一个抑制AP-1活性的人类新基因AC3-33的克隆和初步功能研究
1. 华北煤炭医学院生物科学系, 唐山 063000;
2. 国家人类基因组北方研究中心, 北京 100176
收稿日期: 2007-11-11
修回日期: 2008-01-21
网络出版日期: 2008-05-10
Molecular cloning and preliminary function study of a novel human gene AC3-33 related to suppress AP-1 activity
Received date: 2007-11-11
Revised date: 2008-01-21
Online published: 2008-05-10
Activator protein-1(AP-1)是重要的转录因子, 其活性失调与肿瘤等多种疾病直接相关。本文运用“高通量高内涵细胞筛选技术(high throughput-high content cell-based screening technology)”对650个以未知功能基因为主的人类基因进行AP-1双荧光素酶报告基因筛选(Dual-Luciferase reporter gene screening), 获得了一个可抑制佛波酯(PMA)加离子霉素(Inonmycin)诱导的AP-1活性的人类新基因AC3-33(GenBank中该基因名为C3orf33, No. FLJ31139)。生物信息学分析该基因序列全长1 931 bp, 由6 个外显子和5 个内含子组成, 定位于3q25.31, 从271~1026 有一个编码251 个氨基酸的可读框, 编码一个约29 kDa 的蛋白, 在肾上腺和宫颈等多种组织都有表达。AC3-33 与其他人类已知蛋白质没有明显的同源性, 亚细胞定位于细胞质中, 许多氨基酸序列高度保守。初步实验结果显示AC3-33是一个有重要功能的人类新基因。
关键词: AP-1; 基因克隆; 双荧光素酶报告基因筛选; AC3-33
刘鹏,邓唯唯,高鹏,陆阳,孙博,李明,赵杰,石太平,张秀军 . 一个抑制AP-1活性的人类新基因AC3-33的克隆和初步功能研究[J]. 遗传, 2008 , 30(5) : 575 -585 . DOI: 10.3724/SP.J.1005.2008.00575
Activator protein-1(AP-1) is an important transcription factor, and dysregulation of its activity has been associated with many human diseases, including various cancers. A novel human gene AC3-33 (GenBank name: c30rf33, Accession No. FLJ31139), which can suppress PMA and Ionomycin induced activation of AP-1, was identified from 650 human func-tion-known genes by using the high throughput-high content cell-based screening technology. The gene whose full cDNA length is 1391 bp containing 6 exons and 5 introns is located in the human chromosome 3q25.31. The predicted protein encoded by this gene contains 251 amino acids with a theoretical molecular weight of 29 kDa. Expression of the AC3-33 gene is widly found in adrenal glands and cervix. The amino acid sequences of AC3-33 is highly conserved, and has no homology to other known proteins. Subcellular localization studies show that the AC3-33 protein was localized in the cytoplasm. Our preliminary results showed that AC3-33 is an important novel gene related to supress AP-1 activity.
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