Figure 1

Extracellular 14-3-3η selectively activates extracellular signal-regulated kinase and c-Jun N-terminal kinase/stress-activated protein kinase and potentiates inflammatory and joint damage factors. (A) 14-3-3η leads to the phosphorylation and activation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK). p-MEK, Phosphorylated mitogen-activated protein kinase kinase; p-SAPK, Phosphorylated stress-activated protein kinase. (B) Equal protein loading. (C) The effects were specific for ERK and JNK because phosphorylation of p38 mitogen-activated protein kinase (p38MAPK) by 14-3-3η was not observed. (D) Similarly to tumour necrosis factor α (TNFα), 14-3-3η leads to the induction of inflammatory and joint damage factors. IL, Interleukin; GAPDH, Glyceraldehyde 3-phosphate dehydrogenase; MMP, Matrix metalloproteinase; RANKL, Receptor activator of nuclear factor κB ligand. (E) 14-3-3η induced effects observed with 14-3-3η concentrations that closely approximated the 14-3-3η median rheumatoid arthritis (RA) serum concentrations.