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- W1978600980 abstract "ABSTRACT This study was designed to investigate the mechanism of antiprogestational action of synthetic steroids, danazol (17α-hydroxy-pregn-4-en-20-yno [2,3-d] isoxazol-17-ol) and R2323 (13β-ethyl-17α-hydroxy-18,19-dinor-17α-pregna-4,9,11-trien-20-yn-3-one). Oestrogen primed rabbit uteri were used for this study. The sucrose gradient analysis in the supernatant of 248 000 x g (max.) of the uterine homogenate showed that progesterone8S binding was inhibited by each of the synthetic steroid, and the kinetic study revealed that each steroid was a competitive inhibitor, where Kd of progesterone-protein binding was 8.1 × 10 −10 m , Ki of danazol-protein binding was 2.7 × 10 −8 m and Ki of R2323-protein binding was 6.6 × 10 −9 m . These results indicate that these synthetic steroids bind to progesterone receptor with moderate binding affinities. The modified Anderson's exchange assay of nuclear receptor demontrated that danazol- or R2323-receptor complex can enter into the uterine nuclei in a lesser degree than does progesterone-receptor complex. RNA synthesis by the uterine chromatin was stimulated if the progesterone-receptor complex was added, but this stimulation was inhibited by addition of danazol or R2323. The chromatin RNA transcription was not induced by danazol- or R2323-receptor complex. These results suggest that such a synthetic steroid binds to a progesterone receptor, and the steroid-receptor complex enters into the nucleus but does not activate the chromatin template, thus resulting in the antiprogesational effect." @default.
- W1978600980 created "2016-06-24" @default.
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- W1978600980 date "1978-05-01" @default.
- W1978600980 modified "2023-09-27" @default.
- W1978600980 title "MECHANISM OF ANTIPROGESTATIONAL ACTION OF SYNTHETIC STEROIDS" @default.
- W1978600980 doi "https://doi.org/10.1530/acta.0.0880190" @default.
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