Abstract:
:Human T-cell leukemia virus type I (HTLV-I)-infected T-cell lines constitutively produce high levels of biologically active lymphotoxin (LT; tumor necrosis factor-beta) protein and LT mRNA. To understand the regulation of LT transcription by HTLV-I, we analyzed the ability of a series of deletions of the LT promoter to drive the chloramphenicol acetyltransferase (CAT) reporter gene in HTLV-I-positive MT-2 cells. The smallest LT promoter fragment (-140 to +77) that was able to drive CAT activity contained a site that was similar to the immunoglobulin kappa-chain NF-kappa B-binding site. Since the HTLV-I tax gene activates the nuclear form of NF-kappa B, this finding suggested a possible means of HTLV-I activation of LT production. We found that the LT kappa B-like site specifically formed a complex with NF-kappa B-containing nuclear extract from MT-2, C81-66-45, and other activated T cells. Mutation of the LT kappa B site in the context of the LT promoter (-293 to +77) (mutant M1) reduced the ability of the promoter to drive the CAT gene in HTLV-I-infected and noninfected human T-cell lines. These data suggest a general role for NF-kappa B activation in the induction of LT gene transcription. Activation of LT in HTLV-I-infected cells may explain the pathology associated with HTLV-I infection, including the hypercalcemia that is prevalent in adult T-cell leukemia.
journal_name
J Viroljournal_title
Journal of virologyauthors
Paul NL,Lenardo MJ,Novak KD,Sarr T,Tang WL,Ruddle NHdoi
10.1128/JVI.64.11.5412-5419.1990subject
Has Abstractpub_date
1990-11-01 00:00:00pages
5412-9issue
11eissn
0022-538Xissn
1098-5514journal_volume
64pub_type
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pub_type: 杂志文章
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pub_type: 杂志文章
doi:10.1128/JVI.67.1.360-365.1993
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更新日期:1993-01-01 00:00:00
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