Fig. 1: Hundreds of potential antimicrobial peptides reside in the human proteome.
From: Cell-autonomous innate immunity by proteasome-derived defence peptides
a, AMP sequences (green) in host proteins (grey). Conserved AMPs are indicated in orange, whereas those without conservation data are labelled as NA. b,c, Comparison of predicted amino-acid local-distance difference test (pLDDT) scores (b) and relative solvent-accessible surface area (rASA) (c) in putative AMPs compared with other regions of the same proteins. U-test, ****P < 0.0001. d, Distribution of peptides predicted by in silico proteasomal cleavage of the human proteome, showing only those scoring >5 on the basis of AMP biochemical characteristics. e, CFU count of intracellular S. typhimurium infection of A549 cells treated with bortezomib (50 nM) or untreated, normalized to the cell count. Data are mean ± s.e.m. (n = 6 biological replicates). Unpaired two-tailed Student’s t-test, **P = 0.004. f, Bacterial growth in conditioned medium (<10 kDa). OD, optical density. Diagram of the equipment in f was created with BioRender.com (https://BioRender.com/x10a923). g–i, Growth of S. enterica in medium from HCT116 (h) or A549 (g,i) cells treated with DMSO (control), epoxomicin (1 μM, concentrated medium ×2; g) or bortezomib (50 nM; h,i) for 6 h. Data are mean ± s.e.m. (n = 3 biological replicates). Unpaired two-tailed t-test: NS, P = 0.96, ***P = 0.0007, ****P < 0.0001 (g); **P = 0.0066 (h); *P = 0.0248 (i). j,k, Growth of S. enterica in medium from A549 (j) or HCT116 (k) cells treated with or without bortezomib and followed by proteinase K (1 μg ml–1) for 6 h. Data are mean ± s.e.m. (n = 3 biological replicates). One-way ANOVA: NS, P = 0.38, *P = 0.033 (j); NS, P = 0.675; **P = 0.0038 (k).
