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Literature summary for 4.1.2.27 extracted from
- Sphingosine 1-phosphate lyase deficiency disrupts lipid homeostasis in liver (2010), J. Biol. Chem., 285, 10880-10889.
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Mus musculus | - |
- |
- |
General Information
| General Information | Comment | Organism |
|---|---|---|
| physiological function | in mice with an inactive S1P lyase gene, in addition to the expected increase of sphingoid base phosphates, other sphingolipids including sphingosine, ceramide, and sphingomyelin are substantially elevated in the serum and/or liver. The S1P lyase deficiency results in changes in the levels of serum and liver lipids not directly within the sphingolipid pathway, including phospholipids, triacyglycerol, diacylglycerol, and cholesterol. Lipids in serum and lipid storage are elevated in liver, but adiposity is reduced in the S1P lyase-deficient mice. The S1P lyase deficiency causes widespread changes in the expression pattern of lipid metabolism genes, with a significant increase in the expression of PPAR, a master transcriptional regulator of lipid metabolism. The mRNA expression of the genes encoding the sphingosine kinases and S1P phosphatases, which directly control the levels of S1P, are not significantly changed in liver of the S1P lyase-deficient mice | Mus musculus |
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Release 2023.1 (January 2023)
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