V-SRC AND EJ RAS ALLEVIATE REPRESSION OF C-JUN BY A CELL-SPECIFIC INHIBITOR

被引:84
作者
BAICHWAL, VR [1 ]
PARK, A [1 ]
TJIAN, R [1 ]
机构
[1] UNIV CALIF BERKELEY,DEPT MOLEC & CELL BIOL,BERKELEY,CA 94720
关键词
D O I
10.1038/352165a0
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
THE AP-1 family of transcription factors, which includes the proto-oncogene products c-Jun and c-Fos 1, controls the stimulation of cellular genes by growth factors and the expression of oncogenes, including src and ras 2-8. Transcriptional activation by c-Jun is regulated by a cell-type-specific inhibitor that represses the activity of a transcriptional activation domain (A1) of c-Jun by operating through the adjacent negative regulatory region (delta) (refs 9-11). Here we show that cotransfection of the src or ras oncogene enhances the transcriptional activity of a GAL4:c-Jun hybrid that includes the delta-A1 region of c-Jun, suggesting that the DNA binding and dimerization domain of c-Jun is not required for stimulation by Src or Ras. Moreover, induction of c-Jun activity by Src and Ras occurs in cell lines containing the c-Jun inhibitor but not in a cell line lacking it. The region in c-Jun essential for the stimulatory action of these oncogenes maps to domain A1. These findings suggest the existence of signal-transduction pathways that result in an increase in transcriptional activity of c-Jun and AP-1 by disrupting the c-Jun:inhibitor interaction.
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页码:165 / 168
页数:4
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