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  • 1
    ISSN: 1573-4927
    Schlagwort(e): β-glucuronidase ; gene regulation ; response to androgen ; response to estrogen ; regulatory locus
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Chemie und Pharmazie
    Notizen: Abstract Both enzyme activity and mRNA concentration of β-glucuronidase were measured in kidneys of mice treated with testosterone and the synthetic estrogen, diethylstilbestrol. Six congenic strains, all having a C57BL6/J genetic background but each having a different haplotype of the β-glucuronidase gene complex, were compared. In each strain the induction caused by androgen was partially repressed by estrogen. The extent of this antagonism varied among the six haplotypes and was not coordinate with the extent of induction by androgen alone. Antagonism appears to be regulated by at least two alleles of a new locus,Gus-e, within the β-glucuronidase gene complex. Repression by estrogen, like induction by androgen, appears to take place primarily at the transcriptional level. Kinetic studies revealed that estrogen causes the androgen response curve to plateau earlier and at a lower level. This suggests that estrogen increases the rate of gene deactivation rather than decreasing the rate of gene activation, Isoelectric focusing of β-glucuronidase fromGus-e a andGus-e b mice and their F1 progeny revealed that the genes are regulated incis. Together, these findings support a model in which both sex hormones exert their effects on separate DNA response elements located in close proximity to the gene or within the gene itself.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 1573-4927
    Schlagwort(e): β-glucuronidase ; gene regulation ; response to androgen ; response to estrogen ; regulatory locus
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Chemie und Pharmazie
    Notizen: Abstract Both enzyme activity and mRNA concentration of β-glucuronidase were measured in kidneys of mice treated with testosterone and the synthetic estrogen, diethylstilbestrol. Six congenic strains, all having a C57BL6/J genetic background but each having a different haplotype of the β-glucuronidase gene complex, were compared. In each strain the induction caused by androgen was partially repressed by estrogen. The extent of this antagonism varied among the six haplotypes and was not coordinate with the extent of induction by androgen alone. Antagonism appears to be regulated by at least two alleles of a new locus,Gus-e, within the β-glucuronidase gene complex. Repression by estrogen, like induction by androgen, appears to take place primarily at the transcriptional level. Kinetic studies revealed that estrogen causes the androgen response curve to plateau earlier and at a lower level. This suggests that estrogen increases the rate of gene deactivation rather than decreasing the rate of gene activation, Isoelectric focusing of β-glucuronidase fromGus-e a andGus-e b mice and their F1 progeny revealed that the genes are regulated incis. Together, these findings support a model in which both sex hormones exert their effects on separate DNA response elements located in close proximity to the gene or within the gene itself.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 3
    Digitale Medien
    Digitale Medien
    Chichester [u.a.] : Wiley-Blackwell
    Developmental Genetics 2 (1981), S. 269-277 
    ISSN: 0192-253X
    Schlagwort(e): β-glucuronidase ; androgen ; receptor ; development ; mouse ; kidney ; Life and Medical Sciences ; Genetics
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie
    Notizen: During postnatal development of mouse kidney the androgen responsiveness of epithelial cells for β-glucuronidase induction, cellular hypertrophy, and other enzyme inductions appears coincidentally with a rise in androgen receptor protein. Initially, a low level of receptor is present but no response is seen. Beginning at about 12 days of age responsiveness begins to increase, reaches a half-maximal level at 18-20 days, and full responsiveness by 28-30 days. The limiting factor appears to be levels of androgen receptor protein.Our experiments shed no light on the question of why each androgen responsive cell type in the organism differentiates the capacity to induce a different array of proteins. However, they do suggest that responsiveness of the β-glucuronidase gene does not appear until a minimum threshold level of receptor is exceeded, and that the response of the gene may not be saturated even at the highest levels of receptor reached.
    Zusätzliches Material: 5 Ill.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 4
    Digitale Medien
    Digitale Medien
    Chichester [u.a.] : Wiley-Blackwell
    Developmental Genetics 5 (1984), S. 83-91 
    ISSN: 0192-253X
    Schlagwort(e): temporal genes ; acid hydrolases ; liver ; mice ; hepatocytes ; nonhepatocytes ; Life and Medical Sciences ; Genetics
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie
    Notizen: The cell specificity of expression of three distinct trans acting temporal gene systems determining the developmental control of α-galactosidase, β-galactosidase and β-glucuronidase was tested in mouse liver. For α-galactosidase and β-galactosidase, expression was limited to hepatocytes; no effect was seen in nonhepatocytes. For β-glucuronidase the data suggest that expression of the Gus-t temporal locus is also limited to hepatocytes, and that the smaller enzyme reduction seen in nonhepatocytes of some strains is due to a separate systemic regulatory locus that is also present in the [Gus] gene complex. We conclude that the temporal gene-determined timing mechanisms initiating switches in rates of enzyme synthesis are intrinsic to the cells themselves and are not communicated to adjacent cells. This conclusion applies to the temporal locus for β-glucuronidase that is proximate to its structural gene as well as those for α-galactosidase and β-galactosidase that are distant from the structural genes that they regulate.
    Zusätzliches Material: 5 Tab.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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