| Description | HTLV-1 encodes two proteins that have been reported to drive oncogenesis: Tax and HTLV-1 basic leucine zipper (bZIP) factor (HBZ). HBZ has been shown to enhance viral infectivity and persistence, and facilitates proliferation of HTLV-1-infected lymphocytes [ ]. It has also been shown to attenuates DSB (double-stranded DNA breaks) repair by nonhomologous end joining (NHEJ), in a manner dependent upon the bZIP domain [].HBZ has been shown to negatively regulate basal and Tax-dependent HTLV-1 transcription through its ability to interact with specific basic-leucine zipper (bZIP) proteins. HBZ has been shown to reduce HTLV-1 transcription and virion production. The protein interacts with CREB in vivo and directly in vitro via the bZIP domain of each protein; CREM-Ia and ATF-1 also interact with HBZ-bZIP. The interaction between CREB and HBZ prevents CREB binding to the viral CRE elements in vitro and in vivo, suggesting that the reduction in HTLV-1 transcription by HBZ partly results from the the loss of CREB at the promoter. It has also been shown that HBZ displaces CREB from a cellular CRE, suggesting that HBZ may de-regulate CREB-dependent cellular gene expression [ ]. | Name | HTLV-1 basic zipper factor |
| Short Name | HTLV1ZIPPER | Type | Family |
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