Transcriptional activation by the human herpesvirus-8-encoded interferon regulatory factor.
Transcriptional activation by the human herpesvirus-8-encoded interferon regulatory factor.
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人类疱疹病毒 8 编码的干扰素调节因子的转录激活。
DOI：
10.1099/0022-1317-80-8-2205
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Offermann,MargaretK
中科院分区：
文献类型：
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作者：
Roan,Florence;Zimring,JamesC;Goodbourn,Stephen;Offermann,MargaretK
人类疱疹病毒8型（HHV-8）是一种γ疱疹病毒，被认为是卡波西肉瘤和原发性渗出性淋巴瘤的病毒病原体，编码细胞干扰素调节因子（IRFs）的同源物。HHV-8 IRF同源物（vIRF; ORF K9）先前已显示抑制干扰素和IRF-1的基因诱导，并转化NIH 3 T3细胞或Rat-1细胞。此外，在BCBL-1细胞中表达反义vIRF导致某些HHV-8基因的抑制，这表明vIRF也可能正调控基因表达。我们证明，vIRF激活转录时，直接对DNA的GAL 4 DNA结合域。当在HeLa细胞中共表达时，单独不能激活转录的GAL-vIRF截短构建体可以在反式激活中合作，这表明vIRF的多个区域参与反式激活。这些研究拓宽了vIRF的潜在作用机制，包括转录激活和转录抑制。
Human herpesvirus-8 (HHV-8), a gammaherpesvirus that is thought to be the viral aetiologic agent of Kaposi’s sarcoma and primary effusion lymphoma, encodes a homologue to cellular interferon regulatory factors (IRFs). The HHV-8 IRF homologue (vIRF; ORF K9) has previously been shown to inhibit gene induction by interferons and IRF-1 and to transform NIH3T3 cells or Rat-1 cells. Additionally, expression of antisense to vIRF in BCBL-1 cells results in the repression of certain HHV-8 genes, suggesting that vIRF may also positively regulate gene expression. We demonstrate that vIRF activates transcription when directed to DNA by the GAL4 DNA-binding domain. GAL-vIRF truncation constructs that individually are incapable of activating transcription can cooperate in transactivation when coexpressed in HeLa cells, suggesting that multiple regions of vIRF are involved in transactivation. These studies broaden the potential mechanisms of action of vIRF to include transcriptional activation as well as transcriptional repression.