scholarly journals Apolipoprotein(a) gene transcription is regulated by liver-enriched trans-acting factor hepatocyte nuclear factor 1 alpha.

1994 ◽  
Vol 269 (31) ◽  
pp. 19757-19765 ◽  
Author(s):  
D.P. Wade ◽  
G.E. Lindahl ◽  
R.M. Lawn
Keyword(s):  
Gene Transcription ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Apolipoprotein A ◽  
Nuclear Factor 1

scholarly journals Hepatocyte nuclear factor-1 acts as an accessory factor to enhance the inhibitory action of insulin on mouse glucose-6-phosphatase gene transcription

1998 ◽  
Vol 95 (16) ◽  
pp. 9208-9213 ◽  
Author(s):  
Ryan S. Streeper ◽  
Erin M. Eaton ◽  
Daniel H. Ebert ◽  
Stacey C. Chapman ◽  
Christina A. Svitek ◽  
...  
Keyword(s):  
Gene Transcription ◽  
Fusion Gene ◽  
Insulin Response ◽  
Inhibitory Effect ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Promoter Regions ◽  
Gene Encoding ◽  
Accessory Factor ◽  
Nuclear Factor 1

Glucose-6-phosphatase catalyzes the terminal step in the gluconeogenic and glycogenolytic pathways. Transcription of the gene encoding the glucose-6-phosphatase catalytic subunit (G6Pase) is stimulated by cAMP and glucocorticoids whereas insulin strongly inhibits both this induction and basal G6Pase gene transcription. Previously, we have demonstrated that the maximum repression of basal G6Pase gene transcription by insulin requires two distinct promoter regions, designated A (from −271 to −199) and B (from −198 to −159). Region B contains an insulin response sequence because it can confer an inhibitory effect of insulin on the expression of a heterologous fusion gene. By contrast, region A fails to mediate an insulin response in a heterologous context, and the mutation of region B within an otherwise intact promoter almost completely abolishes the effect of insulin on basal G6Pase gene transcription. Therefore, region A is acting as an accessory element to enhance the effect of insulin, mediated through region B, on G6Pase gene transcription. Such an arrangement is a common feature of cAMP and glucocorticoid-regulated genes but has not been previously described for insulin. A combination of fusion gene and protein-binding analyses revealed that the accessory factor binding region A is hepatocyte nuclear factor-1. Thus, despite the usually antagonistic effects of cAMP/glucocorticoids and insulin, all three agents are able to use the same factor to enhance their action on gene transcription. The potential role of G6Pase overexpression in the pathophysiology of MODY3 and 5, rare forms of diabetes caused by hepatocyte nuclear factor-1 mutations, is discussed.

scholarly journals Nuclear Factor 1 Family Members Interact with Hepatocyte Nuclear Factor 1α to Synergistically Activate L-type Pyruvate Kinase Gene Transcription

2005 ◽  
Vol 280 (48) ◽  
pp. 39827-39834 ◽  
Author(s):  
Shin-ichi Satoh ◽  
Takashi Noaki ◽  
Tatsuya Ishigure ◽  
Shigehiro Osada ◽  
Masayoshi Imagawa ◽  
...  
Keyword(s):  
Pyruvate Kinase ◽  
Gene Transcription ◽  
Family Members ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Kinase Gene ◽  
Hepatocyte Nuclear Factor 1Α ◽  
Nuclear Factor 1

The human beta fibrinogen promoter contains a hepatocyte nuclear factor 1-dependent interleukin-6-responsive element

1993 ◽  
Vol 13 (2) ◽  
pp. 1183-1193
Author(s):  
J Dalmon ◽  
M Laurent ◽  
G Courtois
Keyword(s):  
Binding Site ◽  
Acute Phase ◽  
Interleukin 6 ◽  
Constitutive Expression ◽  
Nuclear Proteins ◽  
Functional Coupling ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Tissue Specific ◽  
Nuclear Factor 1

Acute-phase reactants are liver proteins whose synthesis is positively or negatively regulated during inflammation. The main mediators of this phenomenon are glucocorticoids and interleukin-6 (IL-6), a pleiotropic cytokine that also controls hematopoiesis. Functional analysis of several acute-phase reactant promoter regions has identified two major DNA motifs used by IL-6-regulated genes. The first one corresponds to a CTGG(G/A)AA sequence, and the other is a binding site for members of the C/EBP family of nuclear proteins. We have previously shown that the human beta fibrinogen (beta Fg) promoter contains an IL-6-responsive region, located between bp -150 and -67 (P. Huber, M. Laurent, and J. Dalmon, J. Biol. Chem. 265:5695-5701, 1990). In this study, using DNase I footprinting, mobility shift assays, and mutagenesis, we demonstrate that at least three subdomains of this region are necessary to observe a full response to IL-6. The most distal contains a CTGGGAA motif, and its mutation inhibits IL-6 stimulation. Another, which is able to interact with several distinct nuclear proteins, among them members of the C/EBP family, is dispensable for IL-6 induction but plays an important role in the constitutive expression of beta Fg. Finally, a proximal hepatocyte nuclear factor 1 binding site, already described as the major determinant of beta Fg tissue-specific expression, is also required for IL-6 stimulation. These results indicate a complex interplay between nuclear proteins within the beta Fg IL-6-responsive region and suggest a tight functional coupling between the tissue-specific and inducible elements.

scholarly journals Hepatocyte Nuclear Factor-1α, GATA-4, and Caudal Related Homeodomain Protein Cdx2 Interact Functionally to Modulate Intestinal Gene Transcription

2002 ◽  
Vol 277 (35) ◽  
pp. 31909-31917 ◽  
Author(s):  
François Boudreau ◽  
Edmond H. H. M. Rings ◽  
Herbert M. van Wering ◽  
Richard K. Kim ◽  
Gary P. Swain ◽  
...  
Keyword(s):  
Gene Transcription ◽  
Homeodomain Protein ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Hepatocyte Nuclear Factor 1Α
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