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. 2015 Aug 22;12:74. doi: 10.1186/s12977-015-0200-6

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© Wagner et al. 2015

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 4 — Identification of the PR cleavage site in RIPK1. a Primary sequence of human RIPK1 (aa 449–476 according to NCBI Reference Sequence NP_003795.2) with PR cleavage site between residues 462 and 463. Indicated point mutations were introduced by Quikchange mutatgenesis. b HEK293T cells were transfected with expression plasmids encoding wild-type (wt) RIPK1, RIPK1 with a double-mutation in the PR cleavage site (RIPK1 PR^res), or RIPK1 with a non-sense mutation in the PR cleavage site (RIPK1 ΔC), respectively, along with catalytically active HIV PR (5 ng/well) in the absence (−) or presence (+) of SQV (5 μM). Cell lysates were subjected to SDS-PAGE and immunoblotting (WB). Proteins were revealed using antibodies against c-Myc, β-actin, or HIV-1 PR