Cloned (Comment) | Organism |
---|---|
- |
Homo sapiens |
Protein Variants | Comment | Organism |
---|---|---|
G82D | dominant-negative SK1 mutant, removes the capacity of Ang-1 to inhibit endothelial cell permeability | Homo sapiens |
S225A | transfection with S225A, a nonphosphorylatable mutant of SK1, inhibits basal leakiness, and both S225A and a dominant-negative SK1 mutant remove the capacity of Ang-1 to inhibit endothelial cell permeability | Homo sapiens |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Mus musculus | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
endothelial cell | - |
Homo sapiens | - |
HUVEC cell | - |
Homo sapiens | - |
General Information | Comment | Organism |
---|---|---|
physiological function | mice depleted of isoform SK1 have increased vascular leakiness, whereas mice transgenic for SK1 in endothelial cells show attenuation of leakiness | Mus musculus |
physiological function | overexpression of SK1 results in inhibition of permeability similar to that seen for Ang-1, which rapidly and transiently stimulates SK1 activity and phosphorylation, and induces an increase in intracellular sphingosine 1-phosphate concentration. Knockdown of SK1 by siRNA blocks Ang-1-mediated inhibition of permeability. Transfection with S225A, a nonphosphorylatable mutant of SK1, inhibits basal leakiness, and both S225A and a dominant-negative SK1 mutant remove the capacity of Ang-1 to inhibit endotheial cell permeability. These effects are independent of extracellular sphingosine 1-phosphate | Homo sapiens |