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

BRENDA support

Literature summary for 2.7.1.91 extracted from

  • Wadgaonkar, R.; Patel, V.; Grinkina, N.; Romano, C.; Liu, J.; Zhao, Y.; Sammani, S.; Garcia, J.; Natarajan, V.
    Differential regulation of sphingosine kinases 1 and 2 in lung injury (2009), Am. J. Physiol. Lung Cell Mol. Physiol., 296, L603-L613.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 2.7.1.91

Organism

Organism UniProt Comment Textmining
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
lung
-
 Mus musculus
-

Expression

Organism Comment Expression
Mus musculus treatment with lipopolysaccharid causes significantly enhances isoform SphK1 expression within 6 h, which declines back to baseline levels by 24 h. Expression of isoform SphK2 is gradually induced following lipopolysaccharide treatment and is elevated within 24 h up

General Information

General Information Comment Organism
physiological function isoform SphK1 deficient SphK1-/- mice are much more susceptible to lipopolysaccharide-induced lung injury than wild-type. Overexpression of wild-type SphK1 in lungs protects SphK1-/- mice from lung injury and attenuates the severity of the response to lipopolysaccharide. Overexpression of a ShpK1 kinase-dead mutant in SphK1-/- mouse lungs further exacerbates the response to lipopolysaccharide as well as the extent of lung injury. Wild-type isoform SphK2 overexpression also fails to provide protection and augments the degree of lipopolysaccharide-induced lung injury Mus musculus