Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 2.7.1.91 extracted from

  • Li, X.; Stankovic, M.; Bonder, C.S.; Hahn, C.N.; Parsons, M.; Pitson, S.M.; Xia, P.; Proia, R.L.; Vadas, M.A.; Gamble, J.R.
    Basal and angiopoietin-1-mediated endothelial permeability is regulated by sphingosine kinase-1 (2008), Blood, 111, 3489-3497.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 2.7.1.91

Cloned(Commentary)

Cloned (Comment) Organism
-
 Homo sapiens

Protein Variants

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

Organism UniProt Comment Textmining
Homo sapiens
-
-
-
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
endothelial cell
-
 Homo sapiens
-
HUVEC cell
-
 Homo sapiens
-

General Information

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