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. 2015 Oct 5;35(23):2979–2990. doi: 10.1038/onc.2015.364

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Copyright © 2016 Macmillan Publishers Limited

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

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HCV infection upregulates BCR signaling in human primary B cells and Raji cells. (a) Western blot analysis showing protein expression of NS3, CARD11, Blk and CD79A in lysates isolated from normal (five discrete patients) and HCV-infected (mix: pooled from eight patients) purified B cells. Actin was used as a loading control. (b) Protein expression of NS3, core, CD79A and CD79B in lysates isolated from control and HCV-infected Raji cells was detected by western blot analysis. (c) The model depicts a proposed mechanism for HCV-associated B-cell lymphoproliferative disorders. HCV NS3/4A interacts with CHK2 and downregulates CHK2 activity. Subsequently, this repressed CHK2 activity modulates HuR posttranscriptional regulation of a network of target mRNAs associated with B-cell lymphoproliferative disorders, preferentially those involved in the BCR signaling pathway.