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. Author manuscript; available in PMC: 2012 Jan 5.
Published in final edited form as: Virology. 2010 Oct 28;409(1):113–120. doi: 10.1016/j.virol.2010.09.018

Figure 5. The ability of human Trim5α to affect TAB2 levels and to activate NF-kappaB are genetically separable.

Figure 5

(A) 293T cells were co-transfected with an NF-kappaB-driven Luciferase reporter construct (0.5ug DNA per lane) together with either empty vector LPCX, human Trim5α, human Trim5γ, human Trim22, or either of the chimeras Trim22R-5α, Trim5R-22, or Trim5RB-22 (0.5ug DNA per lane). (B) 293T cells were co-transfected with an NF-kappaB-driven Luciferase reporter construct (0.5ug DNA per lane) together with increasing amounts of either human Trim5α, C35A mutant of human Trim5α, or the chimera Trim5RB-22 (gradient of 0.06ug, 0.2ug, 0.6ug DNA per lane). Luciferase expression was plotted on y-axis as fold induction relative to empty vector LPCX. Protein expression was compared using anti-HA antibody.