4.1.2.27: sphinganine-1-phosphate aldolase
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For detailed information about sphinganine-1-phosphate aldolase, go to the full flat file.
Word Map on EC 4.1.2.27
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4.1.2.27
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sphingolipids
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ceramide
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sphingoid
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egress
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lymphopenia
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dihydrosphingosine-1-phosphate
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medicine
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fingolimod
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s1p-degrading
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sphks
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4-deoxypyridoxine
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steroid-resistant
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analysis
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lyase-deficient
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s1p-dependent
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spinster
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s1p-induced
- 4.1.2.27
- sphingolipids
- ceramide
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sphingoid
-
egress
- lymphopenia
- dihydrosphingosine-1-phosphate
- medicine
- fingolimod
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s1p-degrading
-
sphks
- 4-deoxypyridoxine
-
steroid-resistant
- analysis
-
lyase-deficient
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s1p-dependent
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spinster
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s1p-induced
Reaction
Synonyms
aldolase, dihydrosphingosine 1-phosphate, Dihydrosphingosine 1-phosphate aldolase, dihydrosphingosine phosphate lyase, Dpl1, Dpl1p, LegS2, S-1-P-lyase, S1P lyase, S1P-lyase, S1PL, S1PL2021, Sgpl1, sphinganine 1-phosphate lyase, sphinganine-1-phosphate aldolase, sphinganine-1-phosphate lyase, sphinganine-1-phosphate-alkanal-lyase, sphingosine 1-phosphate lyase, sphingosine phosphate lyase, sphingosine-1-phosphate lyase, sphingosine-phosphate lyase, SPL, SPL1
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Application on EC 4.1.2.27 - sphinganine-1-phosphate aldolase
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analysis
medicine
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use of BODIPY-labeled sphinganine substrate, allows fluorescent product detection by HPLC. The reaction is linear over a 30 min time period
analysis
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easy and sensitive procedure to determine sphingosine-1-phosphate lyase activity. The assay uses C17-sphinganine-1-phosphate as substrate and the aldehyde product, pentadecanal, is quantified as its pentafluorobenzyloxime derivative by GC/MS. Derivatization of pentadecanal is performed as a one-step reaction, and the oxime product is directly injected for GC/MS analysis without any further purification. Limit of detection is 281 fmol. The assay is linear with both protein concentration and incubation time up to 20 microg and 40 min, respectively
analysis
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the addition of sphingosine to cultures of cell lines or primary cells provides a source of intracellular sphingosine 1-phosphate that is susceptible to degradation by the lyase and, hence, increases on inhibition or silencing of the enzyme. Development of a biochemical assay optimized with respect to sphingosine concentration, incubation time, and cell density and establishment for routine use with HEK293 cells. The assay is suitable for the testing of novel active site-directed sphongosine-1-phosphate lyase inhibitors
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some effects of immune modulator FTY720 are due to disruption of sphingosine-1-phosphate metabolism
medicine
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some effects of immune modulator FTY720 are due to disruption of sphingosine-1-phosphate metabolism
medicine
all S1PL-deficient genetic models used display lymphopenia, with sequestration of mature T-cells in the thymus and lymph nodes. In addition to the lymphoid phenotypes, S1PL KO mice also develop myeloid cell hyperplasia and significant lesions in the lung, heart, urinary tract, and bone, and have a markedly reduced life span. Complete absence of S1PL affects both maturation/development and egress of mature T cells from the thymus, whereas low level S1PL activity affects T-cell egress more than differentiation
medicine
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complete loss of SPL activity leads to upregulation of the antiapoptotic proteins Bcl-2 and Bcl-xL and consequently protects against apoptosis induced by chemotherapy and nutrient starvation but not against autophagy
