par Turrini, Filippo;Marelli, Sara;Kajaste-Rudnitski, Anna;Lusic, Marina;Van Lint, Carine 
;Das, A T;Harwig, Alex;Berkhout, Ben;Vicenzi, Elisa
Référence Retrovirology, 12, 1, page (104)
Publication Publié, 2015
;Das, A T;Harwig, Alex;Berkhout, Ben;Vicenzi, ElisaRéférence Retrovirology, 12, 1, page (104)
Publication Publié, 2015
Article révisé par les pairs
| Résumé : | Intracellular defense proteins, also referred to as restriction factors, are capable of interfering with different steps of the viral life cycle. Among these, we have shown that Tripartite motif 22 (TRIM22) suppresses basal as well as phorbol ester-induced HIV-1 long terminal repeat (LTR)-mediated transcription, independently of its E3 ubiquitin ligase activity, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) binding to the U3 region and Tat interaction with the TAR region of the HIV-1 LTR. As basal HIV-1 transcription is driven by the transcription factor specificity protein 1 (Sp1), we have investigated whether TRIM22 could interfere with Sp1-driven transcriptional activation of the HIV-1 LTR. |
