2003年6月
Transduction of dominant negative ATF-1 suppresses the pX gene expression in joint fibroblastic cells derived from HTLV-I transgenic rats
EXPERIMENTAL AND MOLECULAR PATHOLOGY
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- 巻
- 74
- 号
- 3
- 開始ページ
- 309
- 終了ページ
- 313
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1016/S0014-4800(02)00019-9
- 出版者・発行元
- ACADEMIC PRESS INC ELSEVIER SCIENCE
Tax (p40Tax) encoded by the env-pX gene of human T-cell leukemia virus type I (HTLV-I) interacts with cyclic adenosine-3',5'-monophosphate response element binding protein/activation transcription factor 1 (CREB/ATF-1) transcription factors of host cells and activates the viral long terminal repeat (LTR) promoter. This molecular interaction induces augmentation of viral gene expression and may result in development of HTLV-I-associated diseases, including adult T-cell leukemia, HTLV-I associated myelopathy/tropical spastic paraparesis. and HTLV-I uveitis. To inhibit this pathway, a dominant negative molecule of ATF-1, ATF-1DN, was used. We transduced ATF-1DN into joint fibroblastic cells derived from transgenic rats carrying the LTR-env-pX-LTR gene of HTLV-I, using the Sindbis virus-based vectors. Expression of the pX gene in cells transduced with ATF-1DN was lower than that in cells with control transfection. A possible application of ATF-1DN to suppress viral gene expression in HTLV-1 infected cells can be considered. (C) 2003 Elsevier Science (USA). All rights reserved.
- リンク情報
- ID情報
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- DOI : 10.1016/S0014-4800(02)00019-9
- ISSN : 0014-4800
- Web of Science ID : WOS:000183457200014