Title : JNK activation is essential for activation of MEK/ERK signaling in IL-1β-induced COX-2 expression in synovial fibroblasts.

Pub. Date : 2017 Jan 5

PMID : 28054591






6 Functional Relationships(s)
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1 The proinflammatory cytokine interleukin 1beta (IL-1beta) induces prostaglandin E2 (PGE2) production via upregulation of cyclooxygenase-2 (COX-2) expression in synovial fibroblasts. Dinoprostone interleukin 1 beta Homo sapiens
2 The proinflammatory cytokine interleukin 1beta (IL-1beta) induces prostaglandin E2 (PGE2) production via upregulation of cyclooxygenase-2 (COX-2) expression in synovial fibroblasts. Dinoprostone interleukin 1 beta Homo sapiens
3 The proinflammatory cytokine interleukin 1beta (IL-1beta) induces prostaglandin E2 (PGE2) production via upregulation of cyclooxygenase-2 (COX-2) expression in synovial fibroblasts. Dinoprostone interleukin 1 beta Homo sapiens
4 The proinflammatory cytokine interleukin 1beta (IL-1beta) induces prostaglandin E2 (PGE2) production via upregulation of cyclooxygenase-2 (COX-2) expression in synovial fibroblasts. Dinoprostone interleukin 1 beta Homo sapiens
5 In the presence of MAPK inhibitors, IL-1beta-induced COX-2 expression and PGE2 release were both attenuated. Dinoprostone interleukin 1 beta Homo sapiens
6 These observations suggest that JNK1 phosphorylation is necessary for the activation of the MEK/ERK1/2 pathway and the subsequent COX-2 expression for PGE2 release, and p38 independently contributes to the IL-1beta effect in synovial fibroblasts. Dinoprostone interleukin 1 beta Homo sapiens