Anti-JUN monoclonal antibody, clone 5I0

HBZ is expressed by the complex retrovirus, Human T-cell Leukemia Virus type 1, and implicated in pathological effects associated with viral infection. From the nucleus, HBZ alters gene expression by interacting with a variety of transcriptional regulatory proteins, among which is c-Jun. Previously, one of the three HBZ variants, HBZ(US), was reported to decrease c-Jun expression by promoting its degradation. Here we show that another variant, HBZ(S1), produces the opposite effect. In the presence of HBZ(S1), c-Jun expression increases due to its stabilization. Our data suggest that this effect requires the ability of HBZ(S1) to interact with c-Jun. We provide evidence that HBZ(S1) inhibits the proteosomal degradation of c-Jun initiated by the Cop1-containing ubiquitin ligase complex. HBZ(S1) is the most abundant variant in HTLV-1-infected T-cells, and our data indicate that levels of c-Jun expression in infected cells are consistent with effects of HBZ(S1).