TAK1 activation of the mouse JunB promoter is mediated through a CCAAT box and NF-Y

被引:17
作者
Eggen, BJL [1 ]
Benus, GFJD [1 ]
Folkertsma, S [1 ]
Jonk, LJ [1 ]
Kruijer, W [1 ]
机构
[1] Univ Groningen, Inst Biotechnol, NL-9751 NN Haren, Netherlands
关键词
JunB; transforming growth factor beta activated kinase 1; nuclear factor Y; promoter; CCAAT motif;
D O I
10.1016/S0014-5793(01)02928-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
The JunB gene is activated by many stimuli including transforming growth factor beta (TGF beta) family members and interleukin-6 (IL-6). Here the effect of TGFP activated kinase 1 (TAK1), a mitogen activated protein kinase kinase kinase (MAPKKK) implicated in TGF beta, bone morphogenetic protein (BMP) and interleukin-1 (IL-1) signaling, on JunB promoter activity was investigated. Promoter analysis led to the identification of a CCAAT motif in the JunB gene, essential for activation by TAK1. Transfer of this CCAAT element to a heterologous minimal promoter conferred TAK1-responsiveness. The CCAAT-binding transcription factor, nuclear factor Y (NF-Y), activated the JunB promoter and a dominant negative NF-YA construct inhibited TAK1 activation of JunB. Our results demonstrate that JunB gene activation by TAK1 is mediated by the CCAAT-binding factor NF-Y. (C) 2001 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:267 / 271
页数:5
相关论文
共 20 条
[1]
RAF MEETS RAS - COMPLETING THE FRAMEWORK OF A SIGNAL-TRANSDUCTION PATHWAY [J].
AVRUCH, J ;
ZHANG, XF ;
KYRIAKIS, JM .
TRENDS IN BIOCHEMICAL SCIENCES, 1994, 19 (07) :279-283
[2]
POLYMORPHISMS IN THE CODING AND NONCODING REGIONS OF MURINE PGK-1 ALLELES [J].
BOER, PH ;
POTTEN, H ;
ADRA, CN ;
JARDINE, K ;
MULLHOFER, G ;
MCBURNEY, MW .
BIOCHEMICAL GENETICS, 1990, 28 (5-6) :299-308
[3]
COFFER P, 1995, ONCOGENE, V10, P985
[4]
MAPKS - NEW JNK EXPANDS THE GROUP [J].
DAVIS, RJ .
TRENDS IN BIOCHEMICAL SCIENCES, 1994, 19 (11) :470-473
[5]
ACTIVATION OF JUNB BY PKC AND PKA SIGNAL TRANSDUCTION THROUGH A NOVEL CIS-ACTING ELEMENT [J].
DEGROOT, RP ;
AUWERX, J ;
KARPERIEN, M ;
STAELS, B ;
KRUIJER, W .
NUCLEIC ACIDS RESEARCH, 1991, 19 (04) :775-781
[6]
TRANSCRIPTIONAL ACTIVATION BY TGF-BETA-1 MEDIATED BY THE DYAD SYMMETRY ELEMENT (DSE) AND THE TPA RESPONSIVE ELEMENT (TRE) [J].
DEGROOT, RP ;
KRUIJER, W .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1990, 168 (03) :1074-1081
[7]
ACCURATE TRANSCRIPTION INITIATION BY RNA POLYMERASE-II IN A SOLUBLE EXTRACT FROM ISOLATED MAMMALIAN NUCLEI [J].
DIGNAM, JD ;
LEBOVITZ, RM ;
ROEDER, RG .
NUCLEIC ACIDS RESEARCH, 1983, 11 (05) :1475-1489
[8]
Okadaic acid induces transcription of junB through a CCAAT Box and NF-Y [J].
Finch, JS ;
Rosenberger, SF ;
Martinez, JD ;
Bowden, GT .
GENE, 2001, 267 (01) :135-144
[9]
Identification and functional characterization of a Smad binding element (SBE) in the JunB promoter that acts as a transforming growth factor-β, activin, and bone morphogenetic protein-inducible enhancer [J].
Jonk, LJC ;
Itoh, S ;
Heldin, CH ;
ten Dijke, P ;
Kruijer, W .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (33) :21145-21152
[10]
A survey of 178 NF-Y binding CCAAT boxes [J].
Mantovani, R .
NUCLEIC ACIDS RESEARCH, 1998, 26 (05) :1135-1143