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For Carlsson, this marked a shift in how his lab approached GPCR research.

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time of peak hypersensitivity implicate potential contributions of mitogen-activated protein kinase (MAPK development of 7α,25-OHC/GPR183-induced mechano-allodynia was associated with significant activation of MAPKs mechanistic insight into how GPR183 signaling in the spinal cord produces hypersensitivity through MAPK We found that 7α,25-OHC-induced allodynia is dependent on MAPK and NF-κB signaling pathways and results

G-protein signaling activates the MAPK Fus3, which phosphorylates the RGS; however, the role of this RGS phosphorylation peaks early; the phospho-state of RGS controls its localization and influences MAPK

intracellular β2-ADR downstream molecules (G protein-coupled receptor kinase 2 (GRK-2), β-Arrestin 2, p38 MAPK Stimulation of CIA B cells with the β-ADR agonist terbutaline increased pp38 MAPK independent of the The phosphorylation of p38 MAPK, ERK1/2 and CREB in the late phase of arthritis was associated with increased

neuroactive ligand-receptor interaction pathway, serotonergic synapse pathway, PI3K-Akt signaling pathway and MAPK ligand -receptor interaction pathway, serotonergic synapse pathway, PI3K-Akt signaling pathway and MAPK

Moreover, GOA-1 acted upstream of MPK-1/ERK MAPK, JNK-1/JNK MAPK, DBL-1/TGF-β, and DAF-7/ TGF-β, GSA- 1 functioned upstream of MPK-1/ERK MAPK, JNK-1/JNK MAPK, and DBL-1/TGF-β, and GPA-10 functioned upstream