Skip to main content
. Author manuscript; available in PMC: 2018 Oct 17.
Published in final edited form as: Immunity. 2017 Oct 17;47(4):635–647.e6. doi: 10.1016/j.immuni.2017.09.011

Figure 6. Pirk Inhibits Amyloid Formation.

Figure 6

(A–F) ThT fluorescence in Drosophila S2* cells expressing mCherry-fusions of PGRP-LCx (A, B), PGRP-LE (C, D), or Imd (E,F), and either an empty vector (mock) or FLAG-Pirk. Representative images (A, C, E) and quantification (B, D, F) showing mean ± SEM of at least 39 cells pooled from three independent experiments. Scale bar: 10 μm. ****p < 0.0001.

(G) The inhibition of Imd amyloidal polymerization by Pirk, assayed by ThT fluorescence.

(H) Effect of Pirk on TNF-induced necroptosis in HeLa cells expressing wild-type RIPK3 or RIPK3/Imd chimera on TNF-induced necroptosis in HeLa cells. Cells were co-transfected with M45 or Pirk with WT or chimeric Imd-RIPK3. Necroptosis was activated with combined TNF, BV6, and zVAD-fmk treatment. The graph shows individual data points (N = 3) with mean indicated as a bar. Abbreviations: BZ, no TNF stimulation (gray dots); TBZ-, BV6-, and zVAD-fmk-treated cells stimulated with TNFα (black dots).

See also Figure S4 for a model of amyloid signaling and Pirk inhibition.