Fig. 7: The direct recruitment of TRAF6 to LMP1 supports LCL survival.
From: Epstein-Barr virus-driven B cell lymphoma mediated by a direct LMP1-TRAF6 complex
a HA-LMP1(∆371-386)-liTRAF6 mimics the direct recruitment of TRAF6 to CTAR2. Amino acids 371-386 of CTAR2 were replaced by a flexible linker and TRAF6 wild-type. b The forced recruitment of TRAF6 to LMP1 is sufficient to activate NF-κB in the absence of functional CTAR1. TRAF6-/- MEFs were transfected with the indicated HA-LMP1 constructs or HA-LMP1(A204xAxA/∆371-386)-liTRAF6 together with an NF-κB reporter. NF-κB reporter assays were performed. Data are mean values ± SD of six independent experiments. Statistics: one-way ANOVA. c LCL.NGFR-LMP1 cells were transfected with doxycycline-inducible pRTS1-mCherry vectors expressing HA-LMP1(∆371-386)-liTRAF6, HA-LMP1 wild-type or the inactive HA-LMP1(A204xAxA/∆371-386) mutant. Endogenous NGFR-LMP1 activity was silenced by antibody withdrawal and expression of the constructs was induced by the addition of doxycycline. After 16 days, the numbers of DAPI-negative/mCherryhigh cells were analyzed by flow cytometry. The numbers of living cells expressing HA-LMP1 were set to 100%. Data are mean values ± SD of six independent experiments. Statistics: unpaired T-test, two-tailed. p-values: *p ≤ 0.05, **p ≤ 0.01, n.s. (not significant). Source data and exact p-values in the Source Data file.
