An allosteric drug, o,o′-bismyristoyl thiamine disulfide, suppresses HIV-1 replication through prevention of nuclear translocation of both HIV-1 Tat and NF-κB

被引：20

作者：

Shoji, S ^{[1
]}

Furuishi, K

Ogata, A

Yamataka, K

Tachibana, K

Mukai, R

Uda, A

Harano, K

Matsushita, S

Misumi, S

机构：

[1] Kumamoto Univ, Fac Pharmaceut Sci, Dept Biochem, Kumamoto 8620973, Japan

[2] Kumamoto Univ, Fac Pharmaceut Sci, Dept Med Chem, Kumamoto 8620973, Japan

[3] Nissui Pharmaceut Co Ltd, Div Res, Ibaraki, Osaka 3070036, Japan

[4] Natl Inst Hlth, Tsukuba Primate Ctr Med Sci, Tsukuba, Ibaraki 3070843, Japan

[5] Kumamoto Univ, Res Inst AIDS, Kumamoto 8600811, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1998年 / 249卷 / 03期

关键词：

D O I：

10.1006/bbrc.1998.9221

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The efficacy of o,o'-bismyristoyl thiamine disulfide (BMT) was examined in detail against HIV-1 laboratory isolates (HTLV-IIIB, JRFL, and MN), primary isolates (KMT and KMO), and simian immunodeficiency virus (SIVmac251) in vitro. BMT inhibited the replication of HIV-1 in both laboratory and primary isolates in vitro. In addition, BMT exhibited antiviral activity against SIVmac251, Minimizing energy studies of BMT structure reveal that a trans-disulfide of thiamine (holo drug) disulfide (TDS, protodrug) is allosterically transited to the reactive twisted disulfide of BMT (allo drug) by o, o'-bismyristoyl esterification of TDS. BMT inhibits nuclear translocation of both HIV-1 transactivator (Tat) and the cellular transcriptional nuclear factor-kappa B (NF-kappa B), resulting in the suppression of HIV-1 replication. (C) 1998 Academic Press.

引用

页码：745 / 753

页数：9

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