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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Molecular and Cellular Endocrinology 104 (1994), S. 173-181 
    ISSN: 0303-7207
    Keywords: Estrogen ; Estrogen responsive element ; Gene expression ; Hepatocyte growth factor (HGF) ; Mouse ovary
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Molecular genetics and genomics 255 (1997), S. 533-542 
    ISSN: 1617-4623
    Keywords: Key wordsSaccharomyces cerevisiae ; DNA damage induction ; Gene expression ; cis-acting element ; Transcriptional regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract MAG1 and DDI1 are two divergently transcribed DNA damage-inducible genes from Saccharomyces cerevisiae. Previous studies have shown that MAG1 induction requires an upstream activating site (UAS) located between nucleotides −376 and −330. Here we show that a 24-bp oligonucleotide from within the UAS MAG1 region forms a sequence-specific DNA-protein complex with partially purified proteins from S. cerevisiae. Point mutations introduced into the 24-bp oligonucleotide inhibited the formation of the DNA-protein complex and decreased the level of induction of MAG1-lacZ. By determining the transcription and translation start points of both MAG1 and DDI1, an interesting, indeed unprecedented feature of genome organization in eukaryotes was revealed: UAS MAG1 actually lies within the protein-coding region of DDI1. Although tightly linked to each other, and co-induced upon treatment with DNA-damaging agents, DDI1 does not share the UAS MAG1 required for DNA damage induction of MAG1. Furthermore, MAG1 and DDI1 respond differently in the presence of the protein synthesis inhibitor cycloheximide, suggesting that these two genes are regulated by different mechanisms in the absence of de novo protein synthesis.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Keywords: Angiotensin I-converting enzyme ; Gene expression ; Sodium chloride ; Heart ; Inbred rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have recently shown that the angiotensin I converting enzyme (ACE) gene is linked to NaCl-loaded blood pressure in the stroke-prone spontaneously hypertensive rat (SHRSP), and that high-NaCl loading selectively stimulates ACE in the aorta of SHRSP but not in normotensive Wistar-Kyoto (WKY) rats. We therefore investigated the relationship between cardiac ACE and the development of hypertension and left ventricular hypertrophy in response to normal- and high-NaCl diet in these rats. ACE mRNA and ACE activity were measured in left ventricular tissue after completion of hemodynamic characterization of the animals. While SHRSP rats increased blood pressure (P〈0.0001) and heart rate (P〈0.005) in response to high NaCl, blood pressure remained unchanged in WKY. Similarly, relative left ventricular weight increased only in SHRSP after high NaCl (P〈0.002). A significant two- to threefold increase of cardiac ACE mRNA and fourfold stimulation of ACE enzyme activity in response to high NaCl was found in both WKY and SHRSP rats (P〈0.005). The induction of ACE gene expression was significantly more pronounced in SHRSP compared to WKY (P〈0.02), whereas no significant strain differences in left ventricular ACE activity were found after either normal- or high-NaCl diet. Thus, arterial blood pressure and left ventricular weight remained unchanged in the WKY rats despite the activation of left ventricular ACE activity after high-NaCl exposure. These results demonstrate that left ventricular ACE activity is equally upregulated in response to high-NaCl in the normotensive and hypertensive strain, independently from the development of hypertension. We conclude that the pretranslational induction of left ventricular ACE with high-NaCl loading may be important both for the regulation of cardiac angiotensins and kinins and for local therapeutic ACE inhibition in the heart during high-salt status.
    Type of Medium: Electronic Resource
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