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. 2019 Jul 23;9:10689. doi: 10.1038/s41598-019-47069-9

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Silencing the NMT1 or CKIIα genes blocked Tat.AG but not Tat.B-induced HIV-1 transactivation in U38 (A–C) and TZM-bl (D–F) cells. (A,D) RT-PCR confirmation of NMT1, NMT2, CKIIα and CKIIβ genes silencing. (B,E) Western blot confirmation of NMT1, NMT2, CKIIα and CKIIβ genes silencing. Control: non-transduced cells. S: cells transduced with scrambled shRNA. (C,F) Silencing the NMT1 or CKIIα genes blocked Tat.AG-induced increase in CAT enzyme levels (C) and luciferase activity (F), but had no effect on Tat.B-induced viral transactivation. Silencing the NMT2 or CKIIβ genes had no effect on Tat.AG or Tat.B-induced viral transactivation. *P < 0.05, **P < 0.01, ^#P < 0.0001, compared to cells treated with similar concentrations of scrambled (S) shRNA and Tat proteins. Errors bars represent SD.