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- B673f5af0a2ef44338e64a016e5d1d451 NCIT_P378 "BIOCARTA" @default.
- B673f5af0a2ef44338e64a016e5d1d451 type Axiom @default.
- B673f5af0a2ef44338e64a016e5d1d451 annotatedProperty NCIT_P325 @default.
- B673f5af0a2ef44338e64a016e5d1d451 annotatedSource NCIT_C39082 @default.
- B673f5af0a2ef44338e64a016e5d1d451 annotatedTarget "Neutrophils respond to bacterial infection by releasing reactive oxygen species that kill bacteria and by expressing chemokines that attract other immune cells to the site of infection. The multisubunit enzyme NADPH oxidase, expressed by neutrophils, produces reactive oxygen species that are rapidly released in what is known as the respiratory burst. Activity of the NADPH oxidase is induced by fMLP receptor ligands, formylated peptides from bacteria. The fMLP receptor is a G-protein coupled receptor, FPR-1, that activates Map kinase pathways and phospholipase C. Phospholipase C activation releases IP3 and calcium, activating protein kinase C and also activating the transcription factor NFAT, which contributes to activation of chemokine genes. One of the components of the NADPH oxidase is p47phox. PKC activation phosphorylates p47phox to activate NADPH oxidase activity. Activation of Map kinase cascades leads to Erk1/Erk2 dependent p47phox phosphorylation as well as activation of the Elk-1 transcription factor and chemokine gene expression. Inhibition of p38 did not affect p47phox phosphorylation, indicating that p38 is not involved in Erk1/2 activation of the NADPH oxidase. Inhibition of p38 did inhibit NADPH oxidase though, indicating that other pathways contribute to activation of this enzyme. (This definition may be outdated - see the DesignNote.)" @default.