Panagopoulos Ioannis, Mertens Fredrik
Department of Clinical Genetics, University Hospital, SE-221 85 Lund, Sweden.
Oncol Rep. 2009 Mar;21(3):615-24.
CREB3L2 encodes a member of the CREB3 family of transcription factors. We characterized its promoter region, showing that it is asymmetrically bidirectional, also driving the expression of a variant of AKR1D1. It has a CRE binding site which is conserved among mammalians; removal or alteration of it resulted in reduced promoter activity. When transiently transfecting the HEK293 cell line with constructs with partially deleted promoter regions, 5' deletions beyond 1058-bp upstream of the transcription starting site resulted in successive reduction of the activity. The inclusion of the untranslated part of CREB3L2 exon 1 strongly inhibited the promoter activity. Forskolin resulted in a decreased reporter activity, whereas phorbol 12-myristate 13-acetate increased the promoter activity irrespective of the status of the CRE binding site. The presence of the CRE site indicates autoregulation of CREB3L2 and/or regulation via other members of the CREB3 family or a variety of bZIP transcription factors.
CREB3L2编码转录因子CREB3家族的一个成员。我们对其启动子区域进行了表征,表明它是不对称双向的,还驱动AKR1D1一个变体的表达。它有一个在哺乳动物中保守的CRE结合位点;去除或改变该位点会导致启动子活性降低。用启动子区域部分缺失的构建体瞬时转染HEK293细胞系时,转录起始位点上游1058 bp以外的5'缺失导致活性连续降低。包含CREB3L2外显子1的非翻译部分强烈抑制启动子活性。福斯高林导致报告基因活性降低,而佛波酯12-肉豆蔻酸酯13-乙酸酯无论CRE结合位点的状态如何都能增加启动子活性。CRE位点的存在表明CREB3L2的自调控和/或通过CREB3家族的其他成员或多种bZIP转录因子进行调控。