We propose that HNF3 represses AFP promoter activity through indirect mechanisms that modulate the binding or activity of a liver-enriched factor that interacts with the -165 region of the AFP promoter. EMSA analyses using in vivo and in vitro synthesized proteins indicate that HNF3 proteins do not bind DNA from the -205 to -150 region. The repression is abolished by a mutation that is centered at -165. Furthermore, this fragment can confer HNF3-mediated repression on a heterologous promoter. This repression is governed by the region between -205 and -150. We show here that the AFP promoter is dramatically repressed by HNF3 in HepG2 hepatoma cells. The repression is governed, at least in part, by the 250 base pair (bp) AFP promoter. We propose that HNF3 represses AFP promoter activity through indirect mechanisms that modulate the binding or activity of a liver-enriched factor that interacts with the -165 region of the AFP promoter.ĪB - The mouse alpha-fetoprotein gene is expressed at high levels in the fetal liver and is transcriptionally silenced at birth. The AFP blood test is called MSAFP (maternal. AFP is a protein normally produced by the fetal liver and is present in the fluid surrounding the fetus (amniotic fluid), and crosses the placenta into the mother's blood. Furthermore, this fragment can confer HNF3-mediated repression on a heterologous promoter. Alpha-fetoprotein screening is a blood test that measures the level of alpha-fetoprotein in the mothers' blood during pregnancy. N2 - The mouse alpha-fetoprotein gene is expressed at high levels in the fetal liver and is transcriptionally silenced at birth. T1 - The mouse alpha-fetoprotein promoter is repressed in HepG2 hepatoma cells by hepatocyte nuclear factor-3 (FOXA)
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