Nuclear factor I regulates expression of the gene for phosphoenolpyruvate carboxykinase (GTP)

被引:21
|
作者
Crawford, DR
Leahy, P
Hu, CY
Chaudhry, A
Gronostajski, R
Grossman, G
Woods, J
Hakimi, P
Roesler, WJ
Hanson, RW [1 ]
机构
[1] Case Western Reserve Univ, Sch Med, Dept Biochem, Cleveland, OH 44106 USA
[2] Cleveland Clin Fdn, Lerner Res Inst, Dept Canc Biol, Cleveland, OH 44106 USA
[3] Univ Saskatchewan, Dept Biochem, Saskatoon, SK S7N 5E5, Canada
关键词
D O I
10.1074/jbc.273.22.13387
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Nuclear factor-I (NFI) binds to the phosphoenolpyruvate carboxykinase (GTP) (PEPCK) gene promoter immediately 5' to the cAMP regulatory element (CRE), This suggests an interaction between NFI and factors that bind the CRE. Of the four NFI isoforms expressed in mammalian tissues, NFI-A and -B stimulate basal transcription from the PEPCK gene promoter in HepG2 cells, while NFI-C and -X are slightly inhibitory. AU four NFI isoforms abrogate the 20-fold protein kinase Ac (PKAc)-mediated induction of transcription from the PEPCK gene promoter. Normal PKAc-mediated induction was noted when the CRE was moved 10 base pairs 3' of its original location. However if the CRE was moved 5 base pairs 3', placing it out of phase with the other elements in the promoter, or moved 5' to -285 (the P3(I) site in the promoter), some PKA-mediated stimulation was lost. The NFI-C isoform effectively inhibited PKAc induction regardless of the relative positions of the CBE and the NFI binding sites. NFI-C also abrogated cAMP regulatory element-binding protein (CREB)-induced activity of wild type and mutant PEPCK promoters. There was some cooperativity in the binding of CREB and NFI to their respective binding sites but this did not appear to be physiologically important.
引用
收藏
页码:13387 / 13390
页数:4
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