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分离与人类I型T细胞白血病病毒长末端重复序列中一个对tax应答的增强子元件特异性结合的DNA结合蛋白的cDNA。

Isolation of cDNAs for DNA-binding proteins which specifically bind to a tax-responsive enhancer element in the long terminal repeat of human T-cell leukemia virus type I.

作者信息

Tsujimoto A, Nyunoya H, Morita T, Sato T, Shimotohno K

机构信息

Virology Division, National Cancer Center Research Institute, Tokyo, Japan.

出版信息

J Virol. 1991 Mar;65(3):1420-6. doi: 10.1128/JVI.65.3.1420-1426.1991.

DOI:10.1128/JVI.65.3.1420-1426.1991
PMID:1847461
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC239921/
Abstract

One of the gene products of human T-cell leukemia virus type I (HTLV-I), p40tax, activates its own viral transcription in trans through tax-responsive enhancers in viral long terminal repeats. Five species of cDNA clones for proteins that bind to the tax-responsive enhancer element in HTLV-I were isolated from the Jurkat cell library. The beta-galactosidase fusion protein prepared from the lysogen of a clone specifically recognized the cyclic AMP-responsive element in HTLV-I enhancer. The nucleotide sequence of a full-length cDNA clone (TAXREB67) had a coding capacity of 351 amino acids, which contained a basic motif followed by a leucine zipper structure near the carboxy terminus. Its mRNA was detected in human cell lines, including HTLV-I-infected or noninfected hematopoietic cell lines. The mRNA level in Jurkat cells was decreased temporarily by increasing cyclic AMP concentration but increased by increasing Ca2+ concentration. Polyclonal antibodies against the fusion protein specifically recognized a 52-kDa protein in Jurkat cells. Analyses of the function of this protein and its interactions with other cellular factors will be useful to help understand the regulatory mechanism through tax-responsive enhancers in HTLV-I.

摘要

人类T细胞白血病病毒I型(HTLV-I)的基因产物之一p40tax,通过病毒长末端重复序列中的tax反应增强子反式激活其自身的病毒转录。从Jurkat细胞文库中分离出了5种与HTLV-I中tax反应增强子元件结合的蛋白质的cDNA克隆。从一个克隆的溶原体制备的β-半乳糖苷酶融合蛋白特异性识别HTLV-I增强子中的环磷酸腺苷反应元件。一个全长cDNA克隆(TAXREB67)的核苷酸序列具有编码351个氨基酸的能力,在羧基末端附近包含一个碱性基序,随后是一个亮氨酸拉链结构。在包括HTLV-I感染或未感染的造血细胞系在内的人类细胞系中检测到了它的mRNA。Jurkat细胞中的mRNA水平通过增加环磷酸腺苷浓度而暂时降低,但通过增加Ca2+浓度而升高。针对融合蛋白的多克隆抗体特异性识别Jurkat细胞中的一种52 kDa蛋白。对该蛋白功能及其与其他细胞因子相互作用的分析将有助于理解HTLV-I中通过tax反应增强子的调控机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c73/239921/14c802310a10/jvirol00046-0384-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c73/239921/baa648804f78/jvirol00046-0382-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c73/239921/f8e06da9fd24/jvirol00046-0383-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c73/239921/f8ac3219b2fe/jvirol00046-0383-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c73/239921/14c802310a10/jvirol00046-0384-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c73/239921/baa648804f78/jvirol00046-0382-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c73/239921/f8e06da9fd24/jvirol00046-0383-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c73/239921/f8ac3219b2fe/jvirol00046-0383-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c73/239921/14c802310a10/jvirol00046-0384-a.jpg

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