Skip to main content
. 2016 May 12;6:25740. doi: 10.1038/srep25740

Figure 5. TNF-α secretion is relatively controlled by ALPK1 and myosin IIA in MSU-induced monocytes.

Figure 5

(A) Protein knockdown of si-ALPK1 and si-MYH9 by immunofluorescence (left) and quantification of intensity of colour (right) showed they were effective but not complete knockdown. (B) MSU treatment (compared to none) has generally increased intracellular TNF-α levels, including when ALPK1 was knockdown, which could be explained by the limitation in knockdown efficiency (see Fig. 5 A) or other protein kinases that phosphorylated myosin IIA were not eliminated. The most intracellular TNF-α increase was seen with myosin IIA knockdown. (C) MSU-induced TNF-α secretion was reduced with the knockdown of the endogenous ALPK1 or myosin IIA, however no effect was observed for IL-1β secretion. (D) TNF-α secretion was unaffected by the depletion of another kinase that may phosphorylate myosin IIA, myosin light-chain kinase (MLCK), using siRNA for 24 h prior treatment with MSU. Data are representative of results performed in triplicates. *p < 0.0001.