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. Author manuscript; available in PMC: 2010 Mar 1.
Published in final edited form as: Virology. 2008 Dec 10;385(1):183–191. doi: 10.1016/j.virol.2008.11.018

Fig. 1. LMP2A degradation and LMP2A inhibition of EBV lytic replication by c-Cbl.

Fig. 1

(A) BJAB, BJAB-LMP2A+, LMP2A-expressing LCLs and LMP2A-deleted LCLs were infected with c-Cbl shRNAmir or nonesilencing (NS) shRNAmir lentiviruses. Cell lysates were immunoblotted for c-Cbl and GAPDH. Immunoprecipates of LMP2A, Lyn and Syk were immunoblotted for each protein and for phosphotyrosine. (B) EREB2.5 cells were infected with c-Cbl shRNAmir or nonesilencing (NS) shRNAmir lentiviruses. Selected cells were depleted with estrogen and transfected with LMP2A-expressing plasmid or control vector. Cell lysates were immunoblotted for LMP2A, BZLF1, c-Cbl and GAPDH. (C) BJAB cells were transfected with 5 μg of reporter plasmid expressing firefly luciferase under the control of BZLF1 promoter (Zp) with 20 μg of LMP2A and indicated μg of c-Cbl. Average fold induction of luciferase activity to promoterless plasmid with no activator is indicated. Data averaged from three independent experiments are shown ± standard deviation. The data is the representative of three comparable experiments.