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. 2024 Jun 11;221(8):e20231518. doi: 10.1084/jem.20231518

Figure 3.

Figure 3.

HSV-1 inhibits proteasome-dependent NT-NLRP1 degradation. (A) Immunoblots of lysates from primary human keratinocytes treated with anisomycin (1 μM) and/or bortezomib (10 μM) for 24 h. Images are representative of n = 3 biological replicates. (B) Immunoblots of lysates from primary human keratinocytes infected with HSV-1 KOS (MOI 10) for 4 h followed by treatment with talabostat (30 μM) or anisomycin (1 μM) for 24 h. Images are representative of n = 3 biological replicates. (C) Immunoblots of lysates from primary keratinocytes infected with HSV-1 KOS (MOI 10) for 4 h followed by transfection with poly(I:C) (1 μg/ml) for 24 h. Images are representative of n = 3 biological replicates. (D) NTERT2G1 keratinocytes expressing an empty vector or dTAG-NLRP1 were infected with HSV-1 KOS for 4 h followed by treatment with dTAG-13 or dTAGV-1. Membrane permeability was assessed at 8 h after treatment. Data are presented as the mean of three independent experiments ± SEM. Statistical significance was calculated by Student’s t test (*P < 0.05, ***P < 0.001, ****P < 0.0001). (E) Immunoblot of ASC oligomers and lysates from NTERT2G1 keratinocytes expressing dTAG-NLRP1 infected with HSV-1 for 4 h followed by treatment with DMSO, dTAG-13, or dTAGV-1 for 4 h. Images are representative of n = 3 biological replicates. Source data are available for this figure: SourceData F3.