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CBFa(AML/PEBP2)‐related elements in the TGF‐β type I receptor promoter and expression with osteoblast differentiation
Author(s) -
Ji Changhua,
Casinghino Sandra,
Chang David J.,
Chen Yun,
Javed Amjad,
Ito Yoshiaki,
Hiebert Scott W.,
Lian Jane B.,
Stein Gary S.,
McCarthy Thomas L.,
Centrella Michael
Publication year - 1998
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/(sici)1097-4644(19980601)69:3<353::aid-jcb12>3.0.co;2-d
Subject(s) - osteoblast , transcription factor , core binding factor , transfection , runx2 , enhancer , transcription (linguistics) , microbiology and biotechnology , biology , expression vector , promoter , reporter gene , transforming growth factor beta , transforming growth factor , chemistry , gene expression , gene , in vitro , recombinant dna , genetics , linguistics , philosophy
Organization of the transforming growth factor‐β (TGF‐β) type I receptor (TRI) promoter predicts constitutive transcription, although its activity increases with differentiation status in cultured osteoblasts. Several sequences in the rat TRI promoter comprise cis‐ acting elements for CBFa (AML/PEBP2α) transcription factors. By gel mobility shift and immunological analyses, a principal osteoblast‐derived nuclear factor that binds to these sites is CBFa1(AML‐3/PEBP2αA). Rat CBFa1 levels parallel expression of the osteoblast phenotype and increase under conditions that promote mineralized bone nodule formation in vitro. Fusion of CBFa binding sequence from the TRI promoter to enhancer‐free transfection vector increases reporter gene expression in cells that possess abundant CBFa1, and overexpression of CBFa increase the activity of transfected native TRI promoter/reporter plasmid. Consequently, phenotype‐restricted use of cis‐ acting elements for CBFa transcription factors can contribute to the high levels of TRI that parallel osteoblast differentiation and to the potent effects of TGF‐β on osteoblast function. J. Cell. Biochem. 69:353‐363. © 1998 Wiley‐Liss, Inc.