scholarly journals Striking homology between mouse and human transcription enhancer factor-1 (TEF-1)

1993 ◽  
Vol 21 (3) ◽  
pp. 747-748 ◽  
Author(s):  
Cila Blatt ◽  
Melvin L. DePamphills
1997 ◽  
Vol 17 (7) ◽  
pp. 3924-3936 ◽  
Author(s):  
M P Gupta ◽  
C S Amin ◽  
M Gupta ◽  
N Hay ◽  
R Zak

The M-CAT binding factor transcription enhancer factor 1 (TEF-1) has been implicated in the regulation of several cardiac and skeletal muscle genes. Previously, we identified an E-box-M-CAT hybrid (EM) motif that is responsible for the basal and cyclic AMP-inducible expression of the rat cardiac alpha-myosin heavy chain (alpha-MHC) gene in cardiac myocytes. In this study, we report that two factors, TEF-1 and a basic helix-loop-helix leucine zipper protein, Max, bind to the alpha-MHC EM motif. We also found that Max was a part of the cardiac troponin T M-CAT-TEF-1 complex even when the DNA template did not contain an apparent E-box binding site. In the protein-protein interaction assay, a stable association of Max with TEF-1 was observed when glutathione S-transferase (GST)-TEF-1 or GST-Max was used to pull down in vitro-translated Max or TEF-1, respectively. In addition, Max was coimmunoprecipitated with TEF-1, thus documenting an in vivo TEF-1-Max interaction. In the transient transcription assay, overexpression of either Max or TEF-1 resulted a mild activation of the alpha-MHC-chloramphenicol acetyltransferase (CAT) reporter gene at lower concentrations and repression of this gene at higher concentrations. However, when Max and TEF-1 expression plasmids were transfected together, the repression mediated by a single expression plasmid was alleviated and a three- to fourfold transactivation of the alpha-MHC-CAT reporter gene was observed. This effect was abolished once the EM motif in the promoter-reporter construct was mutated, thus suggesting that the synergistic transactivation function of the TEF-1-Max heterotypic complex is mediated through binding of the complex to the EM motif. These results demonstrate a novel association between Max and TEF-1 and indicate a positive cooperation between these two factors in alpha-MHC gene regulation.


2007 ◽  
Vol 67 (19) ◽  
pp. 9055-9065 ◽  
Author(s):  
Tomas Hucl ◽  
Jonathan R. Brody ◽  
Eike Gallmeier ◽  
Christine A. Iacobuzio-Donahue ◽  
Iain K. Farrance ◽  
...  

1996 ◽  
Vol 271 (14) ◽  
pp. 8260-8265 ◽  
Author(s):  
Anthony Azakie ◽  
Sarah B. Larkin ◽  
Iain K. Farrance ◽  
Gabriele Grenningloh ◽  
Charles P. Ordahl

1996 ◽  
Vol 16 (2) ◽  
pp. 205-210 ◽  
Author(s):  
G Quinn ◽  
D S W Boam ◽  
J R E Davis ◽  
J D Glazier ◽  
P Mylona ◽  
...  

ABSTRACT A transcriptional enhancer which has a consensus binding sequence for transcription enhancer factor-1 (TEF-1) has been found 3′ of the hPL3 gene. We examined whether TEF-1 is expressed by the human placenta and whether such expression is co-ordinated with that of human placental lactogen (hPL). Probing Northern blots of total RNA from first trimester and term placenta, the choriocarcinoma-derived cell line JAr and primary cultured cytotrophoblast cells with a cDNA for TEF-1 revealed transcripts of 12–13 kb and 3–4 kb. The level of TEF-1 expression was the same in first trimester as compared with term placenta and in undifferentiated JAr as compared with differentiated cytotrophoblast cells. hPL expression was tenfold higher in term compared with first trimester placenta and, whilst detectable in cytotrophoblast cells, was undetectable in JAr cells. These data show that TEF-1 is expressed by the placenta but is not co-ordinated with hPL expression.


Circulation ◽  
2004 ◽  
Vol 110 (19) ◽  
pp. 2980-2987 ◽  
Author(s):  
Hsiao-Huei Chen ◽  
Catherine J. Baty ◽  
Tomoji Maeda ◽  
Steven Brooks ◽  
Linda C. Baker ◽  
...  

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