Application | Comment | Organism |
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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 | Comment | Organism |
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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 | UniProt | Comment | Textmining |
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Mus musculus | Q62190 | - |
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Source Tissue | Comment | Organism | Textmining |
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Synonyms | Comment | Organism |
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RON receptor tyrosine kinase | - |
Mus musculus |