The transcription of the tyrosinase gene by pterin-4a-carbinolamine dehydratase dimerization with transcription factor hepatocyte nuclear factor 1

1995 ◽  
Vol 5 ◽  
pp. 12
Author(s):  
Y. Wei ◽  
J. M. Wood ◽  
B. Nye ◽  
N. J. Lindsey ◽  
K. U. Schallreuter
Keyword(s):  
Transcription Factor ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Tyrosinase Gene ◽  
Nuclear Factor 1

Mutation P291fsinsC in the Transcription Factor Hepatocyte Nuclear Factor-1  is Dominant Negative

Diabetes ◽  
1998 ◽  
Vol 47 (8) ◽  
pp. 1231-1235 ◽  
Author(s):  
K. Yamagata ◽  
Q. Yang ◽  
K. Yamamoto ◽  
H. Iwahashi ◽  
J.-i. Miyagawa ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Dominant Negative ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Nuclear Factor 1

scholarly journals Pseudopregnancy induces the expression of hepatocyte nuclear factor-1β and its target gene aminopeptidase N in rabbit endometrium via the epithelial promoter

1995 ◽  
Vol 312 (1) ◽  
pp. 31-37 ◽  
Author(s):  
J Olsen ◽  
I Classen-Linke ◽  
H Sjöström ◽  
O Norén
Keyword(s):  
Transcription Factor ◽  
Binding Proteins ◽  
Experimental Manipulation ◽  
Nuclear Hormone Receptor ◽  
Aminopeptidase N ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Parallel Increase ◽  
Nuclear Factor 1

The rabbit endometrium is an excellent model system allowing experimental manipulation of aminopeptidase N (APN) mRNA expression in vivo. By RNase mapping and sequencing of cloned PCR-amplified primer-extended RNA, it was demonstrated that endometrial APN expression is directed by the epithelial APN promoter and is increased in human-choriogonadotropin-induced pseudopregnancy. Cloning and sequencing of the rabbit APN epithelial promoter revealed conservation of the upstream footprint (UF), hepatocyte nuclear factor-1 (HNF1) and Sp1 elements known to be present in the pig and human promoters as well. The pseudopregnancy-induced APN expression was found to be accompanied by a parallel increase in the level of the transcription factor HNF1 beta, whereas a much smaller increase in Sp1 and UF-binding proteins was observed. This indicates that HNF1 beta acts as a switch triggering the pregnancy-induced APN expression. The sequence of the UF element suggests members of the nuclear hormone-receptor superfamily as possible UF-binding proteins, and competition experiments suggest that the chicken ovalbumin upstream promoter transcription factor functions as such in the rabbit endometrium.

scholarly journals Hepatocyte Nuclear Factor 1, a Transcription Factor at the Crossroads of Glucose Homeostasis

2000 ◽  
Vol 11 (suppl 2) ◽  
pp. S140-S143
Author(s):  
MARCO PONTOGLIO
Keyword(s):  
Transcription Factor ◽  
Glucose Homeostasis ◽  
Phenylalanine Hydroxylase ◽  
Large Set ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Expression Of Genes ◽  
Proximal Tubular ◽  
Renal Proximal Tubular ◽  
Nuclear Factor 1

Abstract. Hepatocyte nuclear factor 1 (HNF1) is a transcription factor involved in the regulation of a large set of hepatic genes, including albumin, β-fibrinogen, and α1-antitrypsin. HNF1 is expressed in the liver, digestive tract, pancreas, and kidney. Mice lacking HNF1 exhibit hepatic, pancreatic, and renal dysfunctions. HNF1-deficient mice fail to express the hepatic phenylalanine hydroxylase gene, giving rise to hyperphenylalaninemia. Renal proximal tubular reabsorption of glucose, phosphate, arginine, and other metabolites is affected, producing severe renal glucosuria, phosphaturia, and amino aciduria. Homozygous mutant mice also exhibit a dramatic insulin secretion defect. This dysfunction resembles that exhibited by patients with maturity-onset diabetes mellitus of the young type 3, who carry mutations in the human HNF1 gene in the heterozygous state. These data show that HNF1 is a major regulator of glucose homeostasis, regulating the expression of genes that are expressed in the liver, kidney, and pancreas.