medicine
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following the oral administration of 10 and 100 mg/kg 2-acetyl-4(5)-tetrahydroxybutyl imidazole to male rats, 2-acetyl-4(5)-tetrahydroxybutyl imidazole is rapidly absorbed and reaches a plasma peak level at 1 h post-dosing. Splenic S1P increases and reaches the peak level at 24 h. Blood lymphocyte count decreases as the splenic S1P level increases. 2-Acetyl-4(5)-tetrahydroxybutyl imidazole plasma concentration is linked to splenic S1P concentration using an indirect model incorporated with a four-step signal transduction model. In turn, the S1P level is directly coupled with blood lymphocyte number
medicine
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humanized knock-in mice harboring one allele such as S1PLH/- or two alleles such as S1PLH/H of human S1PL express less than 10 and 20% of normal S1PL activity, respectively. This partial restoration of S1PL activity is sufficient to fully protect both humanized mouse lines from the lethal non-lymphoid lesions that develop in S1PL-/- mice, but fails to restore normal T-cell development and trafficking. The complete absence of S1PL affects both maturation/development and egress of mature T-cells from the thymus, whereas low level S1PL activity affects T-cell egress more than differentiation
medicine
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incubation of lyase-deficient neurons with either sphingosine or S1P results in a similar elevation in cellular S1P, but only S1P addition to the culture medium induces apoptosis. This is not due to S1P acting on the S1P receptor but to hydrolysis of S1P to sphingosine that is phosphorylated by the cells. Although the cells produce S1P from both exogenously added sphingosine as well as sphingosine derived from exogenous S1P, the S1P from these two sources are not equivalent, because the former is primarily produced by SK1, whereas the latter is mainly formed by sphingosine kinase-2
medicine
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mRNA expression for both sphingosine kinase and sphingosine 1-phosphate lyase are up-regulated throughout all four stages in human breast cancer patients
medicine
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thymocyte development in SGPL1-deficient mice which exhibit postnatal discontinuation of early thymocytopoies is starting at 2 weeks after birth. SGPL-/- thymi show a loss of developing thymocytes in the thymic cortex between 2 and 4 weeks of age, whereas mature thymocytes accumulate in the medulla. Increased ceramide levels in the thymus of SGPL1-/- mice abrogates thymic development postnatally by enhanced thymocyte apoptosis and depletion of thymic ETP. Potentially therapeutic immunosuppression by SGPL1 inhibition should benefit from monitoring ceramides to prevent their increase to apoptosis-inducing levels
medicine
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S1P lyase is a therapeutic target for ischemia-reperfusion injury of the heart
medicine
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in fresh human prostatectomy specimens, a remarkable decrease in sphingosine 1-phosphate lyase enzymatic activity is found in tumor samples, as compared with normal adjacent tissues. A significant relationship between loss of sphingosine 1-phosphate lyase expression and higher Gleason score is confirmed. Sphingosine 1-phosphate lyase protein expression and activity are inversely correlated with those of sphingosine kinase-1, the enzyme producing sphingosine 1-phosphate. Sphingosine 1-phosphate lyase and sphingosine kinase expressions are independently predictive of aggressive cancer on tissue microarray
medicine
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inducible sphingosine-1-phosphate lyase knockout mice featuring partial reduction of sphingosine-1-phosphate lyase activity are viable but feature profound reduction of peripheral T cells, similar to the constitutive knockout mice. While thymic T cell development in these mice appears normal, mature T cells are retained in thymus and lymph nodes, leading to reduced T cell numbers in spleen and blood, with a skewing towards increased proportions of memory T cells and T regulatory cells. The inducible knockout mice are protected in experimental autoimmune encephalomyelitis. T cell immigration into the CNS is profoundly reduced
medicine
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inhibition of sphingosine-1-phosphate lyase activity rendes sphingosine 1-phosphate an efficient S1P1 receptor internalizing compound and abrogated sphingosine-1-phosphate-mediated sustained signaling, suggesting that sphingosine-1-phosphate lyase by facilitating S1P1 receptor recycling is essential for sphingosine-1-phosphate-mediated sustained signaling, and that synthetic agonists are functional antagonists because they are not sphingosine-1-phosphate lyase substrates