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MHC II类DRα启动子的异常组成型表达以及SV40 T抗原激活需要一个ATF/CREB结合基序。

An ATF/CREB binding motif is required for aberrant constitutive expression of the MHC class II DR alpha promoter and activation by SV40 T-antigen.

作者信息

Cox P M, Goding C R

机构信息

Eukaryotic Transcription Laboratory, Marie Curie Research Institute, Oxted, Surrey, UK.

出版信息

Nucleic Acids Res. 1992 Sep 25;20(18):4881-7. doi: 10.1093/nar/20.18.4881.

Abstract

Constitutive expression of major histocompatibility complex class II (MHC II) antigens normally occurs in B-lymphocytes and antigen presenting cells of the monocyte/macrophage lineage. However, many malignant tumours and transformed cells express these proteins aberrantly. We demonstrate here that the MHC II DR alpha promoter is constitutively active both in the SV40 large T antigen transformed cell line, COS, and in CV1 cells from which they are derived. As an approach to understanding the molecular mechanisms underlying aberrant DR alpha expression we have examined the cis- and trans-acting requirements for DR alpha transcription in these cell types. Electrophoretic mobility shift assays showed that the region immediately 3' to the X-box was bound by a member of the ATF/CREB family of transcription factors. Using deletions and point mutations in the DR alpha promoter we demonstrate that, in contrast to B-cells, the octamer motif and conserved X- and Y-boxes make only a minor contribution to promoter function while single point mutations in the ATF/CREB motif reduced transcription up to 20-fold. In addition, we show that the DR alpha promoter is activated by SV40 large T-antigen and that activation requires an intact ATF/CREB motif. Similar data were obtained using B16 melanoma cells. These results suggest that the ATF/CREB motif may be a target for transcription deregulation in several transformed cell types.

摘要

主要组织相容性复合体II类(MHC II)抗原的组成型表达通常发生在B淋巴细胞以及单核细胞/巨噬细胞谱系的抗原呈递细胞中。然而,许多恶性肿瘤和转化细胞会异常表达这些蛋白质。我们在此证明,MHC II DRα启动子在SV40大T抗原转化的细胞系COS及其来源的CV1细胞中均呈组成型活性。作为理解异常DRα表达背后分子机制的一种方法,我们研究了这些细胞类型中DRα转录的顺式和反式作用要求。电泳迁移率变动分析表明,紧邻X盒3'端的区域被转录因子ATF/CREB家族的一个成员所结合。利用DRα启动子中的缺失和点突变,我们证明,与B细胞不同,八聚体基序以及保守的X盒和Y盒对启动子功能的贡献很小,而ATF/CREB基序中的单点突变可使转录降低达20倍。此外,我们表明DRα启动子被SV40大T抗原激活,且激活需要完整的ATF/CREB基序。使用B16黑色素瘤细胞也获得了类似的数据。这些结果表明,ATF/CREB基序可能是几种转化细胞类型中转录失调的一个靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db85/334246/7bd44246c9d5/nar00229-0179-a.jpg

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