scholarly journals Regulation of Hepatocyte Nuclear Factor 1 Activity by Wild-Type and Mutant Hepatitis B Virus X Proteins

2002 ◽  
Vol 76 (12) ◽  
pp. 5875-5881 ◽  
Author(s):  
Jie Li ◽  
Zhenming Xu ◽  
Yanyan Zheng ◽  
Deborah L. Johnson ◽  
Jing-hsiung Ou
Keyword(s):  
Transcription Factor ◽  
Dna Binding ◽  
Binding Site ◽  
Core Promoter ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
X Protein ◽  
The Core ◽  
B Virus ◽  
Nuclear Factor 1

ABSTRACT The hepatitis B virus (HBV) core promoter regulates the transcription of two related RNA products named precore RNA and core RNA. Previous studies indicate that a double-nucleotide mutation that occurs frequently during chronic HBV infection converts a nuclear receptor binding site in the core promoter to the binding site of the transcription factor hepatocyte nuclear factor-1 (HNF-1) and specifically suppresses the transcription of the precore RNA. This mutation also changes two codons in the overlapping X protein coding sequence. In this report, we demonstrate that the X protein and its mutant Xmt can physically bind to HNF-1 both in vitro and in vivo. Further analyses indicate that both X and Xmt can enhance the gene transactivation and the DNA binding activities of HNF-1. This finding demonstrates for the first time that the X protein can stimulate the DNA binding activity of a homeodomain transcription factor. Interestingly, while both X and Xmt can stimulate the HNF-1 activities, they differ in their effects: a smaller amount of Xmt is needed to generate greater transactivation and DNA binding activities of HNF-1. This functional difference between X and Xmt may have important implications in HBV pathogenesis and is apparently why they have different effects on the core promoter bearing the HNF-1 binding site.

Mutation P291fsinsC in the transcription factor hepatocyte nuclear factor-1alpha is dominant negative

Diabetes ◽  
1998 ◽  
Vol 47 (8) ◽  
pp. 1231-1235 ◽  
Author(s):  
K. Yamagata ◽  
Q. Yang ◽  
K. Yamamoto ◽  
H. Iwahashi ◽  
J. Miyagawa ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Dominant Negative ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor

The restricted promoter activity of the liver transcription factor hepatocyte nuclear factor 3 beta involves a cell-specific factor and positive autoactivation

1992 ◽  
Vol 12 (2) ◽  
pp. 552-562
Author(s):  
L Pani ◽  
X B Quian ◽  
D Clevidence ◽  
R H Costa
Keyword(s):  
Transcription Factor ◽  
Promoter Activity ◽  
Binding Activity ◽  
Specific Factor ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Cell Type ◽  
Specific Expression ◽  
Cell Type Specific Expression ◽  
Cell Type Specific

The transcription factor hepatocyte nuclear factor 3 (HNF-3) is involved in the coordinate expression of several liver genes. HNF-3 DNA binding activity is composed of three different liver proteins which recognize the same DNA site. The HNF-3 proteins (designated alpha, beta, and gamma) possess homology in the DNA binding domain and in several additional regions. To understand the cell-type-specific expression of HNF-3 beta, we have defined the regulatory sequences that elicit hepatoma-specific expression. Promoter activity requires -134 bp of HNF-3 beta proximal sequences and binds four nuclear proteins, including two ubiquitous factors. One of these promoter sites interacts with a novel cell-specific factor, LF-H3 beta, whose binding activity correlates with the HNF-3 beta tissue expression pattern. Furthermore, there is a binding site for the HNF-3 protein within its own promoter, suggesting that an autoactivation mechanism is involved in the establishment of HNF-3 beta expression. We propose that both the LF-H3 beta and HNF-3 sites play an important role in the cell-type-specific expression of the HNF-3 beta transcription factor.

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