
Activation of the Mouse Proliferating Cell Nuclear Antigen Gene Promoter by Adenovirus Type 12 E1A Proteins
Author(s) -
Yamaguchi Masamitsu,
Hayashi Yuko,
Hirose Fumiko,
Matsuoka Shuhei,
Shiroki Kazuko,
Matsukage Akio
Publication year - 1992
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1992.tb00133.x
Subject(s) - transactivation , microbiology and biotechnology , biology , chloramphenicol acetyltransferase , proliferating cell nuclear antigen , gene , gene expression , transcription (linguistics) , gene product , regulation of gene expression , promoter , transcription factor , dna , genetics , linguistics , philosophy
A plasmid carrying the 5′‐flanking region (– 1584 to + 47 with respect to the transcription initiation site) of the mouse proliferating cell nuclear antigen (PCNA) gene was fused with the chloramphenicol acetyltransferase (CAT) gene, and then cotransfected into mouse N18TG2 cells with expression plasmids for the adenovirus type 12 E1 genes. Expression of E1A gene products elevated the CAT expression by 5‐ to 9‐fold, but expression of the E1B gene product did not. RNase protection analysis revealed that the activation of the PCNA gene promoter by E1A was at the transcription step. Both the 13S E1A and the 12S E1A activated the PCNA gene promoter, indicating that the activation domain of El A resides in a common region(s) of 13S and 12S El A products. The major target region of El A was mapped within the 68 base‐pair region (‐21 to +47) of the PCNA gene, which includes consensus sequences for transcription factors PEA3 and E2P, although the upstream region (–83 to – 21) including ATF(CREB)‐binding consensus had an additional effect in the transactivation.