Rapid activation of insulin-like growth factor binding protein-5 gene transcription during myoblast differentiation

1995 ◽  
Vol 9 (7) ◽  
pp. 913-923 ◽  
Author(s):  
P. Rotwein
Keyword(s):  
Growth Factor ◽  
Gene Transcription ◽  
Binding Protein ◽  
Myoblast Differentiation ◽  
Insulin Like Growth Factor ◽  
Factor Binding ◽  
Rapid Activation

scholarly journals Amino acid regulation of gene transcription of rat insulin-like growth factor-binding protein-1

2000 ◽  
Vol 164 (3) ◽  
pp. R11-R16 ◽  
Author(s):  
A Takenaka ◽  
K Komori ◽  
T Morishita ◽  
SI Takahashi ◽  
T Hidaka ◽  
...  
Keyword(s):  
Amino Acid ◽  
Growth Factor ◽  
Gene Transcription ◽  
Binding Protein ◽  
Present Observation ◽  
Insulin Like Growth Factor ◽  
Amino Acid Deprivation ◽  
Cis Acting ◽  
Factor Binding ◽  
Responsive Element

To investigate the molecular mechanisms of increased transcription of the insulin-like growth factor-binding protein-1 (IGFBP-1) gene in dietary protein-deprived animals, the cis-acting sequence that is involved in this regulation was analyzed. We first showed that IGFBP-1 gene transcription was up-regulated by amino acid deprivation in cultured liver cell lines: H4IIE and HuH-7. Since HuH-7 cells showed a greater increase in IGFBP-1 mRNA in response to amino acid deprivation, this cell line was used in further experiments. Using a promoter function assay, we found that up-regulation of promoter activity responding to amino acid deprivation was abolished by deleting the region between -112 and -81 bp from the cap site from the gene construct. This cis-acting region includes the insulin-responsive element (IRE) and glucocorticoid responsive element (GRE) of IGFBP-1. In summary, the present observation suggests that the 32-bp (-112 to -81) in the IGFBP-1 gene 5' promoter region is involved in the induction of the IGFBP-1 gene in response to amino acid deprivation.

scholarly journals Hepatic nuclear factor 3- and hormone-regulated expression of the phosphoenolpyruvate carboxykinase and insulin-like growth factor-binding protein 1 genes.

1995 ◽  
Vol 15 (3) ◽  
pp. 1747-1758 ◽  
Author(s):  
R M O'Brien ◽  
E L Noisin ◽  
A Suwanichkul ◽  
T Yamasaki ◽  
P C Lucas ◽  
...  
Keyword(s):  
Growth Factor ◽  
Gene Transcription ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Binding Protein ◽  
Nuclear Factor ◽  
Insulin Like Growth Factor ◽  
Binding Studies ◽  
Core Motif ◽  
Factor Binding ◽  
Accessory Factor

The rate of transcription of the hepatic phosphoenolpyruvate carboxykinase (PEPCK) and insulin-like growth factor-binding protein 1 (IGFBP-1) genes is stimulated by glucocorticoids and inhibited by insulin. In both cases, the effect of insulin is dominant, since it suppresses both basal and glucocorticoid-stimulated PEPCK or IGFBP-1 gene transcription. Analyses of both promoters by transfection of PEPCK or IGFBP-1-chloramphenicol acetyltransferase fusion genes into rat hepatoma cells has led to the identification of insulin response sequences (IRSs) in both genes. The core IRS, T(G/A)TTTTG, is the same in both genes, but the PEPCK promoter has a single copy of this element whereas the IGFBP-1 promoter has two copies arranged as an inverted palindrome. The IGFBP-1 IRS and PEPCK IRS both bind the alpha and beta forms of hepatic nuclear factor 3 (HNF-3), although the latter does so with a sixfold-lower relative affinity. Both the PEPCK and the IGFBP-1 IRSs also function as accessory factor binding sites required for the full induction of gene transcription by glucocorticoids. A combination of transient transfection and DNA binding studies suggests that HNF-3 is the accessory factor that supports glucocorticoid-induced gene transcription. In both genes, the HNF-3 binding site overlaps the IRS core motif(s). A model in which insulin is postulated to mediate its negative effect on glucocorticoid-induced PEPCK and IGFBP-1 gene transcription indirectly by inhibiting HNF-3 action is proposed.

Interactions between liver nuclear proteins and the human insulin-like growth factor binding protein 1 promoter in the course of development

1995 ◽  
Vol 132 (5) ◽  
pp. 635-641
Author(s):  
S Babajko
Keyword(s):  
Growth Factor ◽  
Human Insulin ◽  
Gene Transcription ◽  
Binding Protein ◽  
Nuclear Proteins ◽  
Target Sequence ◽  
Insulin Like Growth Factor ◽  
Mobility Shift ◽  
Transcription Activity ◽  
Factor Binding

Babajko S. Interactions between liver nuclear proteins and the human insulin-like growth factor binding protein 1 promoter in the course of development. Eur J Endocrinol 1995;132:635–41. ISSN 0804–4643 Insulin-like growth factor binding proteins (IGFBPs) modulate the bioavailability of the IGFs. Among the six IGFBPs known to date, IGFBP-1 is the most tissue-specific, its expression being limited to the liver and the endometrium. In the liver, IGFBP-1 gene expression is maximal during the perinatal period, with its peak corresponding to a transient rise in gene transcription activity. In this study, interactions between rat liver nuclear proteins and the human IGFBP-1 promoter have been analysed in the course of development, using in vitro DNase I protection and mobility shift assays. Only the interactions between DNA and proteins localized between nt –305 and –268 varied through the period studied (16 days in utero to 70 days postnatally). Three proteins, named Pa, PCI and PC2, interacted with sequences between nt –295 and –285, nt –305 and –295 and nt –285 and –268, respectively. There was a marked perinatal increase in phenotype expression of Pa, which was parallel to that in IGFBP-l gene transcription activity. In addition, DNA-Pa interactions and DNA-PC2 interactions were mutually exclusive. These results suggest that the interaction of Pa with its target sequence(s) prevent PC2 binding and thereby contribute towards increased IGFBP-l gene transcription. Sylvie Babajko, INSERM U.142, Hôpital Saint Antoine, 184 rue du Faubourg St. Antoine, 75571 Paris Cedex 12, France

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