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   <subfield code="a">Specificity of androgen resistance in Mus caroli kidney</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Carol Wilson, Debora Kimberlin, James Griffin, Jean Wilson]</subfield>
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   <subfield code="a">Androgen controls the expression of β-glucuronidase and several other proteins in the kidney of the standard laboratory mouse,Mus musculus. Other species within the genusMus exhibit a variety of response patterns for kidney β-glucuronidase and other markers of androgen action. We have investigated the mechanism of androgen action inM. caroli, aMus species that does not produce β-glucuronidase in response to testosterone. The failure of testosterone to induce β-glucuronidase inM. caroli females cannot be overcome by treatment with dihydrotestosterone, with pharmacological doses of testosterone propionate or dihydrotestosterone propionate, or with a variety of potent androgen analogues. All of these compounds induce kidney β-glucuronidase inM. musculus females and kidney ornithine decarboxylase, submandibular gland renin, and submandibular gland epidermal growth factor in bothM. caroli andM. musculus females. Furthermore, kidney androgen receptor proteins fromM. caroli andM. musculus animals have the same sedimentation characteristics on sucrose density gradients. These data indicate that androgen resistance inM. caroli is not due to deficient 5α-reductase or aberrant hormone metabolism producing suboptimal levels of functional androgen and is not caused by a defective androgen receptor. They suggest that the resistance of β-glucuronidase inM. caroli kidney to induction by androgen occurs at the level of the β-glucuronidase gene.</subfield>
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   <subfield code="a">Mus caroli</subfield>
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