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

BRENDA support

Literature summary for 2.7.10.1 extracted from

  • Caldwell, C.C.; Martignoni, A.; Leonis, M.A.; Ondiveeran, H.K.; Fox-Robichaud, A.E.; Waltz, S.E.
    Ron receptor tyrosine kinase-dependent hepatic neutrophil recruitment and survival benefit in a murine model of bacterial peritonitis (2008), Crit. Care Med., 36, 1585-1593.
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
medicine intact Ron receptor protein enhances survival following cecal ligation and puncture-induced bacterial peritonitis in mice. Ron signaling negatively regulates the response to polymicrobial infection by regulating the activation and recruitment of inflammatory cells necessary for clearing a systemic bacterial burden. This effect may be regulated in part through the Ron-dependent, macrophage-mediated production of cytokines and chemokines, namely monocyte chemoattractant protein-1, interleukin-6, and macrophage inflammatory protein-2, important for neutrophil mobilization Mus musculus

Protein Variants

Protein Variants Comment Organism
additional information mice with a targeted deletion of the Ron tyrosine kinase signaling domain (TK-/-), show a significant decrease in survival time after bacterial infection compared with controls, which is associated with a significant increase in bacterial colony-forming units in the blood and several end-organs. The increased bacterial load is associated with increased liver necrosis and serum alanine aminotransferase levels. Neutrophils from TK-/- mice exhibit decreased spontaneous oxidative burst capacity ex vivo, and a reduced level of neutrophil migration to and translocation within the liver. Loss of Ron signaling results in significantly reduced production of serum monocyte chemoattractant protein-1 and interleukin-6 levels following cecal ligation and puncture, and peritoneal macrophage isolated from TK-/- mice exhibit blunted production of monocyte chemoattractant protein-1, interleukin-6, and macrophage inflammatory protein-2 following stimulation with endotoxin ex vivo Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus Q62190
-
-

Source Tissue

Source Tissue Comment Organism Textmining

Synonyms

Synonyms Comment Organism
RON receptor tyrosine kinase
-
Mus musculus