scholarly journals Kinetics of steroid induction and deinduction of tyrosine aminotransferase synthesis in cultured hepatoma cells.

1975 ◽  
Vol 72 (6) ◽  
pp. 2007-2011 ◽  
Author(s):  
R. A. Steinberg ◽  
B. B. Levinson ◽  
G. M. Tomkins
Keyword(s):  
Tyrosine Aminotransferase ◽  
Hepatoma Cells ◽  
Kinetics Of

The distal enhancer implicated in the developmental regulation of the tyrosine aminotransferase gene is bound by liver-specific and ubiquitous factors

1993 ◽  
Vol 13 (8) ◽  
pp. 4494-4504
Author(s):  
D Nitsch ◽  
G Schütz
Keyword(s):  
Thymidine Kinase ◽  
Specific Binding ◽  
Regulatory Element ◽  
Hepatoma Cell ◽  
Tyrosine Aminotransferase ◽  
Hepatoma Cells ◽  
Hepatoma Cell Line ◽  
Distal Enhancer ◽  
Binding Studies ◽  
Enhancer Sequences

Tyrosine aminotransferase gene expression is confined to parenchymal cells of the liver, is inducible by glucocorticoids and glucagon, and is repressed by insulin. Three enhancers control this tissue-specific and hormone-dependent activity, one of which, located at -11 kb, is implicated in establishing an active expression domain. We have studied in detail this important regulatory element and have identified a 221-bp fragment containing critical enhancer sequences which stimulated the heterologous thymidine kinase promoter more than 100-fold in hepatoma cells. Within this region, we have characterized two essential liver-specific enhancer domains, one of which was bound by proteins of the hepatocyte nuclear factor 3 (HNF3) family. Analyses with the dedifferentiated hepatoma cell line HTC suggested that HNF3 alpha and/or -gamma, but not HNF3 beta, are involved in activating the tyrosine aminotransferase gene via the -11-kb enhancer. Genomic footprinting and in vitro protein-DNA binding studies documented cell-type-specific binding of ubiquitous factors to the second essential enhancer domain, which by itself stimulated the thymidine kinase promoter preferentially in hepatoma cells. These results will allow further characterization of the role of these enhancer sequences in developmental activation of the tyrosine aminotransferase gene.

Differential activity of a tissue-specific extinguisher locus in hepatic and nonhepatic cells

1989 ◽  
Vol 9 (5) ◽  
pp. 1813-1822
Author(s):  
H Gourdeau ◽  
T C Peterson ◽  
R E Fournier
Keyword(s):  
Mouse Chromosome ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Genetic Locus ◽  
Cell Types ◽  
Tyrosine Aminotransferase ◽  
Hepatoma Cells ◽  
Chromosome 11 ◽  
Tissue Specific ◽  
Primary Mouse ◽  
Mouse Chromosome 11

Tissue-specific extinguisher 1 (Tse-1) is a genetic locus on mouse chromosome 11 that can repress expression of several liver genes in trans. This locus is clearly active in fibroblasts, as hepatoma cells retaining fibroblast chromosome 11 are extinguished for both tyrosine aminotransferase and phosphoenolpyruvate carboxykinase gene expression. To assess the activity of Tse-1 in other tissues, we transferred mouse chromosome 11 from several different cell types into rat hepatoma recipients. Tse-1 was active in nonhepatic cell lines derived from each primary germ layer, but Tse-1 activity was not apparent in hybrids between hepatoma cells and primary mouse hepatocytes. These differences in the genetic activity of murine Tse-1 were apparently heritable in cis.

scholarly journals Differential activity of a tissue-specific extinguisher locus in hepatic and nonhepatic cells.

1989 ◽  
Vol 9 (5) ◽  
pp. 1813-1822 ◽  
Author(s):  
H Gourdeau ◽  
T C Peterson ◽  
R E Fournier
Keyword(s):  
Mouse Chromosome ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Genetic Locus ◽  
Cell Types ◽  
Tyrosine Aminotransferase ◽  
Hepatoma Cells ◽  
Chromosome 11 ◽  
Tissue Specific ◽  
Primary Mouse ◽  
Mouse Chromosome 11

Tissue-specific extinguisher 1 (Tse-1) is a genetic locus on mouse chromosome 11 that can repress expression of several liver genes in trans. This locus is clearly active in fibroblasts, as hepatoma cells retaining fibroblast chromosome 11 are extinguished for both tyrosine aminotransferase and phosphoenolpyruvate carboxykinase gene expression. To assess the activity of Tse-1 in other tissues, we transferred mouse chromosome 11 from several different cell types into rat hepatoma recipients. Tse-1 was active in nonhepatic cell lines derived from each primary germ layer, but Tse-1 activity was not apparent in hybrids between hepatoma cells and primary mouse hepatocytes. These differences in the genetic activity of murine Tse-1 were apparently heritable in cis.

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