INDUCTION OF C-FOS MESSENGER-RNA AND AP-1 DNA-BINDING ACTIVITY BY CAMP IN COOPERATION WITH EITHER THE ADENOVIRUS 243-AMINO OR THE ADENOVIRUS 289-AMINO ACID E1A PROTEIN

被引:24
作者
ENGEL, DA
MULLER, U
GEDRICH, RW
EUBANKS, JS
SHENK, T
机构
[1] PRINCETON UNIV,HOWARD HUGHES MED INST,DEPT MOLEC BIOL,PRINCETON,NJ 08544
[2] UNIV VIRGINIA,SCH MED,DEPT MICROBIOL,CHARLOTTESVILLE,VA 22908
[3] UNIV VIRGINIA,SCH MED,CTR CANC,CHARLOTTESVILLE,VA 22908
关键词
TRANSCRIPTION; TRANSCRIPTION FACTOR; TRANSFORMATION; CAMP-DEPENDENT PROTEIN KINASE;
D O I
10.1073/pnas.88.9.3957
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Products of the adenovirus E1A gene can act synergistically with cAMP to activate transcription of several viral early genes and the cellular genes c-fos and jun-B. Transcription factor AP-1-binding activity is also induced by the combined action of E1A and cAMP. Mouse S49 cells were infected with adenovirus variants expressing either the 243- or 289-amino acid E1A protein and treated with the cAMP analog dibutyryl-cAMP. Significant E1A-dependent induction of c-fos mRNA and AP-1-binding activity was observed in cells expressing either E1A protein. These effects absolutely required the presence of cAMP. In contrast, the 243-amino acid protein was a poor activator of the viral early genes E2 and E4 compared with the 289-amino acid protein. These data suggest that the 243- and 289-amino acid E1A proteins both interact functionally with the cAMP signaling system to activate transcription of a cellular gene and AP-1-binding activity. The mechanism involved in this process is probably different from the mechanism of transcriptional activation of viral genes.
引用
收藏
页码:3957 / 3961
页数:5
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