The splice 1 variant of HTLV-1 bZIP factor stabilizes c-Jun.
The splice 1 variant of HTLV-1 bZIP factor stabilizes c-Jun.
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DOI:
10.1016/j.virol.2020.07.013
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发表时间:
2020-10
期刊:
影响因子:
3.7
通讯作者:
Lemasson I
中科院分区:
文献类型:
--
作者:
Polakowski N;Pearce M;Kuguyo O;Boateng G;Hoang K;Lemasson I
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, HBZUS, was reported to decrease c-Jun expression by promoting its degradation. Here we show that another variant, HBZS1, produces the opposite effect. In the presence of HBZS1, c-Jun expression increases due to its stabilization. Our data suggest that this effect requires the ability of HBZS1 to interact with c-Jun. We provide evidence that HBZS1 inhibits the proteosomal degradation of c-Jun initiated by the Cop1-containing ubiquitin ligase complex. HBZS1 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 HBZS1.
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