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. 2019 Aug 19;42(5):1755–1766. doi: 10.3892/or.2019.7282

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Copyright: © Wang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 4. — Association between BTK and MYD88 identified via co-immunoprecipitation, and altered following treatment with ST2825 in MYD88 L265P-expressing ABC DLBCL cells. (A) Immunoprecipitation of cell lysates was performed via pull-down with an anti-MYD88 antibody followed by IB with an anti-BTK antibody. (B) In a reciprocal experiment, pull-down was performed with and anti-BTK antibody and IB with anti-MYD88 antibodies. (C) Immunoprecipitation of BTK with MYD88 was conducted following a 6-h treatment with 20 µM ST2825 or DMSO in MYD88 L265P mutant-ABC DLBCL cells (OCY-LY10 and TMD8). The data present a representative of at least two independent experiments. MYD88, myeloid differentiation primary response gene 88; BTK, Bruton's tyrosine kinase; ABC, activated B cell; DLBCA, diffuse large B-cell lymphoma; IB, immunoblot; IP, Immunoprecipitation; IgG, immunoglobulin G.