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. Author manuscript; available in PMC: 2020 Dec 29.
Published in final edited form as: Nat Immunol. 2020 Jun 29;21(8):857–867. doi: 10.1038/s41590-020-0705-6

Figure 3. YopM recruits host RSK to phosphorylate pyrin and suppress inflammasome activation.

Figure 3

a, b, In vitro kinase assay of purified Myc/His-tagged N-terminal human pyrin (amino acids 1–330) (a, b) or RPS6 (b) incubated with recombinant PKN1 and/or RSK1 (a) or incubated with RSK1, RSK2, or RSK3 (b) in the presence of purified GST or GST-YopM, and analyzed by immunoblot with an antibody specific for phosphorylated serine (a, b) or antibody for phosphorylated RPS6 (b), followed by immunoblot analysis with antibody to Myc or antibody to RPS6. Data are representative of three independent experiments with similar results (a and b). c, IL-1β measurements of culture supernatants of CD14+ monocytes of healthy controls treated with indicated concentrations of SL0101–1 (left) or BRD7389 (right) for 1h and infected with Y. pestis at MOI 10. Results are presented as mean ± s.e.m., for n=5 independent biological replicates. d, ASC speck assay from THP1-ASC-GFP cells transfected with control (negative control, N.C.) or a pool of siRNAs targeting PKN1/2 or RSK1/2/3 with/without siMEFV, and infected with Y. pestis at MOI 10. The cells containing an ASC speck are indicated by red arrows. Data in all panels are representative from three repetitions with similar results.