The Experts below are selected from a list of 228 Experts worldwide ranked by ideXlab platform
Shigeo Yoshida - One of the best experts on this subject based on the ideXlab platform.
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A mammalian steroid action inhibitor Spironolactone retards plant growth by inhibition of brassinosteroid action and induces light-induced gene expression in the dark.
The Journal of Steroid Biochemistry and Molecular Biology, 2004Co-Authors: Tadao Asami, Yusuke Jikumaru, Yukihisa Shimada, Iriko Kaneko, Takeshi Nakano, Shigeo YoshidaAbstract:We screened steroid derivatives and found that Spironolactone, an inhibitor of both 17β-hydroxysteroid dehydrogenase (17β-HSD) and aldosterone receptor, is an inhibitor of phytohormone brassinosteroid (BR) action in plants. Under both dark and light growing conditions, Spironolactone induced morphological changes in Arabidopsis, characteristic of brassinosteroid-deficient mutants. Spironolactone-treated plants were also nearly restored to the wild-type phenotype by treatment with additional BRs. In the Spironolactone-treated Arabidopsis, the CPD gene in the BR biosynthesis pathway was up-regulated, probably due to feedback regulation caused by BR-deficiency. Spironolactone-treated tobacco plants grown in the dark showed expression of light-regulated genes as was observed in the deficient mutant. These data suggest that Spironolactone inhibits brassinosteroid action probably due to the blockage of biosynthesis and exerts its activity against plants. Thus, Spironolactone, in conjunction with brassinosteroid-deficient mutants, can be used to clarify the function of BRs in plants and characterize mutants. The Spironolactone action site was also investigated by feeding BR biosynthesis intermediates to Arabidopsis grown in the dark, and the results are discussed.
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A mammalian steroid action inhibitor Spironolactone retards plant growth by inhibition of brassinosteroid action and induces light-induced gene expression in the dark.
The Journal of steroid biochemistry and molecular biology, 2004Co-Authors: Tadao Asami, Yusuke Jikumaru, Yukihisa Shimada, Iriko Kaneko, Takeshi Nakano, Shigeo YoshidaAbstract:We screened steroid derivatives and found that Spironolactone, an inhibitor of both 17beta-hydroxysteroid dehydrogenase (17beta-HSD) and aldosterone receptor, is an inhibitor of phytohormone brassinosteroid (BR) action in plants. Under both dark and light growing conditions, Spironolactone induced morphological changes in Arabidopsis, characteristic of brassinosteroid-deficient mutants. Spironolactone-treated plants were also nearly restored to the wild-type phenotype by treatment with additional BRs. In the Spironolactone-treated Arabidopsis, the CPD gene in the BR biosynthesis pathway was up-regulated, probably due to feedback regulation caused by BR-deficiency. Spironolactone-treated tobacco plants grown in the dark showed expression of light-regulated genes as was observed in the deficient mutant. These data suggest that Spironolactone inhibits brassinosteroid action probably due to the blockage of biosynthesis and exerts its activity against plants. Thus, Spironolactone, in conjunction with brassinosteroid-deficient mutants, can be used to clarify the function of BRs in plants and characterize mutants. The Spironolactone action site was also investigated by feeding BR biosynthesis intermediates to Arabidopsis grown in the dark, and the results are discussed.
Byeongmoon Jeong - One of the best experts on this subject based on the ideXlab platform.
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drug release from biodegradable injectable thermosensitive hydrogel of peg plga peg triblock copolymers
Journal of Controlled Release, 2000Co-Authors: Byeongmoon JeongAbstract:Abstract An aqueous solution of newly developed low-molecular-weight PEG–PLGA–PEG triblock copolymers with a specific composition is a free flowing sol at room temperature but becomes a gel at body temperature. Two model drugs, ketoprofen and spironolatone, which have different hydrophobicities, were released from the PEG–PLGA–PEG triblock copolymer hydrogel formed in situ by injecting the solutions into a 37°C aqueous environment. Ketoprofen (a model hydrophilic drug) was released over 2 weeks with a first-order release profile, while Spironolactone (a model hydrophobic drug) was released over 2 months with an S-shaped release profile. The release profiles were simulated by models considering degradation and diffusion, and were better described by a model assuming a core-shell structure of the gel.
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drug release from biodegradable injectable thermosensitive hydrogel of peg plga peg triblock copolymers
Journal of Controlled Release, 2000Co-Authors: Byeongmoon JeongAbstract:Abstract An aqueous solution of newly developed low-molecular-weight PEG–PLGA–PEG triblock copolymers with a specific composition is a free flowing sol at room temperature but becomes a gel at body temperature. Two model drugs, ketoprofen and spironolatone, which have different hydrophobicities, were released from the PEG–PLGA–PEG triblock copolymer hydrogel formed in situ by injecting the solutions into a 37°C aqueous environment. Ketoprofen (a model hydrophilic drug) was released over 2 weeks with a first-order release profile, while Spironolactone (a model hydrophobic drug) was released over 2 months with an S-shaped release profile. The release profiles were simulated by models considering degradation and diffusion, and were better described by a model assuming a core-shell structure of the gel.
