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参与人白细胞介素-2基因诱导表达的多个顺式作用元件和反式作用因子的鉴定。

Identification of multiple cis-elements and trans-acting factors involved in the induced expression of human IL-2 gene.

作者信息

Shibuya H, Taniguchi T

机构信息

Institute for Molecular and Cellular Biology, Osaka University, Japan.

出版信息

Nucleic Acids Res. 1989 Nov 25;17(22):9173-84. doi: 10.1093/nar/17.22.9173.

DOI:10.1093/nar/17.22.9173
PMID:2555786
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC335122/
Abstract

Regulated expression of interleukin-2 (IL-2) gene constitutes an essential part in the clonal proliferation of activated T lymphocytes (T-cells). In order to gain insight on the mechanism(s) of the IL-2 gene induction, deletions were introduced in the human IL-2 gene 5'-flanking region and the mitogen inducibility of each deletion mutant was examined in cultured T cell lines. At least four functional regions were identified, they contain potential binding sites for several transcription factors including one NF-kappa B and two octamer binding factor sites. Whereas each of the functional regions (or elements) is required for the maximal induction of the IL-2 gene by mitogen, one such region was found to be dispensable for activation by the HTLV-1-encoded trans-activator, tax-1. Furthermore, the potent immunosuppressive agent, cyclosporin A was found to inhibit the gene induction by mitogen, but not by tax-1.

摘要

白细胞介素-2(IL-2)基因的调控表达是活化T淋巴细胞(T细胞)克隆增殖的重要组成部分。为了深入了解IL-2基因诱导的机制,在人IL-2基因5'侧翼区域引入缺失,并在培养的T细胞系中检测每个缺失突变体的丝裂原诱导性。至少鉴定出四个功能区域,它们包含几个转录因子的潜在结合位点,包括一个核因子κB(NF-κB)和两个八聚体结合因子位点。虽然每个功能区域(或元件)对于丝裂原对IL-2基因的最大诱导是必需的,但发现其中一个这样的区域对于人嗜T淋巴细胞病毒1型(HTLV-1)编码的反式激活因子tax-1的激活是可有可无的。此外,发现强效免疫抑制剂环孢菌素A可抑制丝裂原诱导的基因,但不抑制tax-1诱导的基因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1c/335122/8f24c0bef2b0/nar00139-0273-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1c/335122/0f8a5d30337f/nar00139-0268-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1c/335122/a36d8907e752/nar00139-0270-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1c/335122/b7f2c88188fd/nar00139-0271-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1c/335122/8f24c0bef2b0/nar00139-0273-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1c/335122/0f8a5d30337f/nar00139-0268-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1c/335122/a36d8907e752/nar00139-0270-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1c/335122/b7f2c88188fd/nar00139-0271-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1c/335122/8f24c0bef2b0/nar00139-0273-a.jpg

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