EC Number   |
General Information |
Reference |
|---|
    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 |
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 |
| 4.1.2.27 | malfunction |
the absence of the enzyme is associated with reduced NF-kappaB activation and atypical morphology of mitochondria |
-, 749075 |
| 4.1.2.27 | metabolism |
S1P lyase catalyzes the irreversible degradation of sphingosine 1-phosphate in the final step of sphingolipid metabolism |
714674 |
| 4.1.2.27 | metabolism |
sphingosine-1-phosphate lyase is a key enzyme of sphingolipid metabolism |
716935 |
| 4.1.2.27 | metabolism |
SPL functions as the exit gate of the sphingolipid metabolism |
716860 |
| 4.1.2.27 | physiological function |
a myoblast sphingosine-1-phosphate lyase-knockdown cell accumulates intracellular and extracellular sphingosine-1-phosphate and fails to form myotubes under conditions that normally stimulate myogenic differentiation. Under differentiation conditions, knockdown cells also demonstrate delayed induction of myogenic microRNAs, miR-1, miR-206, and miR-486. Knockdown cells successfully differentiate when treated with an S1P1 agonist, S1P2 antagonist, and combination treatments, which also increase myogenic miRNA levels. Knockdown cells transfected with mimics for miR-1 or miR-206 also overcome the differentiation block |
727464 |
