EC Number   |
General Information |
Reference |
|---|
    4.1.2.27 | drug target |
pharmacological inhibition of sphingosine 1-phosphate lyase prevents the progression of cancer |
770491 |
| 4.1.2.27 | drug target |
sphingosine-1-phosphate lyase is therapeutically inhibited by fingolimod which is an oral drug for relapsing multiple sclerosis (MS). Modification and inhibition of sphingosine-1-phosphate lyase activity by the long-term therapeutic use of fingolimod is safe for the adrenal function in adult patients with MS |
769965 |
| 4.1.2.27 | malfunction |
ablation of sphingosine-1-phosphate lyase expression increases sphingosine-1-phosphate levels and reduces de novo formation and steady-state levels of the glycerophospholipid phosphatidylethanolamine (PE). In spite of its mitochondrial localization, TbSpl depletion has no apparent effect on mitochondrial morphology but results in aggregation of acidocalcisomes |
-, 775832 |
| 4.1.2.27 | malfunction |
congenital sphingosine-1-phosphate lyase deficiency due to biallelic mutations in SGPL1 gene is described in association with primary adrenal insufficiency and steroid-resistant nephrotic syndrome |
769965 |
| 4.1.2.27 | malfunction |
downregulation/inhibition of SPL prevents premature cell cycle progression and mitotic death. Oral administration of an SPL inhibitor to mice prolonges their survival after exposure to a lethal dose (10Gy) of total body ionizing radiation |
714674 |
| 4.1.2.27 | malfunction |
enzyme inhibition causes protein-losing glomerulopathy due to podocyte dysfunction, skin irritation, and platelet activation and may also be associated with pathological alterations in other tissues such as lung, liver, thymus, and the red blood cell system |
749402 |
| 4.1.2.27 | malfunction |
enzyme-deficient mutants display impaired intracellular replication in murine macrophages (associated with an inability to evade the maturing phagosome) |
-, 748668 |
| 4.1.2.27 | malfunction |
hearts of heterozygous SPL knockout mice exhibit reduced SPL activity, elevated sphingosine 1-phosphate levels, smaller infarct size, and increased functional recovery after ischemia-reperfusion injury compared with littermate controls |
713721 |
| 4.1.2.27 | malfunction |
inactivation causes product depletion and accumulation of upstream sphingolipid intermediates |
773439 |
| 4.1.2.27 | malfunction |
inhibition of S1PL with 4-deoxypyridoxine or knockdown of S1PL with siRNA increases intracellular sphingosine-1-phosphate 3fold, potentiates motility of HPAEC cells to extracellular sphingosine-1-phosphate or serum, and augments activated Rac1 as well as stimulates Rac1 and IQGAP1 translocation to the cell periphery |
716696 |
