a source for new drug targets. Further studies of genes involved in the synthesis (de novo and salvage) and degradation of PLs and SLs will reveal their diverse effects on Leishmania pathogenesis. | lld:pubmed |
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