Tata element‐binding protein is important to epidermal growth factor‐dependent induction of H2B histone gene expression in primary hepatocytes from rat

Song, Hea-Jeong; Yun, Kyung-Ah; Son, Min Jung; Park, Seung-Kiel; Kweon, Gi‐Ryang; Hwang, Byungil; Byun, Sang-Hyun; Yoon, Won‐Sang

doi:10.1080/15216549800202972

Cited by 1 publication

(1 citation statement)

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“…Figure 7 shows that deletion of the G6Pase promoter sequence between −231 and −35 resulted in a decrease in the ability of EGF to stimulate basal G6Pase-luciferase gene expression that did not map to a single promoter region. The shortest fusion gene tested, containing the −35 to +66 G6Pase promoter region, also includes a TATA box motif, an element that has been reported to mediate the EGF-stimulated gene expression [28, 29]. To determine whether the G6Pase TATA box also mediates EGF-stimulated G6Pase gene transcription in cultured hepatocytes we generated a site-direction mutation of this element in the context of the −484 to +66 promoter fragment.…”

Section: Resultsmentioning

confidence: 99%

Insulin and epidermal growth factor suppress basal glucose-6-phosphatase catalytic subunit gene transcription through overlapping but distinct mechanisms

Onuma

Oeser

Nelson

et al. 2008

Biochemical Journal

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Synopsis The glucose-6-phosphatase catalytic subunit (G6Pase) catalyses the final step in the gluconeogenic and glycogenolytic pathways, the hydrolysis of glucose-6-phosphate to glucose. We show here that, in HepG2 hepatoma cells, epidermal growth factor (EGF) inhibits basal mouse G6Pase fusion gene transcription. Several studies have shown that insulin represses basal mouse G6Pase fusion gene transcription through FOXO1 but Stoffel and colleagues (Proc. Natl. Acad. Sci. 100:11624, 2003) have recently suggested that insulin can also regulate gene transcription through FOXA2. A combined glucocorticoid receptor (GR)-FOXA2 binding site is located between −185 and −174 in the mouse G6Pase promoter overlapping two FOXO1 binding sites located between (−188 and −182) and (−174 and −168). Selective mutation of the FOXO1 binding sites reduced the effect of insulin whereas mutation of the GR/FOXA2 binding site had no effect on the insulin response. In contrast, selective mutation of the FOXO1 and GR/FOXA2 binding sites both reduced the effect of EGF. The effect of these mutations was additive since the combined mutation of both FOXO1 and GR/FOXA2 binding sites reduced the effect of EGF to a greater extent than the individual mutations. These results suggest that, in HepG2 cells, GR and/or FOXA2 are required for the inhibition of basal G6Pase gene transcription by EGF but not insulin. EGF also inhibits hepatic G6Pase gene expression in vivo but in cultured hepatocytes EGF has the opposite effect stimulating expression, an observation that may be explained by a switch in ErbB receptor sub-type expression following hepatocyte isolation.

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Section: Resultsmentioning

confidence: 99%