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人类免疫缺陷病毒1型反式激活因子通过蛋白酪氨酸磷酸酶介导的核转录因子NF-κB激活诱导单核细胞产生基质金属蛋白酶-9。

Human immunodeficiency virus-1-tat induces matrix metalloproteinase-9 in monocytes through protein tyrosine phosphatase-mediated activation of nuclear transcription factor NF-kappaB.

作者信息

Kumar A, Dhawan S, Mukhopadhyay A, Aggarwal B B

机构信息

Cytokine Research Section, Department of Molecular Oncology, University of Texas M.D. Anderson Cancer Center, 1515 Holcombe St. Box 143, Houston, TX 77030, USA.

出版信息

FEBS Lett. 1999 Nov 26;462(1-2):140-4. doi: 10.1016/s0014-5793(99)01487-8.

DOI:10.1016/s0014-5793(99)01487-8
PMID:10580107
Abstract

We have previously shown that human immunodeficiency virus (HIV)-1-tat induces the production of matrix metalloproteinase-9 (MMP-9) in human monocytes by a mechanism that is not understood. In the present report, we demonstrate that HIV-tat-induced expression of MMP-9 is blocked by inhibitors of protein tyrosine phosphatases (PTPases). PTPase inhibitors also blocked HIV-tat-induced nuclear transcription factor NF-kappaB activation and IkappaBalpha degradation required for MMP-9 induction. These results suggest that HIV-tat induces MMP-9 in human monocytes through activation of PTPase and NF-kappaB.

摘要

我们之前已经表明,人类免疫缺陷病毒1型(HIV-1)反式激活蛋白(tat)可通过一种尚不明确的机制诱导人单核细胞产生基质金属蛋白酶9(MMP-9)。在本报告中,我们证明HIV-tat诱导的MMP-9表达可被蛋白酪氨酸磷酸酶(PTPase)抑制剂阻断。PTPase抑制剂还可阻断HIV-tat诱导的MMP-9表达所需的核转录因子NF-κB激活及IκBα降解。这些结果表明,HIV-tat通过激活PTPase和NF-κB在人单核细胞中诱导MMP-9的产生。

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Human immunodeficiency virus-1-tat induces matrix metalloproteinase-9 in monocytes through protein tyrosine phosphatase-mediated activation of nuclear transcription factor NF-kappaB.人类免疫缺陷病毒1型反式激活因子通过蛋白酪氨酸磷酸酶介导的核转录因子NF-κB激活诱导单核细胞产生基质金属蛋白酶-9。
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