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- W2041548356 abstract "Systemic inflammation arising from the organismal distribution of pathogen-associated molecular patterns is a major cause of clinical morbidity and mortality. Herein we report a critical and previously unrecognized in vivo role for germinal center kinase (GCK, genome nomenclature: map4k2 ), a mammalian Sterile 20 ( STE20 ) orthologue, in PAMP signaling, and systemic inflammation. We find that disruption of gck in mice strongly impairs PAMP-stimulated macrophage cytokine and chemokine release and renders mice resistant to endotoxin-mediated lethality. Bone marrow transplantation studies show that hematopoietic cell GCK signaling is essential to systemic inflammation. Disruption of gck substantially reduces PAMP activation of macrophage Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinases (MAPKs) via reduced activation of the MAPK-kinase-kinases (MAP3Ks) mixed lineage kinases (MLKs)-2 and -3. Extracellular signal-regulated kinase (ERK) and nuclear factor-κB (NF-κB) activation are largely unaffected. Thus, GCK is an essential PAMP effector coupling JNK and p38, but not ERK or NF-κB to systemic inflammation." @default.
- W2041548356 created "2016-06-24" @default.
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- W2041548356 date "2009-03-17" @default.
- W2041548356 modified "2023-10-03" @default.
- W2041548356 title "GCK is essential to systemic inflammation and pattern recognition receptor signaling to JNK and p38" @default.
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- W2041548356 doi "https://doi.org/10.1073/pnas.0812642106" @default.
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