TRANSCRIPTIONAL ACTIVATION OF THE INTERLEUKIN-6 GENE BY HTLV-1 P40TAX THROUGH AN NF-KAPPA-B-LIKE BINDING-SITE

被引：25

作者：

MURAOKA, O ^{[1
]}

KAISHO, T ^{[1
]}

TANABE, M ^{[1
]}

HIRANO, T ^{[1
]}

机构：

[1] OSAKA UNIV, SCH MED,BIOMED RES CTR,DIV MOLEC ONCOL, 2-2 YAMADA OKA, SUITA, OSAKA 565, JAPAN

来源：

IMMUNOLOGY LETTERS | 1993年 / 37卷 / 2-3期

关键词：

INTERLEUKIN-6; HUMAN T-CELL LEUKEMIA VIRUS TYPE-1 P40TAX; TRANSACTIVATION; NF-KAPPA-B BINDING SITE;

D O I：

10.1016/0165-2478(93)90026-X

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The interleukin-6 (IL-6) gene is expressed by various stimuli including cytokines or viral infections, such as human T-cell leukemia virus type I (HTLV-1). However, it has not been well established how HTLV-1 induces the expression of the IL-6 gene. In the present study, we demonstrated that HTLV-1-derived transactivator protein, p40tax, could stimulate endogenous IL-6 gene expression. Furthermore, we showed that the NF-kappaB binding site (IL-6kappaB site) located between -74 and -62 upstream of the cap site of the IL-6 gene was an essential cis-acting element for p40tax-mediated transactivation of the IL-6 gene expression by utilizing a series of 5' deletion mutants of the IL-6 5' flanking region as well as a construct with a mutated IL-6kappaB site. We identified the presence of two nuclear factor complexes that bound to the IL-6kappaB site. One was constitutively expressed, and the other was inducible by p40tax. Taken together, HTLV-1 p40tax directly induces IL-6 gene expression through the IL-6kappaB site, indicating the close association between IL-6 overproduction and HTLV-1 infection.

引用

页码：159 / 165

页数：7

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