Fig. 1.

Effect of HBZ on bZIP factor activities. (1) Tax interacts with CREB to bind to vCREs and then recruits CBP (or p300) to activate viral transcription from the 5′ LTR. (2) HBZ inhibits Tax-dependent viral transcription by interacting with CREB and CBP/p300. (3) HBZ also stimulates its own expression by forming HBZ/JunD heterodimers capable of interacting with Sp1 bound to the 3′ LTR. (4) HBZ can also bind to ATF-3/p53 complexes, reducing ATF3′s ability to enhance p53 activity. (5 and 6) HBZ inhibits the MafB, C/EBPα, c-Jun, and JunB transcriptional activities by promoting their degradation via a proteasome-dependent pathway (5) or by sequestration into nuclear bodies (6). HBZ stimulates JunD activity (7) by inducing expression of ΔJunD, a JunD isoform that is unable to interact with the inhibitor menin. HBZ is also able to activate HMOX1 transcription by forming heterodimers with the small Mafs [42]