Tadao Asami - One of the best experts on this subject based on the ideXlab platform.
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A mammalian steroid action inhibitor Spironolactone retards plant growth by inhibition of brassinosteroid action and induces light-induced gene expression in the dark.
The Journal of Steroid Biochemistry and Molecular Biology, 2004Co-Authors: Tadao Asami, Yusuke Jikumaru, Yukihisa Shimada, Iriko Kaneko, Takeshi Nakano, Shigeo YoshidaAbstract:We screened steroid derivatives and found that Spironolactone, an inhibitor of both 17β-hydroxysteroid dehydrogenase (17β-HSD) and aldosterone receptor, is an inhibitor of phytohormone brassinosteroid (BR) action in plants. Under both dark and light growing conditions, Spironolactone induced morphological changes in Arabidopsis, characteristic of brassinosteroid-deficient mutants. Spironolactone-treated plants were also nearly restored to the wild-type phenotype by treatment with additional BRs. In the Spironolactone-treated Arabidopsis, the CPD gene in the BR biosynthesis pathway was up-regulated, probably due to feedback regulation caused by BR-deficiency. Spironolactone-treated tobacco plants grown in the dark showed expression of light-regulated genes as was observed in the deficient mutant. These data suggest that Spironolactone inhibits brassinosteroid action probably due to the blockage of biosynthesis and exerts its activity against plants. Thus, Spironolactone, in conjunction with brassinosteroid-deficient mutants, can be used to clarify the function of BRs in plants and characterize mutants. The Spironolactone action site was also investigated by feeding BR biosynthesis intermediates to Arabidopsis grown in the dark, and the results are discussed.
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A mammalian steroid action inhibitor Spironolactone retards plant growth by inhibition of brassinosteroid action and induces light-induced gene expression in the dark.
The Journal of steroid biochemistry and molecular biology, 2004Co-Authors: Tadao Asami, Yusuke Jikumaru, Yukihisa Shimada, Iriko Kaneko, Takeshi Nakano, Shigeo YoshidaAbstract:We screened steroid derivatives and found that Spironolactone, an inhibitor of both 17beta-hydroxysteroid dehydrogenase (17beta-HSD) and aldosterone receptor, is an inhibitor of phytohormone brassinosteroid (BR) action in plants. Under both dark and light growing conditions, Spironolactone induced morphological changes in Arabidopsis, characteristic of brassinosteroid-deficient mutants. Spironolactone-treated plants were also nearly restored to the wild-type phenotype by treatment with additional BRs. In the Spironolactone-treated Arabidopsis, the CPD gene in the BR biosynthesis pathway was up-regulated, probably due to feedback regulation caused by BR-deficiency. Spironolactone-treated tobacco plants grown in the dark showed expression of light-regulated genes as was observed in the deficient mutant. These data suggest that Spironolactone inhibits brassinosteroid action probably due to the blockage of biosynthesis and exerts its activity against plants. Thus, Spironolactone, in conjunction with brassinosteroid-deficient mutants, can be used to clarify the function of BRs in plants and characterize mutants. The Spironolactone action site was also investigated by feeding BR biosynthesis intermediates to Arabidopsis grown in the dark, and the results are discussed.
Takeshi Nakano - One of the best experts on this subject based on the ideXlab platform.
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A mammalian steroid action inhibitor Spironolactone retards plant growth by inhibition of brassinosteroid action and induces light-induced gene expression in the dark.
The Journal of Steroid Biochemistry and Molecular Biology, 2004Co-Authors: Tadao Asami, Yusuke Jikumaru, Yukihisa Shimada, Iriko Kaneko, Takeshi Nakano, Shigeo YoshidaAbstract:We screened steroid derivatives and found that Spironolactone, an inhibitor of both 17β-hydroxysteroid dehydrogenase (17β-HSD) and aldosterone receptor, is an inhibitor of phytohormone brassinosteroid (BR) action in plants. Under both dark and light growing conditions, Spironolactone induced morphological changes in Arabidopsis, characteristic of brassinosteroid-deficient mutants. Spironolactone-treated plants were also nearly restored to the wild-type phenotype by treatment with additional BRs. In the Spironolactone-treated Arabidopsis, the CPD gene in the BR biosynthesis pathway was up-regulated, probably due to feedback regulation caused by BR-deficiency. Spironolactone-treated tobacco plants grown in the dark showed expression of light-regulated genes as was observed in the deficient mutant. These data suggest that Spironolactone inhibits brassinosteroid action probably due to the blockage of biosynthesis and exerts its activity against plants. Thus, Spironolactone, in conjunction with brassinosteroid-deficient mutants, can be used to clarify the function of BRs in plants and characterize mutants. The Spironolactone action site was also investigated by feeding BR biosynthesis intermediates to Arabidopsis grown in the dark, and the results are discussed.
