Katoh S, Ozawa K, Kondoh S, Soeda E, Israel A, Shiroki K, Fujinaga K, Itakura K, Gachelin G, Yokoyama K
Tsukuba Life Science Center, RIKEN, Institute of Physical and Chemical Research, Ibaraki, Japan.
EMBO J. 1990 Jan;9(1):127-35. doi: 10.1002/j.1460-2075.1990.tb08088.x.
The mechanism of transcriptional regulation of the H-2Kbm1 major histocompatibility complex (MHC) class I gene by adenovirus type 12 E1A (Ad12-E1A) was studied in transfected rat embryonal fibroblasts. Results of long-term expression of the chloramphenicol acetyl transferase (CAT) gene placed under the control of the 5'-flanking region of the mouse MHC class I gene. H-2Kbm1, and the results of nuclear run-on transcription assays, yield evidence for both positive and negative regulation of H-2Kbm1 by E1A gene product. Deletion studies in the H-2Kbm1 promoter region revealed that a proximal 58 bp upstream sequence (-194 to -136, relative to the cap site) and a distal 316 bp sequence (-1837 to -1521) respectively contribute to positive and negative regulation mediated by the E1A gene product. Both regulatory elements of MHC class I gene promoter region are responsible for the differential expression of the H-2Kbm1 gene in Ad12 transformed cells. A nuclear factor binding to the negative element has been detected only in extracts derived from cells expressing Ad12-E1A.
在转染的大鼠胚胎成纤维细胞中研究了12型腺病毒E1A（Ad12-E1A）对H-2Kbm1主要组织相容性复合体（MHC）I类基因的转录调控机制。氯霉素乙酰转移酶（CAT）基因在小鼠MHC I类基因H-2Kbm1的5'侧翼区控制下长期表达的结果，以及核转录分析的结果，为E1A基因产物对H-2Kbm1的正负调控提供了证据。H-2Kbm1启动子区域的缺失研究表明，近端58 bp上游序列（相对于帽位点为-194至-136）和远端316 bp序列（-1837至-1521）分别对E1A基因产物介导的正调控和负调控有贡献。MHC I类基因启动子区域的这两个调控元件都负责H-2Kbm1基因在Ad12转化细胞中的差异表达。仅在表达Ad12-E1A的细胞提取物中检测到与负调控元件结合的核因子。
