A potentially immunologically inert derivative of the reverse tetracycline-controlled transactivator
Abstract
The archetypical system for regulating heterologous gene expression in mammalian cells involves tetracycline-activated transactivators (rtTA). Binding of such transactivators to tet-operator-controlled promoters induces transcription. Immune responses directed against the transactivator proteins may limit the applicability of this system in immune-competent hosts. To circumvent such immune responses the immune evasion mechanism of the Epstein-Barr virus Nuclear-Antigen 1 was exploited. Our data show that fusion of the rtTA with the EBNA-1 derived Gly-Ala repeat yielded an efficient transactivator with no detectable activity in absence of inducer. Antigenic peptides of the fusion protein were not presented in MHC class I.
Doxycycline Gene therapy Inducible expression Promoter Transcription recombinant-adenoassociated-virus regulated transgene expression cis-inhibition gene repeats degradation activation proteasome cells term