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A mammalian steroid action inhibitor Spironolactone retards plant growth by inhibition of brassinosteroid action and induces light-induced gene expression in the dark.
The Journal of steroid biochemistry and molecular biology, 2004Co-Authors: Tadao Asami, Yusuke Jikumaru, Yukihisa Shimada, Iriko Kaneko, Takeshi Nakano, Shigeo YoshidaAbstract:We screened steroid derivatives and found that Spironolactone, an inhibitor of both 17beta-hydroxysteroid dehydrogenase (17beta-HSD) and aldosterone receptor, is an inhibitor of phytohormone brassinosteroid (BR) action in plants. Under both dark and light growing conditions, Spironolactone induced morphological changes in Arabidopsis, characteristic of brassinosteroid-deficient mutants. Spironolactone-treated plants were also nearly restored to the wild-type phenotype by treatment with additional BRs. In the Spironolactone-treated Arabidopsis, the CPD gene in the BR biosynthesis pathway was up-regulated, probably due to feedback regulation caused by BR-deficiency. Spironolactone-treated tobacco plants grown in the dark showed expression of light-regulated genes as was observed in the deficient mutant. These data suggest that Spironolactone inhibits brassinosteroid action probably due to the blockage of biosynthesis and exerts its activity against plants. Thus, Spironolactone, in conjunction with brassinosteroid-deficient mutants, can be used to clarify the function of BRs in plants and characterize mutants. The Spironolactone action site was also investigated by feeding BR biosynthesis intermediates to Arabidopsis grown in the dark, and the results are discussed.
Iriko Kaneko - One of the best experts on this subject based on the ideXlab platform.
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A mammalian steroid action inhibitor Spironolactone retards plant growth by inhibition of brassinosteroid action and induces light-induced gene expression in the dark.
The Journal of Steroid Biochemistry and Molecular Biology, 2004Co-Authors: Tadao Asami, Yusuke Jikumaru, Yukihisa Shimada, Iriko Kaneko, Takeshi Nakano, Shigeo YoshidaAbstract:We screened steroid derivatives and found that Spironolactone, an inhibitor of both 17β-hydroxysteroid dehydrogenase (17β-HSD) and aldosterone receptor, is an inhibitor of phytohormone brassinosteroid (BR) action in plants. Under both dark and light growing conditions, Spironolactone induced morphological changes in Arabidopsis, characteristic of brassinosteroid-deficient mutants. Spironolactone-treated plants were also nearly restored to the wild-type phenotype by treatment with additional BRs. In the Spironolactone-treated Arabidopsis, the CPD gene in the BR biosynthesis pathway was up-regulated, probably due to feedback regulation caused by BR-deficiency. Spironolactone-treated tobacco plants grown in the dark showed expression of light-regulated genes as was observed in the deficient mutant. These data suggest that Spironolactone inhibits brassinosteroid action probably due to the blockage of biosynthesis and exerts its activity against plants. Thus, Spironolactone, in conjunction with brassinosteroid-deficient mutants, can be used to clarify the function of BRs in plants and characterize mutants. The Spironolactone action site was also investigated by feeding BR biosynthesis intermediates to Arabidopsis grown in the dark, and the results are discussed.
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A mammalian steroid action inhibitor Spironolactone retards plant growth by inhibition of brassinosteroid action and induces light-induced gene expression in the dark.
The Journal of steroid biochemistry and molecular biology, 2004Co-Authors: Tadao Asami, Yusuke Jikumaru, Yukihisa Shimada, Iriko Kaneko, Takeshi Nakano, Shigeo YoshidaAbstract:We screened steroid derivatives and found that Spironolactone, an inhibitor of both 17beta-hydroxysteroid dehydrogenase (17beta-HSD) and aldosterone receptor, is an inhibitor of phytohormone brassinosteroid (BR) action in plants. Under both dark and light growing conditions, Spironolactone induced morphological changes in Arabidopsis, characteristic of brassinosteroid-deficient mutants. Spironolactone-treated plants were also nearly restored to the wild-type phenotype by treatment with additional BRs. In the Spironolactone-treated Arabidopsis, the CPD gene in the BR biosynthesis pathway was up-regulated, probably due to feedback regulation caused by BR-deficiency. Spironolactone-treated tobacco plants grown in the dark showed expression of light-regulated genes as was observed in the deficient mutant. These data suggest that Spironolactone inhibits brassinosteroid action probably due to the blockage of biosynthesis and exerts its activity against plants. Thus, Spironolactone, in conjunction with brassinosteroid-deficient mutants, can be used to clarify the function of BRs in plants and characterize mutants. The Spironolactone action site was also investigated by feeding BR biosynthesis intermediates to Arabidopsis grown in the dark, and the results are discussed.
